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[Senate Hearing 107-628]
[From the U.S. Government Publishing Office]

                                                        S. Hrg. 107-628
 
                       ALZHEIMER'S DISEASE, 2002
=======================================================================

                                HEARING

                                before a

                          SUBCOMMITTEE OF THE

            COMMITTEE ON APPROPRIATIONS UNITED STATES SENATE

                      ONE HUNDRED SEVENTH CONGRESS

                             SECOND SESSION

                               __________

                            SPECIAL HEARING

                     APRIL 30, 2002--WASHINGTON, DC

                               __________

         Printed for the use of the Committee on Appropriations

 Available via the World Wide Web: http://www.access.gpo.gov/congress/
                                 senate

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                                 ______
                      COMMITTEE ON APPROPRIATIONS

                ROBERT C. BYRD, West Virginia, Chairman
DANIEL K. INOUYE, Hawaii             TED STEVENS, Alaska
ERNEST F. HOLLINGS, South Carolina   THAD COCHRAN, Mississippi
PATRICK J. LEAHY, Vermont            ARLEN SPECTER, Pennsylvania
TOM HARKIN, Iowa                     PETE V. DOMENICI, New Mexico
BARBARA A. MIKULSKI, Maryland        CHRISTOPHER S. BOND, Missouri
HARRY REID, Nevada                   MITCH McCONNELL, Kentucky
HERB KOHL, Wisconsin                 CONRAD BURNS, Montana
PATTY MURRAY, Washington             RICHARD C. SHELBY, Alabama
BYRON L. DORGAN, North Dakota        JUDD GREGG, New Hampshire
DIANNE FEINSTEIN, California         ROBERT F. BENNETT, Utah
RICHARD J. DURBIN, Illinois          BEN NIGHTHORSE CAMPBELL, Colorado
TIM JOHNSON, South Dakota            LARRY CRAIG, Idaho
MARY L. LANDRIEU, Louisiana          KAY BAILEY HUTCHISON, Texas
JACK REED, Rhode Island              MIKE DeWINE, Ohio
                  Terrence E. Sauvain, Staff Director
                 Charles Kieffer, Deputy Staff Director
               Steven J. Cortese, Minority Staff Director
            Lisa Sutherland, Minority Deputy Staff Director
                                 ------                                

 Subcommittee on Departments of Labor, Health and Human Services, and 
                    Education, and Related Agencies

                       TOM HARKIN, Iowa, Chairman
ERNEST F. HOLLINGS, South Carolina   ARLEN SPECTER, Pennsylvania
DANIEL K. INOUYE, Hawaii             THAD COCHRAN, Mississippi
HARRY REID, Nevada                   JUDD GREGG, New Hampshire
HERB KOHL, Wisconsin                 LARRY CRAIG, Idaho
PATTY MURRAY, Washington             KAY BAILEY HUTCHISON, Texas
MARY L. LANDRIEU, Louisiana          TED STEVENS, Alaska
ROBERT C. BYRD, West Virginia        MIKE DeWINE, Ohio
                           Professional Staff
                              Ellen Murray
                              Jim Sourwine
                              Mark Laisch
                            Adrienne Hallett
                              Erik Fatemi
                       Bettilou Taylor (Minority)
                        Mary Dietrich (Minority)
                    Sudip Shrikant Parikh (Minority)
                       Candice Rogers (Minority)

                         Administrative Support
                             Carole Geagley

                            C O N T E N T S

                              ----------                              
                                                                   Page

Opening statement of Senator Tom Harkin..........................     1
Opening statement of Senator Arlen Specter.......................     2
Statement of Richard J. Hodes, M.D., Director, National Institute 
  on Aging, National Institutes of Health, Department of Health 
  and Human Services.............................................     3
    Prepared statement...........................................     5
Statement of Orien Reid, Chair, board of directors, Alzheimer's 
  Association....................................................    11
    Prepared statement...........................................    13
Statement of Marilyn Albert, Ph.D., Chair, Medical and Scientific 
  Advisory Committee, Alzheimer's Association....................    15
    Prepared statement...........................................    16
Statement of Carol Gratz, New Hampton, IA, East Central Iowa 
  Chapter, Alzheimer's Association...............................    19
Statement of Gene Gratz, New Hampton, IA, East Central Iowa 
  Chapter, Alzheimer's Association...............................    21
    Prepared statement...........................................    21
Statement of David Hyde Pierce, actor............................    23
    Prepared statement...........................................    24

                       ALZHEIMER'S DISEASE, 2002

                              ----------                              

                        TUESDAY, APRIL 30, 2002

                           U.S. Senate,    
    Subcommittee on Labor, Health and Human
     Services, and Education, and Related Agencies,
                               Committee on Appropriations,
                                                    Washington, DC.
    The subcommittee met at 9:09 a.m., in room SD-106, Dirksen 
Senate Office Building, Hon. Tom Harkin (chairman) presiding.
    Present: Senators Harkin and Specter.

                opening statement of senator tom harkin

    Senator Harkin. The hearing of the Senate Labor, Health and 
Human Services, and Education Appropriations Subcommittee will 
come to order. I welcome everyone here this morning. I thank 
you for the tremendous turnout.
    This is the third year in a row that this subcommittee has 
held a hearing on Alzheimer's disease specifically, either with 
me as chairman or my friend Arlen Specter. I think that is as 
clear a sign as any that there are no party lines when it comes 
to preventing and curing Alzheimer's. This is an equal 
opportunity disease, striking men and women of all races and 
all backgrounds, so it is fitting that Democrats and 
Republicans have worked arm in arm to confront it.
    The fact that we have held so many hearings on Alzheimer's 
also shows how urgently we need answers. A poll released this 
morning shows that 57 percent of Americans are personally 
worried about getting this disease, and for good reason. There 
are currently 4 million people in the United States with 
Alzheimer's and by the year 2050 that number is expected to 
rise to about 14 million. We will be paying $357 billion a year 
in health care costs. That is, unless science can find a way to 
prevent or delay this disease.
    Fortunately, thanks in large part to this subcommittee's 
effort to double funding at NIH, led by Senator Specter and me, 
that goal is in sight. Researchers are finally closing in on 
what causes Alzheimer's. They are using cutting-edge brain 
imaging to figure out how to diagnose it, and they are studying 
everything from folic acid and statins to Advil and gingko 
biloba to see if any of these drugs and supplements can help 
delay it.
    On another front, this Nation has finally recognized the 
importance of family caregivers in helping people with 
Alzheimer's. This disease takes an enormous toll on caregivers, 
not only financially but also emotionally and physically. This 
subcommittee funds two programs to address this need, the 
Family Caregiver Support Program and the Alzheimer's Matching 
Grant Program, and we will continue to give them high priority.
    We are fortunate to have an outstanding panel of witnesses 
here today to discuss these issues. I of course extend a 
special welcome to Carol and Gene Gratz of New Hampton, Iowa. 
It takes a lot of time and courage to come to Washington and 
prepare for a hearing like this, and I want to thank you and 
Kris for being here and for helping remind us what it means to 
battle Alzheimer's and what is involved in caring for a loved 
one who has been stricken with this disease.
    This same goes for the hundreds of patients, family 
members, and friends in the audience, who are here as part of 
the Alzheimer's Association's Capitol Hill Day. Your personal 
stories are worth more than a hundred statistics to Senators 
and Congressmen that you visit today. I commend you for your 
advocacy. We need you here and we need you talking to all of 
your Congressmen and Senators here in Washington.
    So before we turn to our witnesses, I would yield to my 
colleague, the ranking member, Senator Specter, for his opening 
remarks.

               opening statement of senator arlen specter

    Senator Specter. Thank you very much, Mr. Chairman, and 
thank you for your leadership on the effort to cure Alzheimer's 
and on matters of medical treatment in general.
    Thank you, ladies and gentlemen, for coming here today. 
This kind of an outpouring of support in one of the Senate's 
biggest hearing rooms is noted in this city and this country 
and really around the world.
    I thank the Pennsylvania Alzheimer's Association for the 
Humanitarian Award which I received in this room at the outset 
of the session. It was interesting to pose for a moment or two 
for a so-called photo op. I did not realize there were so many 
cameras in the audience. It is just too bad we cannot take 
enough time to have everyone photographed individually with 
Senator Harkin----
    Senator Harkin. So goes life.
    Senator Specter [continuing]. And I might sneak into the 
corner of a picture or two. But we have very, very important 
work to do.
    Senator Harkin has noted that he and I and this 
subcommittee, have led the fight on increasing funding for the 
National Institutes of Health and Alzheimer's. When we started 
our effort to double the NIH funding, we asked the Budget 
Committee for $1 billion, were turned down, took it to the 
floor, and lost 63 to 37. So Tom and I got out our sharp 
pencils and found $1 billion among the priorities.
    Having lost on our effort to increase the funding by $1 
billion, and then the next year we asked for $2 billion. That 
is the way things are done in Washington. We got turned down 
again, and once again we found the money as a matter of 
priorities.
    On this last vote it was 96 to 4 in favor of increasing NIH 
funding. Through the leadership of this subcommittee, the 
funding has almost doubled from $12 billion to $23 billion. 
This year President Bush has taken the lead in asking for $3.4 
billion more. So you can see we are on the move.
    Last year Alzheimer's was funded at almost $600 million, 
and this year we are looking for $650 million. I know that you 
ladies and gentlemen are looking for $1 billion and, frankly, 
so are we.
    I regret that I cannot be present at the news conference 
later. Today happens to be an exceptionally busy day. They are 
all busy days around here, but today is an exceptionally busy 
day because we are going to introduce legislation that will 
allow nuclear transplantation. Some people call it therapeutic 
cloning, but that is a misnomer because it gives the impression 
that it is cloning. Everybody is against reproductive cloning. 
You certainly would not want to create another Arlen Specter. 
But if you wanted to create another Tom Harkin, then there 
would be an argument, an argument in favor.
    But very, very seriously, since stem cells came upon the 
scene in November 1998 this subcommittee has held a series of 
hearings, 14 in number, to encourage their use because they can 
be inserted into the brain, and perhaps will be the ultimate 
answer to Alzheimer's. Now with this nuclear transplantation 
there is a procedure so that a person suffering from 
Alzheimer's, Parkinson's, or other maladies, will not reject 
the cells.
    We have got a tough fight on our hands because there are 
people who want to criminalize cell transplantation. Later this 
morning we are going to be having a news conference and I am 
going to have to excuse myself at about 10 o'clock to attend 
that conference. However, Senator Harkin and I are blessed with 
fellow Senators here, Senator Taylor, Senator Ellen, and I will 
be following very closely what we are doing here and fighting 
very hard to move toward that billion dollars for Alzheimer's 
and more funding for NIH.
    Thank you all for being here and for your battle. Thank 
you, Mr. Chairman. Thank you, Senator Specter.
STATEMENT OF RICHARD J. HODES, M.D., DIRECTOR, NATIONAL 
            INSTITUTE ON AGING, NATIONAL INSTITUTES OF 
            HEALTH, DEPARTMENT OF HEALTH AND HUMAN 
            SERVICES
    Senator Harkin. Our first witness this morning will be Dr. 
Richard Hodes. Dr. Hodes, if you could take the witness table, 
please. Dr. Hodes is the Director of the National Institute on 
Aging, the lead Institute at NIH on Alzheimer's disease. Dr. 
Hodes received his bachelor's degree from Yale University, his 
M.D. from Harvard. He held numerous posts in the National 
Cancer Institute before being named Director of the National 
Institute on Aging in 1993.
    Dr. Hodes has testified several times before this 
subcommittee. We certainly welcome him back. So Dr. Hodes, we 
have your written testimony. It will be made a part of the 
record in its entirety. If you could sum it up for us, I would 
certainly appreciate it.
    Dr. Hodes. Thank you, Mr. Chairman, Senator Specter. It is 
a privilege to be back before this committee once more, joining 
the Alzheimer's Association and all present here. I will take 
these few minutes to summarize for you the progress in 
Alzheimer's research over the past year. The chairman has 
adequately summarized the magnitude of the problem and the 
urgency that faces us and the Nation with an increased number 
of older people at risk for Alzheimer's disease.
    The very positive news is that progress over the past years 
has been extraordinary. I use the one figure that is in the 
written testimony as well to illustrate the nature of the 
process by which basic discovery is translated into application 
for clinical interventions. Over the past year research on risk 
factors for Alzheimer's disease has made important progress. 
Some of the progress was again enumerated in the introduction 
and has identified factors such as high cholesterol, blood 
pressure, high homocysteine levels, factors which we are used 
to thinking of as risk factors for cardiovascular disease and 
which also appear to be risk factors for Alzheimer's.
    The importance of this identification is that it provides 
targets for modifiable risk factors, and then in fact these are 
translated into clinical prevention trials currently underway.
    Similarly, the discovery of Alzheimer's genes has provided 
great clues into the mechanisms underlying that process. We 
have now identified three genes which are responsible for the 
early onset familial forms of Alzheimer's, as well as one gene, 
APOE4, that appears to be a risk factor for the common variety 
of that disease. In the past year it has become evident that an 
additional four genes are likely to be involved in Alzheimer's 
and their identification and characterization will again 
provide new targets for intervention.
    Imaging has allowed us for the first time to identify 
changes in the brain at most early stages, and this is an 
advance that is critical if we are going to learn how to 
intervene before irreparable damage has been done to the brain 
and to follow the effect of therapies by looking at changes in 
brain structure and function through these imaging techniques.
    The past years have provided for the first time animal 
experimental models of Alzheimer's, which again have proved 
extraordinarily useful in identifying the mechanisms that 
mediate the disease and providing ways to test therapies in 
animal models before their introduction to humans, once 
identified as being promising and safe. This currently leads to 
the translation of the information about secretases, for 
example, the proteins which are important in generating the 
plaques that characterize Alzheimer's disease, and drugs to 
inhibit the formation of these amyloid peptides, as well as 
what you have heard about before, the use of some immunologic 
approaches to try to clear or prevent the formation of the 
lesions that characterize Alzheimer's disease.
    These all pass through stages of drug development, 
preclinical testing, and into clinical trials. Whereas a few 
years ago there were no trials that were targeted at 
intervening to prevent rather than treat disease, we are now 
supporting 18 major clinical trials, 7 of which are 
preventions.
    Overall, these past years have seen extraordinary progress. 
As recently as 15 years ago, we knew essentially nothing about 
the genetics or underlying molecular basis for Alzheimer's 
disease. Now we have an extensive knowledge that has been 
translated into useful information.
    As recently as 10 years ago, we knew very little about the 
early risk factors and our ability to identify early stages of 
Alzheimer's through imaging was really in its infancy. Over the 
past 5 years only have we been able to translate this into 
prevention studies. In the past year alone, we have learned 
through animal models to recreate ever more valid and 
legitimate experimental systems which mimic both the anatomic 
lesions and the memory deficit of Alzheimer's disease, and 
these again have provided new and increasing opportunities for 
intervention.

