TABLE OF CONTENTS

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Preventing a Complex Disease Like AD is a Challenge . . . . . . . . . 3

AD Risk Factors We Can’t Control . . . . . . . . . . . . . . . . . . . . . . . . . 3

The Search for AD Prevention Strategies . . . . . . . . . . . . . . . . . . . . 7

The Search for Other Clues That May Contribute to

Prevention Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

What Can You Do? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

A Final Word of Caution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

For More Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
page 

Can Alzheimer’s Disease be Prevented?

Introduction

These days, it seems that newspapers, magazines, and TV are full 

of stories about ways to stay healthy, eat right, and keep fit. Lots 

of people are concerned about staying healthy as they get older. 

They wonder whether they can do anything to prevent diseases that 

happen more often with age, such as Alzheimer’s disease (AD). 

AD has no known cure, and the secrets to preventing it are not yet 

known. But research supported by the National Institute on Aging 

(NIA) and other public and private agencies offers tantalizing 

clues about the origins and development of AD. These findings are 

raising hopes that someday it might be possible to delay the onset 

of AD, slow its progress, or even prevent it altogether. Delaying 

by even 5 years the time when AD symptoms begin could greatly 

reduce the number of people who have the disease.

The National Institute on Aging, part of the Federal Government’s National 

Institutes of Health, has primary responsibility for research on AD and agerelated decline in cognitive abilities (such as thinking, decision-making, 

and language skills). This responsibility is part of a larger mission to 

understand the nature of aging and find ways to help people stay physically, 

emotionally, and cognitively healthy for as long as possible. 

Several years ago, NIA, the National Institute of Mental Health, and the 

National Institute of Neurological Disorders and Stroke launched The 

Cognitive and Emotional Health Project, which has begun to identify and 

describe the diverse lifestyle factors that possibly affect the emotional 

health and cognitive abilities of older adults. Further research on the most 

promising factors will be necessary to determine whether any will result 

in strategies that can help people remain mentally and emotionally vibrant 

as they age. The hope is that successful strategies will also contribute to 

our knowledge of what goes wrong in the brain during the development of 

neurodegenerative diseases like AD.

page 

Can Alzheimer’s Disease be Prevented?

Preventing a Complex Disease Like AD 

is a Challenge

Many diseases, such as diabetes, heart disease, and arthritis, are 

complex. They develop when genetic, environmental, and lifestyle 

factors work together to cause a disease process to start and then 

progress. The importance of these factors may differ for each 

person. AD is one of these complex diseases. It develops over 

many years, and it appears to be affected by a number of factors 

that may increase or decrease a person’s risk of developing the 

disease. We don’t have control over some of the risk factors for 

AD. We can do something about other possible AD risk factors, 

though. The effect on any particular person of risk factor changes 

will likely depend on his or her genetic makeup, environment, 

and lifestyle. 

AD Risk Factors We Can’t Control

Age is the most important known risk factor for AD. The risk of 

developing the disease doubles every 5 years over age 65. Several 

studies estimate that up to half the people older than 85 have AD. 

These facts are significant because of the growing number of 

people 65 and older. More than 34 million Americans are now 65 

or older. Even more significant, the group with the highest risk of 

AD—those older than 85—is the fastest growing population group 

in the country.

Genetics is the other known AD risk factor that a person can’t 

control. Scientists have found genetic links to the two forms of AD. 

Early-onset AD is a very rare form of the disease that can occur 

in people between the ages of 30 and 65. In the 1980s and early 
Can Alzheimer’s Disease be Prevented?

page 

1990s, researchers found that mutations (or changes) in certain 

genes on three chromosomes cause early-onset AD. If a parent has 

any of these genetic mutations, his or her child has a 50-50 chance 

of inheriting the mutant gene and developing early-onset AD. 

Late-onset AD, the more common form, develops after age 65. In 

1992, researchers found that certain forms of the apolipoprotein E 

(APOE) gene can influence AD risk:

APOE ε2, a rarely occurring form, may provide some 

protection;

APOE ε3, the most common form, plays a neutral role; and

APOE ε4, which is found in about 40 percent of people with 

AD; APOE ε4 lowers the age of onset and thus increases risk. 

(Having this gene form does not mean that a person will definitely develop AD; it only increases risk. Many people who 

develop AD do not have the APOE ε4 form.) 

Researchers are now intensively searching for other risk factor 

genes that may be linked to late-onset AD. Discovering these 

genes is essential for understanding the very early biological steps 

leading to AD and for pinpointing targets for drug development and 

other prevention or treatment strategies. It’s also critical for developing better ways to identify people at risk and determining how 

AD risk factor genes may interact with other genes or with lifestyle 

or environmental factors to affect AD risk in any one individual. 