                           prepared statement

    We have a promise beyond what we expected a few years ago 
and as we continue in this promise to prevent and treat 
Alzheimer's disease we continue as well to recognize the need 
to care for those with Alzheimer's and those many caregivers 
who are also affected, and so research on trying to ease the 
burden to caregivers as well as the present quality of life of 
those afflicted is a part of our research agenda as well.
    Again, I thank you for the opportunity once more to appear 
before you and look forward to answering questions that you 
might have. Thank you.
    [The statement follows:]
               Prepared Statement of Dr. Richard J. Hodes
    Senator Harkin and Members of the Committee: Thank you for inviting 
me to appear before you today to discuss Alzheimer's disease (AD), an 
issue of interest and concern to us all. I am Dr. Richard Hodes, 
Director of the National Institute on Aging (NIA), the lead federal 
agency for Alzheimer's disease research. I am delighted to be here this 
morning to tell you about the progress we are making toward 
understanding, treating, and preventing AD.
    As you know, AD is a major public health issue for the United 
States, and it has a devastating impact on individuals, families, the 
health care system, and society as a whole. Approximately 4 million 
Americans are currently battling the disease, with annual costs 
estimated to exceed $100 billion. Moreover, the rapid aging of the 
American population threatens to increase this burden several-fold in 
the coming decades. However, despite the grim statistics, we have made, 
and are making, tremendous progress.
    Until very recently, preventing or curing AD was considered, at 
best, a distant possibility. Our understanding of AD's underlying 
biology was limited, and for this reason it was difficult even to 
predict what might be effective as a treatment or preventive.
    Today, the picture is considerably brighter. Through laboratory and 
population-based scientific studies, we have identified a number of 
risk factors for AD, including both genetic and possible lifestyle 
factors. Research supported by the NIA, the National Institute of 
Neurological Disorders and Stroke (NINDS), and the National Institute 
of Mental Health (NIMH) has identified several genes that can cause AD, 
thereby helping us identify pathways affecting its development or 
progression, which will lead to better molecular predictors of the 
disease even before it is clinically apparent. The development and 
refinement of powerful imaging techniques that target anatomical, 
molecular, and functional processes in the brain will give us an 
improved ability to diagnose AD early, while the patient can still take 
an active role in decision-making. These techniques, along with better 
neuropsychological tests, are also enabling us to identify people who 
are at very high risk of one day developing the disease and to 
determine just how the disease starts in brain. This knowledge, in 
turn, may allow early intervention in persons long before the disease 
affects their level of functioning.
    Most importantly, we are making significant advances toward 
effectively treating, or even preventing, AD. NIA is currently 
supporting 18 AD clinical trials, seven of which are large-scale 
prevention trials. These trials are testing agents such as estrogen, 
anti-inflammatory drugs, and anti-oxidants for their effects on slowing 
progress of the disease, delaying AD's onset, or preventing it 
altogether. We eagerly await the results of these trials.
    As we search for effective preventive interventions and treatments 
for AD, it is becoming clear that, rather than seeking only a ``magic 
bullet'' that will, by itself, prevent or cure the disease, we may be 
able to identify a number of potential interventions that together can 
be used to reduce risk. Several recent studies have highlighted this.
    For example, a recent study in the New England Journal of Medicine 
\1\ indicates that elevated blood levels of the amino acid 
homocysteine, already considered a risk factor for cardiovascular 
disease, are associated with an increased risk of developing AD. The 
relationship between AD and homocysteine is of particular interest 
because blood levels of homocysteine can be reduced, for example, by 
increasing intake of folic acid (or folate) and vitamins B6 and B12. 
And, in fact, in a separate study in the Journal of Neuroscience,\2\ 
NIA researchers show that folic acid may protect AD transgenic mice 
against death of neurons in one of the brain regions most affected in 
AD. NIA has ongoing clinical trials of these substances to test whether 
supplementation can slow the rate of cognitive decline in cognitively 
normal men as well as in women at increased risk for developing heart 
disease. A pilot clinical trial to determine effective treatment levels 
of folate/B6/B12 for lowering plasma homocysteine levels in persons 
with AD is ongoing, and a full-scale clinical trial on people diagnosed 
with AD is due to start in 2003. Other studies have indicated that the 
use of statins, the most common type of cholesterol-lowering drugs, may 
lower the risk of developing AD. A clinical trial to determine whether 
statins slow the rate of disease progression in AD patients is planned 
for fall 2002.
---------------------------------------------------------------------------
    \1\ S. Sesdradri, A. Beiser, J. Selhub, et al., ``Plasma 
Homocysteine As A Risk Factor For Dementia and Alzheimer's Disease,'' N 
Eng J Med, 346:7, pp. 476-483.
    \2\ I. Kruman, T.S. Kumaravel, A. Lohani, W. Pedersen, R.G. Cutler, 
Y. Kruman, N. Haughey, J. Lee, M. Evans, and M.P. Mattson, ``Folic Acid 
Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons 
and Sensitize Them To Amyloid Toxicity in Experimental Models of 
Alzheimer's Disease,'' Journal of Neuroscience, 22:5, pp. 1752-1762.
---------------------------------------------------------------------------
    Another promising area of study is the role of mentally stimulating 
activities throughout life as a factor capable of maintaining cognitive 
health or even reducing the risk of cognitive decline or AD. Through 
its Advanced Cognitive Training for Independent and Vital Elderly 
(ACTIVE) study, NIA is currently exploring whether three specific 
interventions (on memory, reasoning, and speed of processing) can 
maintain or improve functioning in unimpaired, community-dwelling older 
adults. In addition, NIA-supported researchers recently found that more 
frequent participation in activities such as reading, doing crossword 
puzzles, or playing card games is associated with a reduced risk of 
later developing AD.\3\
---------------------------------------------------------------------------
    \3\ Wilson RS, Mendes de Leon CF, Barnes LL et al., ``Participation 
in Cognitively Stimulating Activities and Risk of Incident Alzheimer 
Disease,'' JAMA 287: 742-748.
---------------------------------------------------------------------------
    In addition to these exciting clinical findings, NIA-supported 
investigators are beginning to unravel AD's complex etiology. For 
example, until very recently, just four of the approximately 30,000 
genes in the human genome were conclusively known to affect the 
development of AD pathology. Three of these genes cause early onset AD, 
and only one is associated with the more common form of the disease, 
late-onset AD (LOAD). Recent genetic studies suggest that as many as 
four additional and as yet unidentified genes may also be risk factors 
for LOAD, and regions in several different chromosomes have been 
identified as likely locations for these genes. Finding new risk factor 
genes will help identify pathways affecting the development or 
progression of AD and may eventually lead to better predictors of the 
disease even before it is diagnosed.
    To facilitate the identification of the remaining AD risk factor 
genes, NIA is planning an expansion of its National Cell Repository. A 
national resource for research on AD, the Repository was created to 
collect and distribute DNA, cells, and information from families with 
multiple members with AD and related dementias. Its activities include 
the production of a catalog of cell lines and DNA samples that are 
available for qualified scientists to study. The expansion will allow 
researchers to more rapidly identify the underlying genetic mechanisms 
and environmental risk factors that interact to cause the more common 
late-onset form of AD. Understanding these mechanisms will provide 
opportunities for the design of effective diagnostic, therapeutic, and 
preventive interventions.
    The process of translating basic science findings into clinical 
interventions is a challenging but critical component of AD research. 
For example, a promising finding gained through basic research efforts 
was the ability of an immunization strategy to prevent or reverse 
formation of amyloid plaques in mouse models of AD. In collaboration 
with NINDS, NIA has issued a Request for Applications (RFA) and funded 
a number of studies to better understand the science underlying the 
vaccine approach. Similarly, NIA-funded studies are providing exciting 
new evidence on the identity of the snipping enzyme that cuts the 
amyloid beta molecule out of its precursor protein, and ways to blunt 
its activity. These interventions may be capable of preventing the 
formation of amyloid plaques.
    In addition, NIA-supported researchers have recently made a 
surprising discovery about the role of amyloid plaques in AD pathology. 
In one study, investigators found that amyloid beta oligomers, or small 
precursor components of amyloid plaques, inhibited brain mechanisms 
thought to be involved in memory formation in rats.\4\ In another, 
scientists used an immunization strategy to treat plaque-containing AD 
transgenic mice. Although the amount of plaques in the mice's brains 
remained constant, the mice very quickly regained cognitive 
functioning.\5\ These findings suggest that amyloid plaques themselves 
may not be responsible for AD's cognitive symptoms, and that a related 
pathology--perhaps a precursor molecule such as the amyloid beta 
oligomer--is the true culprit. This insight, in turn, may lead to the 
development of new and effective treatments for the disease.
---------------------------------------------------------------------------
    \4\ Walsh DM et al. Naturally secreted oligomers of amyloid 
 protein potently inhibit hippocampal long-term potentiation 
in vivo. Nature 416: 535-539, 2002.
    \5\ Dodart J-C et al. Immunization reverses memory deficits without 
reducing brain A burden in Alzheimer's disease model. Nature 
Neuroscience 2002: Advance online publication.
---------------------------------------------------------------------------
    Although the findings are still preliminary, these studies 
illustrate the importance of continued basic research to help us 
understand the mechanisms behind AD development and pathology, and the 
ways in which basic research findings can suggest new prevention and 
treatment strategies.
    Scientists funded by NIA, NINDS, and NIMH are also developing and 
refining powerful imaging techniques that hold promise of earlier and 
more accurate diagnosis of AD, as well as improved identification of 
people who are at risk of developing the disease and a more complete 
understanding of normal and abnormal age-related changes in the brain. 
For example, recent studies suggest that positron emission tomography 
(PET) scanning of metabolic changes in the brain and magnetic resonance 
imaging (MRI) scanning of structural brain changes may be useful tools 
for predicting future decline associated with AD and other 
neurodegenerative diseases.
    Researchers have also developed a new way of using functional MRI 
(fMRI), a technique for visualizing activity of brain structures, that 
is both easier on the person being tested and capable of imaging 
smaller structures in the brain than has been possible in the past. 
Using this new technique, investigators assessed the hippocampus, an 
area of the brain involved in memory formation, in people between 20 
and 88 years of age. They found that activity in certain regions of the 
hippocampus declines normally with age, but that decline in a specific 
region, the entorhinal cortex, is abnormal and may reflect an illness 
or condition such as AD. They conclude that some age-related memory 
loss is normal, due to ordinary hippocampal changes, but that 
individuals with dysfunction in the entorhinal cortex may be at 
increased risk of progressing to full-blown AD.\6\ These studies, if 
confirmed by ongoing longitudinal observation of the patients, hold the 
promise, for the first time, of being able to distinguish between the 
subtle brain changes that occur with normal aging and those that are a 
harbinger of clinical AD.
---------------------------------------------------------------------------
    \6\ Small SA et al. Imaging hippocampal function across the human 
life span: Is memory decline normal or not? Annals of Neurology 51: 
290-295, 2002.
---------------------------------------------------------------------------
    These methodologies may also be useful for evaluating the efficacy 
of drugs in stemming the progression of AD or preventing its onset 
altogether. However, these and other emerging imaging techniques, while 
promising, require further testing and analysis before they can be 
routinely adopted in the clinical setting.
    Another very important area of research involves easing the burden 
on caregivers of AD patients. In a sense, the AD ``patient'' is not 
only the person with the disease, but the entire family unit. Most 
Americans with AD are cared for outside the institutional setting by an 
adult child or in-law, a spouse, another relative, or a friend. The 
financial costs of this care can be devastating to families; the 
average lifetime cost per person for patients with AD is approximately 
$174,000.\7\ In addition to these financial burdens, caregivers 
frequently experience emotional stress and physical strain.
---------------------------------------------------------------------------
    \7\ Ernst, RL and Hay, JW The US economic and social costs of 
Alzheimer's disease revisited. American Journal of Public Health 84: 
1262-1264, 1994.
---------------------------------------------------------------------------
    NIA is investing in new approaches to assist these caregivers. A 
first priority is to assess the magnitude of the problem. For example, 
the ongoing Aging, Demographic, and Memory Study (ADAMS) has been 
designed to assess dementia and AD among Americans, the burden on 
caregivers, the economic cost of dementia to families and to society, 
and the burden of dementia over the course of the illness.
    NIA is also supporting a study of a combined behavioral and drug 
intervention on patients with mild AD. In this study, caregivers will 
be key participants in the behavioral intervention, and the researchers 
hypothesize that this participation will reduce caregivers' 
psychological stress. In addition, NIA is supporting a large, multi-
site clinical trial, REACH (Resources for Enhancing Alzheimer's 
Caregiver Health), to examine the effectiveness of various 
interventions to strengthen family members' capacity to care for 
individuals with AD. Thus far, the study has recruited over 1,200 
caregiver/care recipient pairs at six different sites across the 
country to participate in 12 different interventions. REACH is designed 
to show us what works to support caregivers and at what cost; we 
anticipate that the first findings from this trial may be available 
within the next several years. The NIMH is supporting a major project 
called the Clinical Anti-psychotic Trial of Intervention Effectiveness 
for Alzheimer's Disease (CATIE-AD) designed to help identify effective 
treatments for behavioral problems in AD, to help reduce the burden of 
care for both providers and families.
    Fifteen years ago, we did not know any of the genes that could 
cause AD, and we had no idea of the biological pathways that were 
involved in the development of brain pathology. Now, we know the 3 
major genes for early-onset disease and one of the major risk factor 
genes for late-onset disease, and we have extensive knowledge of 
pathways leading to the development of AD's characteristic amyloid 
plaques in the brain. Ten years ago, we could not model the disease in 
animals. Today, transgenic mice are an invaluable resource for modeling 
amyloid plaque development in the brain and in testing possible 
therapies. Five years ago, we did not have any prevention trials funded 
and had no ways of identifying persons at high risk for the disease. 
Now, we have seven ongoing prevention trials, and scientists are 
identifying persons at high risk for developing AD by imaging, 
neuropsychological tests, and structured clinician interviews. And as 
recently as one year ago, we did not understand anything about how 
plaques and tangles relate to each other. Now, through the creation of 
the first double transgenic mouse to produce both plaques and tangles, 
we know that plaques in the brain can influence the development of 
tangles in brain regions susceptible in AD. Recent findings also 
suggest that there are some common mechanisms of disease in a number of 
neurodegenerative disorders, which will further inform research in AD.
    It is difficult to predict the pace of science or to know with 
certainty what the future will bring. However, the progress we have 
already made will help us speed the pace of discovery, unravel the 
mysteries of AD's pathology, and develop safe, effective preventions 
and treatments, to the benefit of older Americans.
    Thank you for giving me this opportunity to share with you our 
progress on Alzheimer's disease. I would be happy to answer any 
questions you may have.

    Senator Harkin. Dr. Hodes, thank you very much.
    I am going to ask you to stay, if you could, and we will 
have the next panel up.
    I will yield to Senator Specter. He does have to leave.
    Senator Specter. Thank you, Mr. Chairman. I appreciate the 
opportunity to ask a few questions of you, Dr. Hodes, at this 
time because I am going to have to excuse myself, as I said 
earlier.
    The funding for Alzheimer's, as well as the funding for all 
of the other National Institutes of Health, depends to a 
significant extent on the sense of the Congress, really the 
sense of the American people, as to how well the money is being 
spent and what are the results. We have had estimates on 
Parkinson's, for example, that we may be within 5 years of a 
cure.
    While I know it is difficult to make a quantitative 
evaluation, I would be interested, to the extent that is 
consistent with your scientific methodology, if you can give us 
some estimate as to a time line for a cure on Alzheimer's?
    Dr. Hodes. Well, I apologize for the fact that I think I 
cannot responsibly quote a specific time in terms of years. But 
I can certainly share an exceptional sense of optimism 
projecting from the pace of discovery as summarized over these 
past 15 years. This pace is bringing us closer to interventions 
and cures than we ever dreamed possible a few years ago.
    The fact that we were able to bring into clinical trials 
interventions which have the promise for preventing disease is 
extraordinary. I can tell you that the results of some of these 
ongoing prevention trials, for example, will be coming to 
fruition over the next 3 to 5 years. That is not an estimate of 
when we know we will have success, but it is an estimate of 
when we should have the first results on some of the large-
scale prevention trials which have real promise of success.
    Senator Specter. So you are saying, in terms of prevention, 
the prospects are good that the scientific research has a 
realistic possibility of preventing Alzheimer's?
    Dr. Hodes. Yes. I think that we have over these past years 
uncovered now multiple potential targets. We have identified 
risk factors and learned how to modify those risk factors. Some 
of these risk factors are behavioral, some of them are 
biochemical and genetic. The more targets we have for 
intervention, the greater the chance that one or more of them 
is going to be successful. And yes, the pace of progress over 
these past years gives good reason to propose a realistic 
vision of a cure and/or prevention for Alzheimer's disease over 
the years to come.
    Senator Specter. When we talk about raising the funding 
this year by approximately $50 million, from $600 to $650 
million, what tangible evidence can you give Senator Harkin and 
myself as ammunition to deal with our colleagues in the Senate 
as to why that increase ought to be given? What can you tell us 
that we can pass on to the other Members of the Senate?
    Dr. Hodes. I can provide some general statements and then 
some rather more specific. In the general sense, the greatest 
argument for a continued increase in funding is the quality of 
scientific opportunities. Each discovery, be it in genetics, in 
risk factors, in relief of caregivers, creates opportunities, 
which then need to be followed by additional research.
    In particular, as basic research has provided opportunities 
for treatment and prevention, we have come to a stage of 
carrying out multiple clinical trials. Now, if we were to carry 
out only one clinical trial at a time, awaiting its result 
before going on to the next, I think this would be an 
unpardonable delay in eventually reaching success. So our 
approach has been to capitalize on the funding that has been 
made available to fund all of the most outstanding 
opportunities for clinical trials.
    Clinical trials, for prevention in particular, require the 
inclusion of thousands of individuals followed for several 
years. They are expensive studies. Each of these studies may 
cost in the range of $25 to $50 million. In order to carry out 
those several, each of which is responsive to outstanding 
current scientific opportunities, an increase in budget would 
be enormously helpful and important.
    Senator Specter. Okay. The billion dollar question. Dr. 
Hodes, what can you accomplish with $1 billion that you cannot 
accomplish with $650 million?
    Dr. Hodes. Well, we would be able, simply arithmetically, 
by that comparison to support 50 percent more research than we 
do. Fifty percent more research would easily be carried out by 
supporting uncompromised quality of both basic science to try 
to produce the opportunities for translation in the years to 
come as well as an increased speed of expeditiously following 
up on current opportunities to follow all of the candidate 
interventions for both treatment and prevention.
    Senator Specter. Dr. Hodes, I would like you to give some 
thought when you go back to your office, to your laboratory, to 
see if you can quantify more specifically. I appreciate the 
answers you have given, but we started funding Alzheimer's with 
$3.9 million in 1976 and now it is up to $600 million and you 
want to go to $1 billion. To the extent that you could give 
some hard estimates or some hard information--for example my 
colleagues can understand that you could possibly get 50 
percent more research from $1 billion versus $650 million. That 
kind of arithmetic is about the limit of our capability.
    But see if you cannot give us something really tangible, as 
tangible as possible.
    Dr. Hodes. Absolutely. I would be pleased to provide 
concrete examples.
    [The information follows:]

    Recent research advances have created important new opportunities 
for research that will accelerate progress toward interventions for 
early diagnosis, treatment, and prevention of AD.
    Recent scientific advances, largely the result of NIH-supported 
research, have illuminated significant genetic and cellular mechanisms 
that underlie AD. For example, four genes that affect the development 
of AD have already been identified, and recent studies suggest that for 
late-onset AD (the more common form of the disease) there may be at 
least four more risk factor genes. Efforts to pinpoint their exact 
location will help identify pathways affecting the development or 
progression of AD and may eventually lead to better predictors of the 
disease even before it is clinically apparent.
    In addition, scientists are developing and refining powerful 
imaging techniques that target anatomical, molecular, and functional 
processes in the brain. These new techniques hold promise of earlier 
and more accurate diagnosis of AD, as well as improved identification 
of people who are at risk of developing the disease. For example, 
recent studies suggest that positron emission tomography (PET) scanning 
of metabolic changes in the brain and magnetic resonance imaging (MRI) 
scanning of structural brain changes may be useful tools for predicting 
future decline associated with AD and other neurodegenerative diseases. 
Researchers have also developed a new method of functional MRI (fMRI), 
a technique for visualizing activity of brain structures, that is both 
easier on the person being tested and capable of imaging smaller 
structures in the brain than has been possible in the past. These 
methodologies may also be useful for evaluating the efficacy of drugs 
in stemming the progression of AD or preventing its onset altogether. 
However, these and other emerging imaging techniques, while promising, 
require further testing and analysis before they can be routinely 
adopted in the clinical setting.
    Research findings at the molecular level have created new and 
unprecedented opportunities for translation of basic research into 
clinical applications. The process is necessarily deliberate; as new 
target molecules are identified, interventions must be developed, 
tested in animal models for safety and efficacy, and only then moved 
into human trials. At the same time, clinical trials are needed today 
to test treatment interventions that have already shown promise in 
animal models, including promising new vaccines that ``wash'' amyloid 
from the brain and treatments that target enzymes called secretases, 
which begin the formation of amyloid plaques in the brain by snipping a 
protein into fragments that re-form as plaques. This research area is 
of tremendous interest to researchers in industry and academia as well 
as at other NIH Institutes, and this interest is leading to expanded 
opportunities for partnership.
    Trials are also needed for interventions that prevent AD onset or 
progression. Examination of a number of possible AD preventives is 
underway--for example, the AD Prevention Trial using vitamin E and 
donepezil, as well as trials testing the effect of estrogen, anti-
inflammatory drugs, and antioxidants. Candidate interventions that 
lower amyloid burden in animal models of AD are being identified with 
increasing frequency. Targeting specific abnormal cellular pathways 
uncovered by recent discoveries, including plaque and tangle formation 
and death of brain cells, are pointing to design of new interventions 
to prevent the onset of AD. Prevention trials are among the most costly 
of research projects, but, if successful, the payoff in terms of 
reduced disease and disability will be significant.
    Critical opportunities that could be supported with increased funds 
in fiscal year 2003 include:
    (1) Epidemiology studies to identify additional genetic causes and 
risk factors for AD, information that will provide new targets for 
treatment and prevention.
    (2) Testing of new methods for early diagnosis of AD, based on 
imaging and markers of early brain changes. Early diagnosis is critical 
to effective treatment and prevention, before onset of symptoms and 
death of brain cells.
    (3) Pre-clinical trials in newly created animal models of AD, which 
permit rapid testing of potential treatments based on new genetic and 
molecular targets.
    (4) Clinical trials of AD prevention. Candidates for prevention, 
based on human epidemiology and animal model studies, require clinical 
trials. These include anti-inflammatory agents, anti-oxidants, 
estrogen, statins, immunization with amyloid peptide, and secretase 
inhibitors.
    (5) Development of interventions to reduce caregiver burden and 
strengthen family members' capacity to care for AD patients.
    It must be noted that this estimate is based on our assessment of 
scientific opportunities over the next five years, without 
consideration of economic constraints or other competing priorities of 
the Federal government. This level of support must be integrated with 
other research efforts of the NIH.