In 2003, the NIA announced a major expansion of AD genetics 

research efforts. The AD Genetics Study is collecting genetic 

material from individuals in families with two or more living 

brothers or sisters who have late-onset AD. This valuable resource 

♦

♦

♦


page 

Can Alzheimer’s Disease be Prevented?

will allow geneticists to speed up the discovery of additional AD 

risk factor genes.

The Search for AD Prevention Strategies

Though we can’t do much about our age or genetic profile, recent 

research suggests that maintaining good overall health habits may 

help lower the chances of developing several serious diseases, 

including ones affecting the brain. This booklet describes a number 

of health, lifestyle, and environmental factors that could make a 

difference in AD and that are being actively studied by scientists. 

Many of these potential factors have been identified in observational and animal studies. At present, they are only associated with 

changes in AD risk. Only further research, including clinical trials, 

will reveal whether, in fact, these factors can help to prevent AD. It 

is important to understand that the degree to which a person might 

be helped by any of these factors may be very slight, especially 

if the person has inherited a bad form of a risk factor gene. That 

is why it is so important to also focus on other parts of the AD 

prevention research mission. At the same time that scientists are 

examining lifestyle factors, many others are developing drugs that 

can enhance protective biochemical pathways or block pathways 

that lead to cognitive decline and AD. 

Investigating heart disease risk. High levels of blood cholesterol 

are a known risk factor for heart disease. In recent years, basic 

research in laboratories as well as population and animal studies 

have suggested there may also be a connection between high levels 

of blood cholesterol and development of AD. These findings led 

scientists to wonder whether drugs that lower blood cholesterol 
Can Alzheimer’s Disease be Prevented?

page 

might also lower the risk of developing AD or reduce its rate of 

progression. Recent population and animal studies have raised the 

possibility that statins, the most commonly prescribed cholesterol 

lowering drugs, may reduce the risk of dementia. Other studies, 

though, have found no association between statins and dementia 

risk. Thus, it is not clear at this time whether statins affect the onset 

or progression of AD. To help answer this question, the NIA is 

currently funding a clinical trial to determine whether one particular statin slows the progression of AD. 

Other research has found that a high level of the amino acid homocysteine is associated with an increased risk of developing AD. 

High levels of homocysteine are known to increase heart disease 

risk, and NIA studies in mice have shown that high levels of this 

amino acid can make neurons stop working and die. The relationship between AD risk and homocysteine levels is particularly 

appealing because blood levels of homocysteine can be reduced 

by increasing intake of folic acid and vitamins B6 and B12. An 

NIA-funded clinical trial is currently studying whether reducing 

homocysteine levels with folic acid and vitamin B6 and B12 

supplements will slow the rate of cognitive decline in older adults 

with AD.

Examining high blood pressure. Scientists also have found associations among AD, high blood pressure that begins in midlife, and 

other risk factors of stroke, such as age, diabetes, and cardiovascular 

disease. It is known that even in relatively healthy older adults, high 

blood pressure and other stroke risk factors can damage blood vessels 

in the brain and reduce the brain’s oxygen supply. This damage 

may disrupt nerve cell circuits that are thought to be important to 

decision-making, memory, and verbal skills. Scientists are studying 


page 11

Can Alzheimer’s Disease be Prevented?

the connections between AD and high blood pressure in hopes that 

knowledge gained will provide new insights into both conditions.

Learning about diabetes and insulin resistance. Large-scale 

population studies suggest that diabetes is associated with several 

types of dementia, including AD and vascular dementia (a type 

of dementia associated with strokes, sometimes referred to as 

multi-infarct dementia). These studies have found that AD and 

type 2 diabetes share several characteristics, including increasing prevalence with age, genetic predisposition, and deposits of 

two different kinds of damaging amyloid protein (in the brain for 

AD and in the pancreas for type 2 diabetes). Abnormal glucose (a 

type of sugar) regulation, a key element of diabetes, also has been 

associated with development of AD. Scientists are working to learn 

more about this association.

Researchers also are becoming increasingly interested in the 

possible role of insulin resistance (a condition in which the body 

produces insulin but cells do not use it properly) in AD. Too much 

insulin in the blood (which happens as a result of insulin resistance) may encourage inflammation and oxidative stress, both of 

which contribute to the damage seen in AD. 