    Senator Specter. Thank you very much, Dr. Hodes.
    Thank you, Mr. Chairman.
    Senator Harkin. Thank you, Senator Specter.
    I just noticed, looking at the record, we have got it 
pretty even. When I was chairman we almost doubled it and when 
you were chairman we almost doubled it. That is pretty good.
    Senator Specter. It looks like if we have another change in 
chairmanships we will double it again.
    Let me tell you ladies and gentlemen, while I prefer to be 
chairman to ranking, when Senator Harkin and I shift the gavel 
it is seamless, absolutely seamless. It keeps going the same 
way.
    Senator Harkin. That is true, absolutely.
    Thank you very much, Dr. Hodes.
    I would like to call up our next panel if I could then. 
Orien Reid, Chair of the National Board of Directors; Dr. 
Marilyn Albert; Carol and Gene Gratz; and David Hyde Pierce. We 
will go in that order, and I would first recognize Ms. Orien 
Reid, the Chair of the National Board of Directors of the 
Alzheimer's Association.
    Ms. Reid was a consumer reporter on television and radio 
for 26 years and recently formed a media consulting business. 
Ms. Reid earned her bachelor of arts degree from Park College 
and a master's degree from the Atlanta University School of 
Social Work. She lives in Laverock, Pennsylvania. I am not sure 
I know where that is, but it sounds like a nice place to be.
    Ms. Reid. Suburban Philadelphia.
    Senator Specter. One additional comment about Ms. Reid, Mr. 
Chairman. She is a very, very familiar figure on Philadelphia 
television and when she speaks people listen.
    Senator Harkin. Politicians listen, right?
    Senator Specter. So do statesmen.
STATEMENT OF ORIEN REID, CHAIR, BOARD OF DIRECTORS, 
            ALZHEIMER'S ASSOCIATION
    Ms. Reid. Thank you. Thank you, Senators. Thank you, thank 
you so much.
    Senator Specter. Adlai Stevenson defined a statesman as a 
dead politician.
    Ms. Reid. Well, I am not ready to die.
    Thank you so much. Thank you, Senator Specter.
    Senator Harkin. Orien Reid, welcome. All your statements 
will be made part of the record in their entirety. If you would 
just sum it up for us, I would appreciate it. Again, I thank 
you for your great leadership.
    Ms. Reid. I certainly will. Thank you so much for inviting 
me to testify at this very important hearing today. As you 
noted, I serve as Chair of the National Board of Directors of 
the Alzheimer's Association.
    I am here this morning to speak for my own family because, 
you see, today is a very special day. It is my mother's 
birthday, and had she not been killed by Alzheimer's disease 
she would be 86 years old today. So I just feel her spirit with 
me today and I want to speak for her and for my grandmother, my 
aunt, and my uncle, all of whom had Alzheimer's disease.
    I also speak for the hundreds of families, Alzheimer's 
families who are gathered in this room today, and for the 
millions of families like us. We are here today to thank you 
for your consistent leadership on issues that matter to the 
Alzheimer's community. We are here to tell you that we support 
your continued efforts to increase funding for Alzheimer's 
research and services. We know that you are on our side. We are 
here to enlist others to support your effort to increase 
medical research funding in general and specifically for 
Alzheimer's disease.
    Now, I would like to submit and present to you for the 
record the Alzheimer's national public policy program to 
conquer Alzheimer's disease. You will have that. Today 
Alzheimer's advocates from across the country will deliver this 
national program personally to their own Senators and 
Representatives.
    My request today is an urgent one. It is to ask you to 
increase appropriations for Alzheimer's research by $200 
million this year and to a billion dollars a year as soon as 
possible.
    We thank you for your support of our goal, which in 
particular we are very happy that you chose to reflect it as 
part of the language of your committee report last year. We 
have seen your commitment to Alzheimer's disease research 
funding through the years.
    The problem is we are running out of time to find an end to 
this disease. It is time now. The time is now for Congress to 
make this investment. The two experts in Alzheimer's research 
that I have sitting here will tell you about, and Dr. Hodes has 
just told you about, some of the scientific opportunities that 
exist today. If we are going to prevent the 14 million baby 
boomers from getting Alzheimer's disease, we have got to do 
something today.
    The experts know the science, but I along with 19 million 
other caregivers know what it is like to live with this 
disease. I watched Alzheimer's disease destroy my mother, a 
beautiful woman with a beautiful mind, a woman who counseled 
eminent leaders like Dr. Martin Luther King Junior and the 
former Mayor of Atlanta, Maynard Jackson.
    My family and I made major sacrifices and I do not regret 
that a bit. But what I do regret is the fact that this disease 
robbed my children of their childhood. It also took the money 
that I had saved for their college education and it left scars 
that continue to affect their lives. Today my children and I 
all live in fear because we do not want to live this nightmare 
all over again. I am only 16 years younger than my mother was 
when she was diagnosed with this disease. It is also very 
disconcerting to me to learn that African Americans may be at a 
higher risk for Alzheimer's disease. That does not make me feel 
comfortable.
    Today there are 14 million baby boomers in the United 
States who will get Alzheimer's disease if we do not find a way 
to stop it. We cannot save Medicare if 14 million baby boomers 
get Alzheimer's disease because the cost of treating people 
with Alzheimer's disease is estimated to climb from $31.9 
billion in 2000 up to $49.3 billion in 2010, just 8 years away, 
even though Medicare does not pay for most of the long-term 
care.
    We cannot preserve Medicare and Medicaid if we do not find 
a way to stop this disease. That can only be done through 
research.
    In addition to research, there are some important programs 
before your committee. We are happy to hear that you are going 
to continue your support of the family caregiver support 
program and we urge you to continue your support to expand the 
Alzheimer's matching grant program to all 50 States, to reach 
rural, underserved, and minority populations.

                           PREPARED STATEMENT

    You can see how your support has helped thousands of their 
families with Alzheimer's disease. As my beloved friend Maureen 
Reagan used to say, she hoped that we would be the last 
generation to face this disease without hope. You are our only 
hope so that we will not have to. Please help us.
    Thank you.
    [The statement follows:]
                    Prepared Statement of Orien Reid
    Senator Harkin, Senator Specter and other members of the 
Subcommittee: Thank you very much for inviting me to testify today at 
this very important hearing. I serve as chair of the Board of Directors 
of the Alzheimer's Association. I am here to speak for my own family--
my mother, my aunt, my uncle, and my grandmother--all of whom had 
Alzheimer's disease. I also speak for the hundreds of Alzheimer 
families gathered in this room today, and for the millions of families 
like us across the country.
    We are here to thank you for your constant leadership on issues 
that matter to the Alzheimer community, and to tell you that we support 
you in your continued efforts to increase funding for Alzheimer 
research and services. We know you are on our side. We are here to 
enlist others to support your effort to increase medical research 
funding in general, and specifically for Alzheimer's disease.
    I would like to present to you and submit for the record the 
Association's National Public Policy Program to Conquer Alzheimer's 
Disease. Today, Alzheimer advocates from across the country will 
deliver this National Program personally to their own Senators and 
Representatives.
    Today I am here with an urgent request--to ask you to increase 
appropriations for Alzheimer research by $200 million this year, and to 
$1 billion a year as soon as possible. We applaud you for your support 
of our goal, reflected in the language of your Committee Report from 
last year and your commitment to Alzheimer's disease research funding 
through the years.
    There is no time to wait--now is the time for Congress to make this 
investment. You have two experts in Alzheimer research here to tell you 
about the exciting scientific opportunities that exist today--new 
opportunities we must pursue in order to prevent 14 million baby 
boomers from getting Alzheimer's disease. I will leave the discussion 
of the science to the researchers--my knowledge is in the area of what 
it means to live with Alzheimer's disease.
    My own personal experience with this horrible disease reflects 
those of 19 million Americans who have a family member with Alzheimer's 
disease. Our experiences, combined with the knowledge that the 
Alzheimer's disease process begins in the brain as many as 20 years 
before a person is seriously impaired, have created our sense of 
urgency and driven us to this call for action.
    It devastated me to watch the disease destroy the beauty and mind 
of my mother--a woman who had counseled imminent leaders like the late 
Dr. Martin Luther King, and former Atlanta Mayor, Maynard Jackson. My 
mother's Alzheimer's disease forced major changes in my personal and 
professional life. I don't regret those sacrifices for a moment. My 
mother was worth it. But this disease didn't just take a toll on me, 
but also robbed my son and daughter of their childhood, took the money 
I had saved for their college education, and left an indelible mark on 
them that continues to affect their lives.
    My children and I are terrified by the prevalence of this disease 
in our family. I'm now 16 years younger than my mother when she was 
diagnosed with Alzheimer's. My greatest fear is that it has started to 
eat away at my brain too, and that my children will be forced to live 
this nightmare all over again. Recent studies showing that African-
Americans may be at higher risk of Alzheimer's disease does nothing to 
ease my mind.
    I am not alone in my fears. Today there are 14 million baby boomers 
in the United States who will get Alzheimer's disease, if we don't find 
a way to stop it. Think about the implications. For example, it is 
difficult to see how you can save Medicare, if 14 million baby boomers 
get Alzheimer's disease. Alzheimer's poses a threat to Medicare even 
before the baby boomers have all retired. The cost to Medicare of 
treating people with Alzheimer's disease is estimated to soar from 
$31.9 billion in 2000 to $49.3 billion in 2010, even though Medicare 
does not pay for most of the long term care they need.
    The survey conducted by Peter D. Hart Research Associates and being 
released today by the Alzheimer's Association found that Americans are 
also concerned about health care costs. More than eight in ten voters 
say that paying for health care costs is the biggest financial 
challenge facing the elderly today--far outpacing housing, the cost of 
utilities and food. There is no way to preserve Medicare and Medicaid, 
and rein in health care costs, if we do not find a way to stop 
Alzheimer's disease, and that can only be done through research.
    In addition to medical research, there are important programs 
before your Committee that are providing immediate help to people who 
are living with Alzheimer's disease. We urge you to continue your long-
standing support, and fund further expansion of the Alzheimer matching 
grant program to support model programs in all fifty states to reach 
underserved communities, particularly minority populations and rural 
areas. And we thank you for your support of the Family Caregiver 
Support Program.
    The Alzheimer's Disease Demonstration Grants to States Program 
helps states assure that community services are accessible and 
appropriate for the unique needs of people with Alzheimer's and their 
families. While these grants are very small--$250,000 to $350,000 per 
year for a three-year period--they have had a huge impact by:
  --providing services to individuals who were previously left out, 
        especially minorities and rural populations;
  --changing the larger health and long term care systems so that 
        states to do a better job of serving people with Alzheimer's 
        disease;
  --developing partnerships along with new public and private resources 
        to continue and expand programs upon conclusion of the 
        demonstration;
  --developing ``best practice'' service delivery models that are being 
        replicated within and beyond the state; and
  --generating an Alzheimer's Disease Resource Room on the 
        Administration on Aging website that features information on 
        successful strategies that can be replicated in communities 
        across the country.
    Let me give you a few examples of the innovations your investment 
has brought in the states that have received these grants:
  --In Maine, dementia teams that are linked to university specialists 
        now go to the homes of people in isolated rural areas and 
        regularly consult with their family physicians.
  --A mobile dementia day care program now serves small towns in 
        Georgia that cannot support a full time adult day care center.
  --Latino families in South Central Los Angeles now have a 
        comprehensive Alzheimer community services program, and the 
        initial seed money from the federal government has been totally 
        replaced with locally raised funds. This program has now been 
        replicated in the African American and Asian American 
        communities.
  --Oregon has trained all of the case managers in its long term care 
        system to understand the special needs of people with dementia 
        and, as a result, the entire system is more responsive to those 
        needs.
  --A current grant in Rhode Island is focused on developing a model of 
        consumer directed respite care provided by and for minority 
        elders. It is also creating a model of workforce development, 
        including Certified Nursing Assistant (CNA) training and the 
        establishment of career ladders for CNA's.
    In each case, the state has partnered with local Alzheimer's 
Association chapters to apply for and implement the grant. We urge you 
to appropriate $25 million to allow these innovations to go forward in 
every state. As states and health care systems redefine their services 
to meet the needs of a growing aging population, this program will help 
assure that people with Alzheimer's disease do not fall through the 
cracks.
    Alzheimer's disease is an epidemic, and we simply cannot wait to do 
something about it. The Alzheimer's Association continues its own 
investment in Alzheimer research--nearly $120 million to date. We will 
do everything we can to bring as much private money as we can into the 
search for the answers. But we all know it will take your support, and 
the resources of the NIH to harness and stop this disease.
    To allow researchers to capitalize on new knowledge gained through 
past investments in research and reach answers in time to make a 
difference, Congress must provide an additional $200 million this year 
for a government-wide assault on Alzheimer's disease. We are asking you 
to join us in this effort. Time is running out for our children and 
grandchildren, and for 14 million baby boomers who may be living with a 
sentence of Alzheimer's disease. Please, for all of us, act now. Thank 
you.

    Senator Harkin. Thank you, Ms. Reid. Great testimony. Thank 
you for your leadership.
    Next we will turn to Dr. Marilyn Albert, Professor in 
Psychiatry and Neurology at Harvard Medical School and Director 
of Gerontology Research Unit at the Massachusetts General 
Hospital. Dr. Albert also serves as Chair of the Alzheimer's 
Association's Medical and Scientific Advisory Committee. She 
received her Ph.D. in psychology from McGill University. 
Welcome, Dr. Albert.
STATEMENT OF MARILYN ALBERT, Ph.D., CHAIR, MEDICAL AND 
            SCIENTIFIC ADVISORY COMMITTEE, ALZHEIMER'S 
            ASSOCIATION
    Dr. Albert. Thank you very much, Senator Harkin, Senator 
Specter. It is a great honor to speak to you this morning in my 
position as Chair of the Medical and Scientific Advisory 
Committee of the Alzheimer's Association.
    I wanted to begin by commending you for your past and very 
strong support of research funding for the NIH and for 
Alzheimer's Association in particular. My research colleagues 
around the country are certain that it is that strong support 
that has enabled us to learn so much about Alzheimer's disease 
so quickly over the last 20 years. We believe it is this 
progress that has put us on the brink of finding truly 
effective treatments for the disease in the coming years.
    In my written statement that I submitted for the record, I 
identified five major research areas where we believe an 
infusion of money would be greatly helpful. But in the brief 
time allotted to me, what I would like to do is talk to you 
about the research area that I know the best, the one that I 
work in, which is longitudinal clinical research for the early 
diagnosis of Alzheimer's disease.
    As you may know, recent studies have demonstrated that the 
pathology of Alzheimer's disease begins many years before 
clinical dementia can be diagnosed. Most of my colleagues 
believe that when we get effective treatments for the disease 
it is highly unlikely that they are going to be benign, and yet 
it is going to be critically important to intervene before 
substantial damage has been done to the brain.
    So the kind of work that I do has been involved in trying 
to identify people before the disease symptoms become full-
blown, when intervention would be of the greatest benefit. The 
work of my research colleagues and of several other groups 
around the country has been using cognitive testing, neuro-
imaging, genetics to try to identify individuals who have 
memory problems that are relatively mild and be able to predict 
when those symptoms are going to progress and which of those 
individuals are going to go on to meet criteria for Alzheimer's 
disease in subsequent years.
    Now, when I started this phase of my work 10 years ago, it 
seemed sort of incredible in retrospect, but I thought that we 
would have clear answers within 5 years. It turns out, on the 
basis of our research, that people progress with varying rates, 
people with mild memory difficulty. Some progress quite quickly 
and do develop Alzheimer's disease within a very short period 
of time. Some progress very slowly and seem to be going in the 
direction of developing the disease, but do not within even a 
decade. Some who appear to be at high risk actually remain 
stable, and we have a great deal of difficulty then predicting 
what is going to happen to people over time.
    So that, although we have made a great deal of progress, it 
has been much harder than we ever anticipated, it has required 
much more time, many more subjects, and of course that 
translates into many more dollars.
    We believe that we are on the right track. We have 
anticipation that pharmaceutical companies will be close to 
adopting some of the methods that we have used to help screen 
drugs that might be effective for the disease and study 
patients to determine whether or not the drugs that they have 
developed actually slow down the progress of the disease. But 
it is really going to take considerably more effort to get the 
answers that we are seeking.
    This one research effort I think illustrates how much more 
complicated and expensive long-term clinical research is on a 
day to day basis and why it is so important for us to have 
additional research dollars for this problem as well as the 
many others that Dr. Hodes just described.

                           PREPARED STATEMENT

    Like my other colleagues in the Alzheimer's Association, I 
want to emphasize how important it is for us to have additional 
funding for research in this area. As Orien just said to you, 
it is not an exaggeration to say that if we do not find 
effective treatments for Alzheimer's disease there is no health 
care system in the world that will be able to support the 
problem that we will face.
    Thank you.
    [The statement follows:]
                  Prepared Statement of Marilyn Albert
    Mr. Chairman and members of the Subcommittee: Thank you for 
inviting me to participate in this very important hearing on 
Alzheimer's disease--the epidemic of the 21st century. Others on this 
panel are here to describe the human side of Alzheimer's and its 
enormous cost--to individuals, to families, to our health care system 
and our national economy. The case for the war against Alzheimer's is 
clear. My task, as a scientist, is to convince you we can win this 
war--if we are willing to put the resources into the fight.
    The possibility of ending Alzheimer's disease as we know it has 
never been more real. We have reached this historic point because of 
your unflagging support of funding for the National Institutes of 
Health as a whole, and for Alzheimer's disease research in particular. 
We are now poised to yield enormous return on that prior investment.
    When I started my own research on Alzheimer's disease 22 years ago, 
there were a relative handful of scientists working in the field. NIH 
was investing about $12 million in Alzheimer research. We were just 
beginning to understand the basic mechanisms of the disease. Only a 
handful of papers on Alzheimer's disease found their way to 
publication. Caregivers struggling with the disease were starting to 
find each other and forming the local support groups that would soon 
become the Alzheimer's Association.
    How the world has changed! This July, the Alzheimer's Association 
will convene the 8th International Conference on Alzheimer's Disease 
and Related Disorders in Stockholm. More than 4,000 scientists working 
on Alzheimer's disease will gather to report new findings on the 
biology, epidemiology, genetics, environmental risk factors, diagnosis, 
treatment, and prevention of Alzheimer's disease. This year alone, more 
than 3,000 peer-reviewed papers on Alzheimer's research will appear in 
leading American and international journals.
    We have come this far, this fast, because of the systematic care 
with which the National Institute on Aging has nurtured and developed 
the field of Alzheimer research, creating a scientific infrastructure 
that has made possible not only the rapid accumulation of knowledge, 
but an unprecedented sharing of data among laboratories and the 
translation of basic science to clinical studies.
    All of this work is directed toward two objectives:
    First, to delay and prevent the onset of disease in the tens of 
millions of people who are now at risk. We now understand that the 
process that leads to Alzheimer's may start in a person's brain many 
years before he or she becomes clinically impaired. That gives us a 
window of time to prevent the devastation of Alzheimer's in millions of 
today's babyboomers--if we can find effective and affordable 
therapeutic interventions, and if we can identify those individuals who 
are at risk so that we can intervene early enough to make a difference.
    The second and equally important goal is to treat and delay the 
progress of Alzheimer's in those for whom we cannot prevent disease.
    Both of these goals are within reach. But Alzheimer's disease has 
turned out to be much more complicated than we originally thought. That 
is why we need a $1 billion investment from NIH, to pursue 
simultaneously the immediate opportunities in 5 essential and 
interrelated areas of research.
    First, we must continue basic biomedical research to find the last 
pieces of the complex puzzle of Alzheimer's disease, to complete our 
understanding of how and why brain cells shrink and die. We are 
constantly learning more about the two major characteristic of 
Alzheimer's--the amyloid plaques and neurofibulary tangles--and how 
they interact. We know how plaques are formed and deposited in the 
brain and how they act as toxins. Now, scientists are working 
aggressively to block their formation. We are assembling the same type 
of information about the formation of tangles. And evidence is mounting 
that inflammation and oxidative stress may play an important role in 
the disease. Neuroscience, and the study of Alzheimer's disease 
particularly, is one of the most exciting and promising areas of basic 
science today. We will continue to attract the best minds to the field 
as long as we maintain our investment here.
    Second, we must conduct large scale clinical trials to test 
potential therapies to slow or halt onset and progression of disease 
and to prevent or delay disability. Basic research is identifying 
multiple targets for such therapies, and observational studies have 
suggested that drugs already used widely by middle-aged and older 
people may have a protective effect. The only way to figure out how to 
turn all of this discovery into safe and effective treatment is to do 
large-scale, controlled clinical trials of each of these interventions 
that holds promise.
    These trials--especially prevention trials--are very expensive. We 
have to recruit large numbers of people who do not yet have Alzheimer's 
disease and follow them long enough to see whether the compound has the 
desired effect. And we have to test for variability by race and 
ethnicity. At the urging of Congress and under the leadership of the 
National Institute on Aging, NIH is investing in a number of these 
trials already, at costs as high as $25 million for a single trial. But 
if we are going to take advantage of the window of time we have before 
large numbers of babyboomers succumb to the disease, there must be a 
steady infusion of funds for additional trials to validate initial 
results and to explore new potential therapies as rapidly as science 
identifies their potential.
    Third, we have to do the longitudinal clinical studies that will 
tell us who is really at risk of getting Alzheimer's disease and to 
find the surrogate markers that will make it possible to identify 
people before the disease is apparent. We are not just doing science 
for science's sake. We have a moral obligation to make sure that the 
people who can benefit from what we learn get the treatment they need, 
and that they get it early enough to make a difference.
    This is the kind of work I do. For the past 10 years, my research 
team has been following people with mild memory difficulty to try to 
see if we can predict which ones will get worse and which one's won't 
and what factors influence progression. We started with a relatively 
small group of subjects, but as we learned more about how complicated 
the disease is and how slowly it progresses, and as other research has 
brought us new tools and new questions, our research has grown. We have 
increased the number of people we are following. We are looking at 
people who are normal as well as those with memory difficulties. And we 
are now able to take the enormous scientific progress that has been 
made by others and apply it in our clinical studies. When we started, 
we were excited that we could use CAT scans to ``see'' the brain. Now, 
we are using three types of structural imaging that give us 
extraordinary ability to measure changes in the brain over time. We are 
applying increased knowledge of genetics to look at its influence on 
cognitive performance and imaging measures in our subjects. We have 
also been able to confirm the findings of other researchers by looking 
at the impact of anti-inflammatories in our population.
    All of this takes money. Our own research--this one clinical study, 
for example--now costs $2.5 million a year. And it requires a sustained 
commitment of funds for a decade or more. Without a continued 
substantial increase in funding from Congress, NIA will be forced to 
make impossible choices between multi-year funding for these large 
scale clinical studies and funding for new investigator-initiated basic 
science. If we are going to find the answers to Alzheimer's in time to 
make a difference, there must be enough money in the system to do both.
    Fourth, we need to track down the linkages between vascular disease 
and Alzheimer's. This is an increasingly promising avenue of research 
with enormous potential payoff. Evidence from a number of longitudinal 
studies here and abroad suggests there is a direct relationship between 
vascular disease and Alzheimer's. Vascular abnormalities in the brain, 
on top of the lesions of Alzheimer's disease, appear to make cognitive 
impairment worse. Vascular risk factors like high cholesterol and high 
blood pressure may be significant risk factors for Alzheimer's disease 
as well. And there is now some accumulating evidence that statins--
cholesterol-lowering drugs--may have a protective effect.
    Many of the long-term population-based studies of heart disease, 
like the Framingham Study and the Nurses Health Study, now have cohorts 
that have aged. These studies have accumulated a lifetime of data on 
their subjects, which we can examine now to study the risks for 
cognitive decline.
    The public health implications of this avenue of research are 
enormous, particularly for racial and ethnic groups disproportionately 
affected by vascular disease. We already know a lot about primary and 
secondary prevention of vascular disease. Now, we may have a route to 
prevention of Alzheimer's as well, for a significant number of people 
at risk. It will take increased resources at the National Heart, Blood, 
and Lung Institute as well as the NIA to pursue this research as 
rapidly as possible.
    Fifth, we must find more effective ways to treat Alzheimer's 
disease. No matter how quick and successful we are in finding a way to 
prevent Alzheimer's disease, millions of Americans like Mr. and Mrs. 
Gratz will still be living with a diagnosis of Alzheimer's for the 
foreseeable future. Congress must continue to invest resources in the 
search for more effective and affordable treatments to improve the 
quality of life and delay the disabling impact of the disease. This 
requires investment in:
  --drug discovery for direct treatment of Alzheimer's and for the 
        management and treatment of the behavioral symptoms that make 
        care so difficult and costly;
  --health services research and demonstrations to find effective ways 
        to manage comorbid medical conditions in people with 
        Alzheimer's who cannot self-manage those conditions and to 
        prevent avoidable illness, injury, and hospitalization;
  --social and behavioral research to improve the quality of care and 
        the quality of life for persons with Alzheimer's and their 
        caregivers in every setting.
    The Alzheimer demonstration grant program, which other witnesses 
have discussed, is a critical piece of this research agenda. I join in 
urging the subcommittee to increase funding of that highly successful 
program to $25 million to allow all 50 states to participate.
    In conclusion, I want to acknowledge the enormous task this 
subcommittee faces in balancing the competing demands in this most 
important part of the federal budget, which touches so directly on the 
health and well-being of every American family. Finding room in that 
budget for the investment needed to keep 14 million Americans from 
getting Alzheimer's disease is one of the most important things this 
subcommittee can do for our long term economic and social security. 
Thank you.

    Senator Harkin. Thank you very much, Dr. Albert.
    Next we turn to Carol and Gene Gratz, who are from New 
Hampton, Iowa, a small town that I have been to many, many 
times in the northeastern part of the State. Gene was diagnosed 
with Alzheimer's last June. Carol and Gene have been married 
for 12 years. They are here with their 11-year-old son, Kris.
    Again, I want to thank you both for taking all the time and 
the trouble to travel here and to give us some personal insight 
as to what has happened to you just in the last year or so 
since Gene was diagnosed. So Carol, we will recognize you if 
you would like to kick it off.
STATEMENT OF CAROL GRATZ, NEW HAMPTON, IA, EAST CENTRAL 
            IOWA CHAPTER, ALZHEIMER'S ASSOCIATION
    Ms. Gratz. Mr. Chairman and members of the subcommittee: 
Thank you very much for giving me the opportunity to testify 
this morning. I am truly honored to be here representing my 
home State of Iowa and our East Central Iowa Chapter of the 
Alzheimer's Association. My name is Carol Gratz and I am here 
today with my husband Gene and our 11-year-old son, Kristopher, 
who is sitting right behind me.
    We have traveled here to Washington from New Hampton, Iowa, 
a rural community of approximately 3800 people, to ask you to 
please do everything to increase funding for the Alzheimer's 
research so a cure or prevention can be found as soon as 
possible. Our plea for increased research funding is extremely 
personal. Ten months ago Gene, at age 57, was diagnosed with 
Alzheimer's disease.
    The symptoms of Gene's disease actually started appearing 4 
years ago. Gene at 53 began having problems with his short-term 
memory and was having great difficulty in dialing a phone or 
reading a newspaper. Naturally, our first instinct was to see 
an eye doctor. However, the eye doctor could find no medical 
explanation for Gene's vision problems.
    Over 2 years, he continued to have problems with his vision 
and his memory, but rarely complained, so I was not fully aware 
of the extent of Gene's problems. By this time he was having 
trouble driving and also decided he could no longer endure a 2-
hour daily commute to his job as a forklift driver. He found a 
new job as a produce manager closer to our home and he worked 
there for about a year. The produce manager's job involved 
substantial amounts of paperwork, which he had great difficulty 
doing because of his vision problems.
    In January 2000, Gene changed jobs a second time and wound 
up with a position on an assembly line at a local manufacturing 
plant. The assembly line work involved repetitive tasks and did 
not require reading or writing, so Gene did well at his job.
    However, in April 2001, with a slowdown in the assembly 
line, it forced him to switch jobs in the plant, and he had to 
begin to read blueprints, which he had trouble doing as his 
vision was very poor. His supervisor asked him to visit a 
doctor for a checkup.
    By this time I knew that Gene's vision problems and short-
term memory problems were not normal and began researching his 
symptoms on the Internet. My search took me to the Alzheimer's 
Association web site. I contacted our local chapter and the 
people at the East Central Iowa Chapter were extremely helpful, 
and sent us many information packets as well as a list of 
doctors in our community.
    After seeing a general practitioner and multiple visits to 
various specialists, we were referred to the University of Iowa 
hospital for additional testing. Finally, in June of 2001 we 
got the terrible news that Gene had Alzheimer's disease. We 
were also told that he had a rare form of the disease that 
attacked his eyesight as well as his memory.
    As you might imagine, in the past year it has been very 
difficult for our family in many ways. Gene can no longer work, 
drive a car, or read a newspaper. He has also had to give up 
his favorite hobby of woodworking because his doctor has told 
him it is not safe to use power tools.
    Gene is on one of the newer Alzheimer's medicines, which 
helps maintain his moods and his functions. His doctor 
evaluates him every 6 months, but we are putting a lot of miles 
on our car as we must travel 2\1/2\ hours to Iowa City for 
every appointment. There are no doctors in our local community 
specializing in Alzheimer's.
    I have had to switch jobs, dealing with unsympathetic 
employers who would not grant my repeated requests for time off 
to take Gene to multiple appointments in Iowa City. I was lucky 
enough to find a job closer to home at a manufacturing plant. 
My employer is very accommodating and sympathetic and I 
currently work the third shift from 8:30 p.m. to 6:30 a.m., 
which allows me to be home with Gene during the day and help my 
son with his homework after school and also fix dinner for my 
guys before going off to work.
    While the disease has been very difficult on Gene and me, 
it has been especially difficult for our son, Kris. He is 11 
years old and seeing his father struggle to do many things that 
other dads do is very tough.
    Gene and I learned a great deal about Alzheimer's. I know 
the scientists are studying the genetic aspects and that is why 
we have chosen to advocate for increased research funding, in 
hopes that a cure or a prevention can be found soon to save our 
son from this dreadful disease.
    We also want to let people know that Alzheimer's is not 
just for seniors, it is for younger people, too.
    I would like to thank you very much for giving me the 
opportunity to be here today and I commend you for everything 
you have done to help the Alzheimer's research and funding. 
Thank you very much.
    I would like to introduce my husband, Gene, to say a few 
words.
    Senator Harkin. Thank you, Carol.
    Gene.
STATEMENT OF GENE GRATZ, NEW HAMPTON, IA, EAST CENTRAL 
            IOWA CHAPTER, ALZHEIMER'S ASSOCIATION
    Mr. Gratz. Senators Harkin and Specter, I am very, very 
happy and really feel privileged to be here. My eyesight, like 
Carol says, is not real good. I had to make kind of a scribbly-
scratch notepad. She did a pad for me on a tape recorder, but 
it is kind of hard to listen to that too and still talk to 
everybody.
    But the worst thing, I guess, in this whole deal: I lost my 
oldest boy, 18 years old, in a car accident, and now I am going 
to lose my son, Kris, to Alzheimer's, and I am the one that has 
got it. He is going to be without a father eventually. 
Hopefully it is not going to be soon. The doctors tell me it is 
going to be a long time down the road.
    But we need the funding. We need that extra funding to get 
this thing killed and get it dead. That is the only reason I 
came here.
    The paperwork that I was given, I really cannot remember 
most of it. But I can tell you that I raise a few small 
animals, about all I can do anymore. I have got a new Dodge 
pickup sitting in the garage that I cannot drive. And my son 
wants to drive already, but good old Marty, our sheriff in 
town, he says I cannot teach him out in the field. But Kris 
wants to know how.

                           PREPARED STATEMENT

    But anyway, it makes life miserable. I was extremely 
independent all my life. I ran major businesses. And to have it 
happen to me like this--it came from my father and my 
grandfather. We have got to stop it in this generation, have 
got to stop it. I do not care what it costs. We have got to get 
the funding in some way, shape, or form to get this disease 
killed.
    Thank you very much, gentlemen. I wish I could be of more 
assistance, but I did my best I could do. Thank you.
    [The combined statement follows:]
               Prepared Statement of Carol and Gene Gratz
    Mr. Chairman and members of the Subcommittee: Thank you very much 
for giving me the opportunity to testify this morning. I am truly 
honored to be here, representing my home state of Iowa and the East 
Central Iowa Chapter of the Alzheimer's Association.
    My name is Carol Gratz and I am here today with my husband, Gene 
and our 11-year old son Kris, who is sitting right behind me. We have 
traveled to Washington from New Hampton, Iowa, a rural community of 
approximately 3,800 people, to ask you to please do everything you can 
to increase funding for Alzheimer research so that a cure or prevention 
can be found as soon as possible. Our plea for increased research 
funding is extremely personal because 10 months ago, at the age of 57, 
Gene was diagnosed with Alzheimer's disease.
    The symptoms of Gene's disease actually started appearing about 5 
years ago. When Gene was 53, he began having some problems with his 
short-term memory and his vision. He complained of not being able to 
see very well and was having great difficulty dialing the telephone and 
reading the newspaper. Gene went to the eye doctor, who did not find 
any explanation for the vision problems.
    Since the eye doctor could find no explanation for Gene's vision 
problems we did not pursue the issue. Gene continued to experience 
difficulties with his vision and memory for another two years but he 
rarely complained, so I was not fully aware of the extent of his 
problems. He was also having trouble driving and decided that he could 
no longer endure the daily two-hour commute to his job as a forklift 
operator at a John Deere warehouse. He found a new job as a produce 
manager at a small grocery store much closer to our home, and we 
thought that would solve all of his problems. Gene lasted about a year 
at his new job but the amount of paperwork he was required to do 
combined with the frequent inventory reports caused him a lot of stress 
due to his continuing vision problems.
    In January 2000, Gene left the small grocery store and took a job 
on the assembly line at a plant that manufactures horse trailers and 
trailers for NASCAR races. Since the assembly line work involved 
repetitive tasks and did not require reading or writing, Gene was able 
to handle the job. Gene was doing well until April 2001 when a slowdown 
in assembly line work forced him to switch jobs in the plant. In his 
new assignment, Gene was required to read blueprints, which was 
impossible for him to do with his poor vision. Gene told his supervisor 
that he was having trouble reading the blueprints and his supervisor 
suggested that he visit a doctor for a check-up.
    By this time, I knew that Gene's vision and short-term memory 
problems were not normal and with my daughter's help, began researching 
his symptoms on the Internet. Our search led us to the Alzheimer's 
Association website and we contacted our local chapter. The people at 
the East Central Iowa chapter were extremely helpful and sent us an 
information packet as well as a list of doctors in our community. We 
went to a general practitioner, a neurologist and a neuropsychologist. 
We were also referred to the University of Iowa hospitals for 
additional testing. Finally, in June 2001, we got the terrible news 
that Gene had Alzheimer's disease. We were also told that Gene had a 
very rare form of the disease that was attacking his eyesight as well 
as his memory.
    As you might imagine, this past year has been very difficult for 
our family in many ways. Gene can no longer work, drive a car or read 
the newspaper. He has also had to give up his favorite hobby of 
woodworking because his doctor told him that it is not safe to use 
power tools anymore.
    Gene is on one of the newer Alzheimer's drugs which is helping to 
maintain his functioning and mood swings. His doctors evaluate him 
every six months but we are putting a lot of miles on our car because 
we must travel two and a half hours to Iowa City for every appointment. 
There are no doctors in our rural community who specialize in treating 
Alzheimer's.
    I have had to switch jobs and deal with an unsympathetic employer 
who would not grant my repeated requests for time off to take Gene to 
his multiple appointments in Iowa City. I was lucky enough to find 
another job, closer to home, at an employee-owned manufacturing plant. 
My new employer has been very accommodating and sympathetic. I 
currently work the third shift, from 8:30 p.m. until 6:30 a.m., which 
allows me to be home with Gene during the day, help Kris with his 
homework after school and fix dinner for ``my guys'' before going off 
to work. This schedule also gives me piece of mind since Gene and Kris 
are generally sleeping during the hours that I am at work and I don't 
have to worry about their safety.
    While this disease has been hard on both Gene and me it has been 
especially difficult for our son Kris. He is only 11 years old and 
seeing his father struggle to do many of the things that other dads do 
is very tough. With assistance from the Alzheimer's Association, we 
found a counselor who has been working with Kris to help him cope with 
the changes we've experienced due to Gene's diagnosis.
    Gene and I have learned a great deal about Alzheimer's and we know 
that scientists are actively studying the genetic aspects of the 
disease. We worry that Kris is at risk and we've chosen to advocate for 
increased research funding in the hope that a cure or prevention will 
be found and our son will be spared from this dreaded disease. We have 
also decided to speak out about Alzheimer's to let everyone know that 
it is not just older people who suffer from the disease. Younger people 
get it too and the impact of Alzheimer's is especially painful when it 
strikes early. Alzheimer's has taken so much from our family. It has 
robbed Gene of his career and hobbies and has threatened our financial 
future. But worst of all, it has stolen Gene's second chance at being a 
father. Gene's son from his first marriage was killed in a tragic car 
accident a few years before we met so we were thrilled when we learned 
that I was pregnant with Kris and that Gene would get another chance at 
fatherhood.
    In closing, I want to thank you again Senators Harkin and Specter 
for giving me the opportunity to share how Alzheimer's disease has 
impacted my family. I commend you for all that you have done to 
increase research funding and raise awareness about Alzheimer's and am 
grateful for your leadership in the U.S. Senate. As you will hear from 
the others who are speaking today, scientists are on the verge of 
finding ways to prevent and treat Alzheimer's disease and the actions 
we take today may save future generations--including my son--from this 
devastating illness. Thank you.

    Senator Harkin. Thank you both very much.
    You said you want to be of more help. What you are doing is 
of immense help. We must put a human face on this. Senators, 
Congressmen, researchers have to know the human toll that this 
is taking. These are not just statistics. They are real people 
with real families, working hard, getting hit like this.
    The fact that you, Carol--just think about that, everybody. 
She works from 8:30 p.m. to 6:30 a.m. every night so she can be 
home to get Kris off to school, get him home from school, take 
care of Gene during the day. That is the kind of toll it takes 
on families. You are a brave woman, and you are a brave man.
    Mr. Gratz. She is, she is a fantastic woman, and I thank 
God I married her.
    Senator Harkin. You are lucky to have her for a wife, I 
will tell you that. She is great.
    Mr. Gratz. I have got a piece of gold sitting next to me 
and I know that.
    Senator Harkin. So thank you very much for sharing your 
story with us.
    Mr. Gratz. Thank you very much.
    Senator Harkin. Now we turn to David Hyde Pierce. I did not 
know that was his real name. I always thought it was Niles 
Crane. So we all know Niles from Frasier. He has won three Emmy 
Awards, a Golden Globe Award; obviously, someone that is known 
nationally.
    He is also a national board member of the Alzheimer's 
Association and an extraordinarily committed advocate in the 
effort to cure Alzheimer's. Mr. Pierce testified before the 
subcommittee last year and, Niles, we certainly welcome you 
back again.
STATEMENT OF DAVID HYDE PIERCE, ACTOR
    Mr. Pierce. Thank you, Dr. Harkin. I appreciate that.
    Senator Harkin. The floor is yours. Thanks.
    Mr. Pierce. I am very pleased to be back here. Thank you 
for inviting me back to testify.
    My grandfather, my father, and, I recently found out, one 
of my dad's sisters all suffered from Alzheimer's and dementia. 
In my written testimony I say that over the years my fears of 
Alzheimer's have increased, but I have to tell you, sitting 
here today, listening to the breakthroughs in research and the 
leadership that people like Orien provide and the incredible 
bravery of Gene and Carol and their son, Kris, my fears have 
evaporated and they are replaced by hope and determination.
    We are so close to catastrophe and we are so close to a 
cure. That is why I am here urging you, in spite of the 
enormous challenges you face today, to maintain your commitment 
to medical research for Alzheimer's and as soon as possible to 
increase funding to a billion dollars a year.
    Today the Alzheimer's Association is releasing a national 
survey by Peter D. Hart Research Associates regarding 
Americans' feelings about Alzheimer's disease. The survey 
confirms what I have seen every day, that Americans of every 
age are terrified by the threat of Alzheimer's disease and that 
they overwhelmingly support the shared efforts of this 
committee and the Alzheimer's Association to increase funding.
    I am going to give you just some of the results. Ninety-
five percent of Americans believe that Alzheimer's disease is a 
serious concern for this country. Senators Harkin and Specter, 
you have led this Congress in the effort to double funding for 
the NIH. The survey shows that Americans support the work. In 
fact, in this election year these voters say medical research 
is one of the most important areas for Federal spending, 
ranking second only to education and ranking above military 
spending.
    Three-quarters of Americans specifically support the 
proposal to increase funding to $1 billion a year. Here is the 
amazing thing: 77 percent of people 65 and older support that, 
which you would expect, but 75 percent of Americans 18 to 34 
also support this increase in funding.
    Mr. Chairman, members of the committee, we understand that 
the world has changed since we were all here last year, and we 
understand that because of that there are many competing 
priorities before this subcommittee. But one of the lessons 
that we have learned over the last months is that when 
Americans are faced with a real threat and a terrible enemy, we 
stand together and we marshall our resources to fight.
    For 14 million Americans, Alzheimer's disease is that 
threat. Alzheimer's disease is that enemy. The case for 
increasing funding to a billion dollars is overwhelming and the 
support for increasing funding is overwhelming.

                           PREPARED STATEMENT

    You by convening this hearing demonstrate your own concerns 
about this looming crisis and your dedication to preventing it. 
I want to thank you on behalf of the Alzheimer's Association, 
on behalf of all the families dealing with this disease, on 
behalf of everyone in this room, and certainly today in honor 
of our dear friend Maureen Reagan, for whom this was her 
greatest goal.
    Thank you very much.
    [The statement follows:]
                Prepared Statement of David Hyde Pierce
    Mr. Chairman and Members of the Subcommittee, thank you for 
inviting me back to testify before your Subcommittee. As you know, I am 
a National Board member of the Alzheimer's Association. You have heard 
my personal story before. Both my grandfather and my father died of 
Alzheimer's disease.
    With each year that passes, my fear grows--my fear that the disease 
process that destroyed their memories, and ultimately their lives, has 
begun developing in my own brain. My fear grows not just for myself, 
but also for my generation--the 14 million baby boomers who will get 
Alzheimer's disease if we don't find a way to beat this dreadful 
disease.
    At the same time, my hope grows. Today I testify with more 
enthusiasm, more confidence that scientists are on the verge of a 
breakthrough. My hope is joined with a sense of urgency. In the quest 
to find a breakthrough for Alzheimer's disease, this nation is in a 
race against time.
    In the midst of the enormous challenges you face, I urge you to 
maintain your commitment to medical research funding for Alzheimer's 
disease, and increase funding to $1 billion a year as soon as possible. 
In this race against time, we can't afford to slip.
    Today, the Alzheimer's Association is releasing a national survey 
by Peter D. Hart Research Associates regarding Americans' concerns 
about Alzheimer's disease. I ask that the survey analysis be submitted 
for the record. This survey confirms what I see every day--that 
Americans of every age are terrified by the threat of Alzheimer's 
disease, and that they overwhelmingly support the shared efforts of 
this Subcommittee and the Alzheimer's Association to increase funding 
for Alzheimer research to $1 billion annually. I would like to share 
just a few of the findings from the survey.
    Ninety-five percent of Americans believe that Alzheimer's disease 
is a serious problem facing our nation. Perhaps they know as well as we 
in this room do--our window of time is very short. Perhaps they know 
that this disease can strike anyone, even a President of the United 
States.
    Senator Harkin and Senator Specter, you have led this Congress in 
the effort to double funding for NIH. Our survey shows that Americans 
support your work. In fact, in this election year, voters say medical 
research is one of the most important areas for federal spending, 
ranking second only to education spending, and placing ahead of 
spending on the military.
    More importantly, however, to those of us who sit before you 
today--three fourths of Americans agree with the proposal that Congress 
should increase funding for Alzheimer research to $1 billion per year. 
There is a broad coalition of voters who unite behind this proposal, 
with large majorities of both young (75 percent of 18-34 year olds) and 
old (77 percent 65 years old and older) agreeing that funding for 
Alzheimer research should be increased.
    Half of us in the room already have the time bomb of Alzheimer's 
disease ticking away in our brains, each and every day. Congress must 
find a way to defuse this bomb, before it destroys our brains and 
ultimately our entire selves.
    The American people have every right to be afraid of this horrible 
disease. By the middle of the century, 14 million of today's baby 
boomers will have Alzheimer's disease. For most of them, the process 
that will destroy their memories, their lives, and their savings has 
already begun.
    Mr. Chairman. We know there are many competing priorities before 
this Subcommittee, and we understand the fiscal constraints you face as 
you balance those priorities. But as we look to the future of the 14 
million baby boomers and indeed, the future of each and every American, 
the case for $1 billion investment in Alzheimer research is 
overwhelming. This hearing demonstrates your own concern about the 
looming crisis and your commitment to averting it. On behalf of 
everyone in the Alzheimer's Association, for every family dealing with 
Alzheimer's disease, and for all of us sitting here before you, thank 
you.

    Senator Harkin. Thank you very much.
    Dr. Hodes, do you want to come back up. We have got an 
extra chair there. Just join David there.
    I again know he has to leave soon, but I would yield to 
Senator Specter for any comments or questions.
    Senator Specter. Thank you very much, Mr. Chairman.
    I want to thank especially Mr. and Mrs. Gratz for coming in 
and providing some real insights for not only this 
subcommittee, but really for all America, on the kinds of 
difficulties which you have had to face. You are very brave and 
I thank you for coming in.
    I would like to ask Ms. Reid and Mr. Pierce, with the 
family backgrounds that you have and with the obvious 
additional risks which you face, Orien, what do you think about 
the intensive work being done by NIH to try to prevent the 
onset of Alzheimer's?
    Ms. Reid. I think NIH has been doing an outstanding job and 
I am looking forward. You know, we can invest at the 
Association, we already have invested almost $120 million into 
research. But we know that the real resources come from NIH. 
They are the ones who are going to be able to really jump-start 
the effort and continue at the pace that they are continuing at 
to find a cure for this disease.
    I am absolutely desperate for us to find a way to prevent 
this disease.
    Senator Specter. Mr. Pierce, how do you look to your 
future?
    Mr. Pierce. Well, I tell you, what I have noticed, I have 
worked for the Association for a few years and I have used this 
quote of 14 million in the year 2050 so often I have forgotten 
that that 14 million is not going to happen in the year 2050. 
It is happening now. I have friends who are beginning to suffer 
from this. I look to my brother and my sisters and other 
members of my family and I just wonder when.
    So I applaud the NIH for its efforts, but I am really 
impassioned about doubling our research while there is time.
    Senator Specter. Dr. Albert, in your capacity as a 
psychiatrist would you care to offer an opinion as to the 
desirability of having people at random take a test to find out 
what their gene consistency is, the so-called genome, with a 
view to seeing if there is some latent problem that a person 
may have which could be acted upon in a preventive way? Or does 
it open up Pandora's box for too many worries that you cannot 
really effectively deal with?
    Dr. Albert. As you probably know, there are four genes that 
have been identified that are associated with risk for 
Alzheimer's disease, and three of them are fortunately 
extremely rare. They only affect people who are primarily young 
and they occur in families where in every generation multiple 
individuals have the disease. These genes are dominant genes, 
which means if you carry the mutation you will definitely get 
the disease.
    For those individuals, genetic testing along with genetic 
counseling is often available. It is not discouraged if people 
understand the consequence of finding the answer and if the 
genetic counselors feel as if it is appropriate to do the 
testing.
    The other gene that we know about is a gene that increases 
risk for Alzheimer's disease late in life. All of us carry some 
form of that gene and all that it does in its particular risk 
form is to increase the likelihood that you will get it across 
your lifetime. That is called the APOE gene and it is the APOE4 
form of the gene that increases risk.
    There are multiple organizations, health care organizations 
throughout the country, that have met and determined that this 
sort of genetic testing is not to be recommended because it 
does not tell you within a short period of time what is going 
to happen to you. In fact, in my own research we have looked at 
that gene and we have tried to see whether or not it tells us, 
if you have trouble with your memory, whether or not you will 
get Alzheimer's disease in 4 or 5 years. It is of no 
informative value. It does not help at all.
    But in general, people feel that knowing that you have a 
slightly increased risk by having genetic testing is not to be 
recommended.
    Senator Specter. Thank you very much, Dr. Albert, and thank 
you all. Senator Harkin has urged me to urge you to get behind 
us on this nuclear transplant issue. You ladies and gentlemen 
come from all over the country. Our staff can tell you which 
Senators need to hear from you. If you are from Tennessee, 
illustratively, and you write to your Senators, Dr. Frist for 
example, that could be very, very influential. He is the one 
physician in the Senate, and he is not alone in needing 
counvincing.
    We have a very, very tough battle and your lives, the lives 
of your loved ones, and the lives of millions of Americans may 
need to turn on the availability of nuclear transplants. To 
criminalize that kind of medical research and tie the hands of 
scientists, will drive many scientists out of the United States 
to other countries, will severely impact medical research, and 
severely impact the ability of medical research to find a cure 
for Alzheimer's.
    Thank you very much, Mr. Chairman.
    Senator Harkin. Thank you, Senator Specter.
    I just wanted to echo what Senator Specter just said. There 
is so much confusion out there on this issue. I do not know of 
anyone that I have really met, I do not know of anyone on this 
committee or in the Senate, that is in favor of human cloning. 
We are all opposed to human cloning. That is not somatic cell 
nuclear transplantation.
    So a number of us have bills in to criminalize, actually 
criminalize, and put severe civil penalties on anyone who would 
transplant that to a uterus for the purpose of human life. But 
to cut off the research for nuclear transplantation and the 
great promise that it holds to me is just really 
unconscionable, to try to cut that off when so many people are 
suffering and this holds such great promise for so many people.
    So we are going to have a big debate here in the Senate in 
May on this issue, probably before the Memorial Day break. But 
I think it is going to be an extremely, extremely close vote. 
So we really need your help.
    Dr. Hodes, you talked about a study in which scientists 
used an immunization strategy to reverse the formation of the 
amyloid plaques in mice. I have followed this quite closely and 
we really got excited about it because it looked like it might 
be a possibility for the development of vaccine for 
Alzheimer's.
    But then I was surprised when I picked up the paper and 
read that the vaccine was permanently shelved after 15 patients 
who were taking it developed meningitis. Can you inform us or 
enlighten us a little bit about this? What happened? Are we 
still looking at a possible vaccine? Just what has happened to 
that, because it looked like it was so promising.
    Dr. Hodes. Yes, I can relate to you in a limited extent at 
least what occurred. I say limited extent because this was a 
study that was carried out by a pharmaceutical company, Elan. 
NIH was not involved in its support and so I do not have the 
level of information that I might otherwise have.
    But precisely as you described, on the basis of animal 
experimentation, humans were immunized with an amyloid peptide 
that was designed to treat the buildup of that protein 
abnormally in the brains of individuals with Alzheimer's 
disease. In the first phase of the study, a number of 
individuals were treated with one immunization to see if any 
side effects would appear. In that initial study there were 
none.
    The study then moved on to a second stage, in which 
individuals were immunized multiple times, which was the 
process that appeared to be effective in the mouse and animal 
models. It was a number of individuals after the second 
immunization who developed symptoms consistent with 
inflammation of the brain and spinal cord and led to the 
cessation of the study.
    In answer to your question about what this means for the 
future, I think it is important to understand that, although 
this is enormously disappointing, that it is not entirely 
unexpected nor unusual that the first attempt at a new approach 
to treatment is met with the discovery of side effects.
    The National Institutes of Health continues to support 
basic research looking at alternative strategies that use 
immune therapy targeted towards finding something that will be 
therapeutic without the unacceptable side effects that occur. 
So the very impressive initial scientific discoveries remain 
reason for hope. There is continued experimentation to try to 
find nontoxic variants of an immunization approach to 
Alzheimer's disease, all this at the same time that we examine 
the alternatives, other approaches, as many as we can find in 
opportunities provided by basic research at multiple levels.
    Senator Harkin. So there is under your Institute some 
ongoing basic research into immunological approaches, for 
example?
    Dr. Hodes. Yes, precisely so. In an initiative that was 
encouraged by the White House 2 years ago and was funded last 
year, there is specifically funding of a large cohort of 
investigators who are looking at different aspects of immune 
approaches to Alzheimer's disease in animal model systems.
    Senator Harkin. These initial studies by Elan--they went 
through all the safety tests, so it was pretty shocking that it 
turned out like that. Again, you are right, this was not an NIH 
thing. This was through a private drug company.
    But can you assure me that there are researchers that are 
being funded by NIH that are looking at what happened and 
perhaps sort of, in my own nonscientific way of saying it, 
backing down from that and starting over again with that type 
of research on a vaccine?
    Dr. Hodes. Certainly attempts to try to----
    Senator Harkin. Let me say this. We are trying to find out, 
why did it not cause the inflammation in mice? It passed the 
safety studies, then, as you mentioned, after multiple 
vaccinations resulted in problems. Well, there is something in 
there that needs to be looked at. I was just wondering, is NIH 
funding any research in the area to find out what might have 
gone wrong there?
    Dr. Hodes. The NIH is funding research looking at 
approaches in animal models to determine which of them might be 
more or less prone to the kind of complication that you 
mention. Actual studies on the patients who underwent these 
clinical trials and who suffered the side effects is being 
carried out by Elan and those precise studies on those patients 
are not a part of NIH-supported research.
    But certainly the efforts to understand what in immune 
therapy is likely to cause those side effects and how it can be 
avoided is most certainly a part of the ongoing research 
supported by NIH.
    Dr. Albert. Senator Harkin, if I might just add one brief 
word. As Dr. Hodes mentioned, we do not know all the details of 
what went on because it was done by the pharmaceutical company. 
But the initial safety studies were done with a very small 
number of people. I think it was no more than about 30 people 
that were in those studies. In the larger trial there were over 
300, and that is when you increase the possibility of having 
side effects. So I think that is the primary reason why the 
side effects were not identified early on; and as Dr. Hodes 
said, because they gave multiple injections and it was only 
after two or more that people developed side effects.
    But there are many reasons to be optimistic, because the 
particular strategy that they used included a large portion of 
this protein that we know to be important for Alzheimer's 
disease. Some people feel, for example, that if they used a 
smaller part of the protein it might be just as efficacious and 
not harmful.
    Senator Harkin. So you think it still holds some promise?
    Dr. Albert. Absolutely.
    Senator Harkin. And we should continue the research and 
development into that.
    Dr. Albert, one other aspect of this that is intriguing to 
me is this idea of use it or lose it, using your brain. Someone 
told me you are working on a book about that right now.
    Dr. Albert. That is correct. It is very nice of you to ask.
    Senator Harkin. Well, let us talk about this book.
    Dr. Albert. It is called ``Keep Your Brain Young.''
    Senator Harkin. When can we expect it out?
    Dr. Albert. It is actually out right now.
    Senator Harkin. Oh, it is?
    Dr. Albert. Yes, within the last few weeks.
    Senator Harkin. Oh my goodness. Well, I will have to get a 
copy of that. What are you advocating?
    Dr. Albert. In fact, research has shown over the last 
decade or so that it is important to be both physically and 
mentally active. It makes sense to us that being mentally 
active might be helpful to the brain, form more connections, 
but recent research has demonstrated that physical activity 
seems to work and interact with mental activity to be 
beneficial for the brain.
    Basic animal research suggests that that might be because 
the brain releases certain kinds of protective factors that 
help it respond to injury. There is very recent exciting 
research that being physically active in a so-called enriched 
environment helps with neurogenesis, the generation of new 
nerve cells, particularly in the part of the brain that has to 
do with memory.
    So there are several avenues that people can take just in 
their daily lives to maximize function.
    Senator Harkin. In your book are you specific to saying do 
certain things? Are there certain types of things?
    Dr. Albert. The book is based on scientific evidence and so 
we outline a number of things that are available. As Dr. Hodes 
mentioned, there are a number of prevention trials that are 
ongoing looking at the effects of vitamin E, ibuprofen, 
statins, estrogen. We talk about those as well. We talk about 
the importance of stress and data on the fact that high levels 
of stress hormones in the brain are bad for it.
    Senator Harkin. Let me ask another question to anyone here. 
Again, there is a lot of talk, I do not know if studies have 
been done, or at least preliminary types of things, to indicate 
that certain types of vitamins, folic acid, maybe some of the B 
vitamins, gingko biloba, others--in fact, before my older 
brother passed away a couple of years ago he had been having 
some problems with memory, and his doctor actually prescribed 
gingko biloba to him to take, which I found interesting. This 
would be 3, almost 4 years ago now.
    What can you tell us about that? Antioxidants, things like 
that, these are things I read about, but is there any basis for 
that at all, Dr. Hodes?
    Dr. Hodes. I think for each of the agents you have 
mentioned--and we can discuss them in more detail--the answer 
is yes, there is something to it. Yes, there is a basis for 
considering the possibility they will be effective, but for 
none of them is there as yet definitive incontrovertible 
evidence of effectiveness.
    Those are precisely the situations where we think it 
important to conduct rigorous clinical trials as expeditiously 
as possible. So that currently for vitamin E, for other 
antioxidants, for folate, for B12, for gingko biloba, among 
other agents, there are prevention trials that are currently in 
progress. These are randomized trials in which the individuals 
taking the drugs or supplements, the physicians who are taking 
care of them, do not know the identity of the drug.
    Then over a period of years observations will determine 
whether those individuals who did or did not take a particular 
agent are more or less likely to develop Alzheimer's disease. 
These studies most definitely have the ability to determine 
whether there is a significant effect of these agents or not. 
We have every reason to hope that one or more of them will be 
effective. But at the same time we convey this optimism, it is 
important to convey to the public that none of them is yet 
proven and none of them can be recommended in the absence of 
further scientific evidence.
    Senator Harkin. Any other observations on that at all?
    Ms. Reid. No, except to tell you that I take them all.
    Senator Harkin. Well, I would guess on that side they 
cannot harm you.
    Dr. Hodes. I guess responsibly it is important to qualify 
that last statement, that they cannot harm you. Certainly if 
these agents were absolutely without risk it would be hard to 
deny the logic that says why not try them. But in fact, even 
for the most benign of them, agents such as vitamin E, it has 
been shown that at some of the dosage levels that people are 
taking that they can interact with other drugs and can 
predispose to problems. So that one does have to be quite 
cautious.
    Senator Harkin. Well, you are right in terms of interaction 
with other drugs and stuff. That is why we always say you 
should make sure that your health care provider knows all you 
are taking and stuff like that, and do the research and do your 
own reading on it yourself, and take matters into your own 
hands.
    But I am not certain, Dr. Hodes, that I would agree fully 
with you on that. Certainly anything taken in excess can hurt 
you. An aspirin, if you take a bottle, will kill you. People 
die every year. We have hundreds of deaths in this country from 
aspirin. But to take things like, I do not take gingko, but 
vitamin E or folic acid, the B drugs, I think taken in dosages 
that have been at least recommended by various studies over the 
years, I cannot see how that would ever harm anybody.
    Obviously, if you overdosed or something like that on 
anything----
    Dr. Hodes. I think I agree very much with what you said. It 
is important to distinguish between recommendations that are 
well-founded on experience or doses of vitamins, including 
folate or the B vitamins--quite right, there are 
recommendations for daily intake that are consistent with 
health and have minimal side effects.
    But for some of the agents being recommended, being used by 
some for treatment or prevention of Alzheimer's, the evidence 
is simply not clearcut, and it is in those cases where the risk 
of overdosing, if you will, exists, because what constitutes a 
safe or dangerous dose is not as well determined as it is for 
some of these other agents.
    Senator Harkin. One of the reasons I have been pushing for 
years for that National Center on Complementary and Alternative 
Medicine to do more research in that area, because the RDA's 
that we have today were established--help me out here--60 years 
ago, something like that?
    Dr. Hodes. Many are quite old, correct.
    Senator Harkin. I think they are 60 or 70, something like 
that. The recommended daily allowances were set up as the 
minimums, as I understand it, to prevent things like vitamin C 
deficiencies. They were set up as the bare minimums that you 
need.
    Other medical researchers over the years have said, well, 
that may be fine, but in some of these cases actually boosting 
those levels up will help your immunological system.
    So I am not certain that just taking RDA's or recommended 
daily allowances is effective at all in some of these cases. I 
know I will bet you there are millions of people out there 
leading healthful lives that take much more than the 
recommended daily allowances of a lot of different vitamins, 
like E and A and everything else. But again, we need more 
research in that area.
    Dr. Hodes. That is certainly an area I think where we agree 
entirely on that last statement. We in studies such as the 
gingko biloba trial are working closely with Steve Strauss and 
the National Center for Complementary and Alternative Medicine 
to assure that the best kind of science is applied with an open 
mind to the efficacy and safety of agents such as this.
    Senator Harkin. I might just say, for the benefit of 
everyone here, that there is really pretty extensive research 
going on through that National Center on gingko biloba. I 
assume you work together with them on that, Dr. Hodes. Do you?
    Dr. Hodes. We do. That study is being carried out 
collaboratively with that center.
    Senator Harkin. Very good.
    Mr. Pierce, you may have told us last year, but remind us: 
How old were your father and grandfather when they were 
diagnosed?
    Mr. Pierce. We noticed the symptoms in my grandfather in 
his mid-eighties. Well, actually in his case the diagnosis was 
done on autopsy after he passed away, which was in his early 
nineties. My dad was in his late seventies, early eighties. I 
actually do not know about his sister, but they were of a 
contemporary age, so I imagine it was the same.
    Senator Harkin. Is it not true you really cannot diagnose 
still today Alzheimer's until you do an autopsy? Is that not 
right, Dr. Hodes?
    Dr. Hodes. That is true, that is the definitive test. But 
the ability to diagnose during life has improved greatly with 
more extensive testing of biology function imaging, so that in 
the hands of people well versed the accuracy of that diagnosis 
can be in the range of 90 percent or more.
    Senator Harkin. Getting to the funding level, you mentioned 
how many people would be affected in the future and you are 
right, that baby boom generation is here now. They are alive 
right now.
    We have all this talk about what we are going to do to save 
the Medicare system because of the onset of the baby boom 
generation and people living longer. A lot of people are 
scratching their heads on how to fund it.
    I saw a figure about a year ago that said that if we could 
just delay the onset of Alzheimer's by 5 years, we would have 
no problem in Medicare funding. That would decrease the cost of 
Medicare so much that we would have no problems. Think what it 
would do if we could actually find a cure of Alzheimer's. Then 
we really could provide prescription drugs for everyone under 
Medicare and things like that.
    Eighteen clinical trials, is that what you said, Dr. Hodes?
    Dr. Hodes. Correct.
    Senator Harkin. Can you give us some idea of some that you 
think really are looking good?
    Dr. Hodes. We do not have information from them as they are 
in progress. The way that these studies are done, because they 
are masked or blinded so that individuals do not know what they 
are taking, leads to the consequence that in general we do not 
know the outcome until a study is over. Now, it is monitored 
carefully and confidentially, so that if we should find an 
overwhelming positive result or evidence of toxicity, a 
negative effect, early, the study would be stopped. But this is 
the unusual circumstance. So in general we will not know the 
outcome until the studies are terminated and the data analyzed.
    Senator Harkin. I am just going to ask a question of 
everyone in the audience. How many people here in this audience 
today take multi-vitamins on a daily basis and supplement that 
with maybe other doses of vitamin E or the B vitamins or 
vitamin C or other things like that? I am just curious as to 
how many people do that here. How many people here take that on 
a daily basis?
    [A show of hands.]
    Look around, Dr. Hodes. I'd better raise my hand, too, 
because I do also.
    I think there is a great sense among people that somehow we 
know what our bodies are telling us, that we need this, and we 
better get the researchers going on this. That is not in your 
bailiwick. That is in that other center, NCCAM. That is why I 
am trying to push them.
    I will close up. Again, talking about the caregiver portion 
of this, we cannot lose sight of the fact that as we proceed in 
the funding for research that we have to be very cognizant of 
support for caregives. The toll that this takes on families is 
incredible. The Gratzes, it just tears our hearts out.
    I have been blessed in my own family. We have not really 
had Alzheimer's in my own family, but we do have very dear and 
close friends with this disease. Joann Hutchins, who I have 
known all my adult life, is now in a nursing home and does not 
recognize her husband. Watching this as a close personal 
friend, it is just mind-boggling what this does to families.
    My elementary school teacher lived across the street from 
me until about 5 years ago. Mary King was wonderful. She 
actually got me started in school. She was the first one who 
ever read a book to me. All of a sudden, she got hit with 
Alzheimer's. It came on really suddenly, like within a year, 
and she could not take care of herself, and now she is in a 
nursing home. So you see, we just have to make sure we do not 
forget about that aspect of it, the caregivers.
    To the Gratz family, you are extremely courageous. All I 
can say is, Kris, you chose well when you chose these parents, 
I can tell you that. They are very brave parents. We need them 
to keep telling their story. I know it is tough, but people 
have to understand the human dimensions of this. These are not 
just statistics on pieces of paper. These are our friends, our 
relatives, our loved ones, our family members.
    I have found around here that many times the most powerful 
way to get to someone here is just to give them that human 
story. That is what we need you to do while you are here today 
and tomorrow, I do not want to say lobbying, I want to say 
educating the Members of Congress. But do not take no for an 
answer. Get in to see these people, because obviously we do 
what we can here, but we need support--I mean we here on this 
committee--we need the support of our fellow Senators.
    I will say right here now to all of my friends who are 
here, I love you dearly and this is a cause of mine that I took 
up a long time ago. I might just say again--I should have said 
this when Senator Specter was here. I said when I was chairman 
we doubled Alzheimer's funding, when he was chairman he has 
doubled it. Well, now it is my turn again, and I intend to do 
it again.
    But we need the support of our fellow Senators to do this. 
I cannot do it by myself and Senator Specter cannot do it by 
himself. The two of us working together can do a lot, but we 
cannot do everything. We do need a lot of help here and we need 
help in the House of Representatives, too. That is why it is so 
important what you are doing here.
    I just cannot tell each of you how important it is for you 
to get to these offices and to talk to people and bring them 
the human dimensions of what we are talking about. And yes, 
tell them about Medicare, tell them about the impact on the 
money. They need to understand that, too.
    We will continue to do our job here to support Dr. Hodes 
and the National Institute and to support all of NIH here. It 
is not just in Dr. Hodes' Institute. There is research that 
affects this in just about every Institute, I think, going 
throughout the whole spectrum of the Institutes at NIH. Dr. 
Hodes has the lead agency, but there are a lot of others that 
are out there.
    So again, I just want to thank you all for being here.
    Orien, thank you very much for your great leadership. You 
are a wonderful spokesperson. You get the point across. You 
have a great persona. We need people like you to get those 
points across. So God bless you and thank you so much.
    David, thank you again also. People look to people like 
you. You are a well-known person in this country and people 
like you. Again, your persona comes across as someone that 
people like and they trust. Your words, your leadership, can be 
very powerful in moving us here and getting the American people 
to understand the dimensions of this. So I congratulate you. I 
thank you for the leadership.
    To Dr. Albert and to Carol and Gene again, please continue 
to tell your story and please continue to get the word out on 
what we can do. Hopefully, we are going to have some 
breakthroughs here. You are a young man and hopefully pretty 
soon we are going to have some breakthroughs here that will 
help you out. That is my fervent hope, my wish, and now we have 
just got to get the money behind it.
    Mr. Gratz. I really appreciate you guys letting us be here. 
I guess one thing we have to do with Alzheimer's, when times 
are bad you have got to laugh at it a little bit. It makes the 
day go better. Sometimes you have got to act a little crazy, 
but that is okay, too, because it makes your day go better.
    The folks in New Hampton, I want to get them out of their 
houses instead of hibernating anymore. I mean, I walk around, I 
was kind of pushed aside for quite a while until they finally 
realized that I was the sort that was not going to go away.
    Senator Harkin. Good for you.
    Mr. Gratz. And I will be there until the Lord says it is 
time for me to leave.
    Senator Harkin. Just remember, you are not alone. You have 
got everybody here. You are not alone and we are with you.

                         CONCLUSION OF HEARING

    Thank you all very much for being here, that concludes our 
hearing.
    [Whereupon, at 10:29 a.m., Tuesday, April 30, the hearing 
was concluded, and the subcommittee was recessed, to reconvene 
subject to the call of the Chair.]

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