Possible relationships between cognitive decline, AD, and diabetes 

are being explored in the Religious Orders Study, which involves 

a large group of older priests, nuns, and brothers who have been 

working with scientists funded by the NIA since 1993. This study 

has provided a wealth of information about many aspects of AD, 

including the possible link between diabetes and cognitive decline 

and AD. In one analysis involving more than 800 study participants, researchers examined tests of five “cognitive systems” 
Can Alzheimer’s Disease be Prevented?

page 12

involved with word and event memory, information processing 

speed, and the ability to recognize spatial patterns. They found that 

diabetes was associated with declines in some cognitive systems 

but not others. The researchers also found a link between those 

with diabetes and an increased risk of developing AD. 

The NIA is funding several clinical trials to determine whether 

treating different aspects of diabetes might affect AD development 

or progression. For example, the NIA is supporting clinical trials 

to evaluate the effect of a drug called rosiglitazone on changes 

in cognitive abilities in people with mild cognitive impairment 

(MCI, a condition in which a person has memory problems but 

not other AD problems; this condition often progresses to AD). 

Rosiglitazone makes cells more sensitive to insulin. The NIA 

is also supporting a study that is evaluating cognitive and brain 

structure changes using magnetic resonance imaging (MRI). This 

study, called ACCORD-MIND (Memory in Diabetes) has been 

added to the ongoing National Heart, Lung, and Blood Institute 

ACCORD (Action to Control Cardiovascular Risk in Diabetes) 

clinical trial. ACCORD is evaluating a variety of approaches for 

managing glucose, blood pressure, and blood lipids. 

Examining social engagement and intellectually stimulating 

activities. Findings from studies of animals, nursing home 

residents, and older people living in the community have suggested 

a link between social engagement and cognitive abilities. Having 

lots of friends and acquaintances and participating in many social 

activities is associated with reduced cognitive decline and decreased 

risk of dementia in older adults. In the NIA-funded Chicago Health 

and Aging Project, a high level of social engagement was associated 

with a significant reduction in cognitive decline. 


page 15

Can Alzheimer’s Disease be Prevented?

Studies also have shown that keeping the brain active is associated with reduced AD risk. In the Religious Orders Study, for 

example, investigators periodically asked more than 700 participants to describe the amount of time they spent in seven activities 

that involve significant information processing. These activities 

included listening to the radio, reading newspapers, playing puzzle 

games, and going to museums. After following the participants for 

4 years, investigators found that the risk of developing AD was 47 

percent lower, on average, for those who did the activities most frequently than for those who did them least frequently. Other studies 

have shown similar results. In addition, a growing body of research, 

including other findings from the Religious Orders Study, suggests 

that, even in the presence of AD plaques, the more formal education 

a person has, the better his or her memory and learning ability.

Another NIA-funded study also supports the value of lifelong 

learning and mentally stimulating activity. In this study of healthy 

older people and people with possible or probable AD, scientists 

found that during their early and middle adulthood, the healthy 

older people had engaged in more mentally stimulating activities 

and spent more hours doing them than did those who ultimately 

developed AD.

The reasons for these findings aren’t entirely clear, but scientists 

have come up with four possibilities:

These activities may protect the brain in some way, perhaps by 

establishing a “cognitive reserve.”

Perhaps these activities help the brain become more adaptable 

and flexible in some areas of mental function so that it can compensate for declines in other areas.

♦

♦
Can Alzheimer’s Disease be Prevented?

page 16

Less engagement with other people or in intellectually stimulating activities could be the result of very early effects of the 

disease rather than its cause.

Perhaps people who engage in these activities have other 

lifestyle features that may protect them against developing AD.

The only way to really evaluate some of these possibilities is by 

testing them in a controlled way in a clinical trial.

Several clinical trials have directly examined whether memory 

training and similar types of mental skills training can actually 

improve the cognitive abilities of healthy older adults and people 

with mild AD. In the Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) trial, certified trainers provided 

10 sessions of memory training, reasoning training, or speed of 

processing training to healthy adults 65 years old and older. The 

sessions improved participants’ mental skills in the area in which 

they were trained. Even better, these improvements persisted for at 

least 2 years after the training was completed. In another study, 25 

participants with mild AD worked with researchers to learn how to 

improve their ability to carry out various tasks, such as how to put 

names and faces together, recall the names of objects, and pay bills 

correctly. Compared to another group with mild AD who received 

more generic mental stimulation activities, people in the “cognitive 

rehabilitation” group improved their abilities more, and their 

abilities were still improved 3 months later.

Investigating physical activity. Accumulating evidence suggests 

that being physically active may benefit more than just our hearts 

and waistlines. Research in older animals has shown that both 

physical and mental function improve with aerobic fitness. Two 

♦

♦


page 19

Can Alzheimer’s Disease be Prevented?

studies in aging adults have shown similar results. The first study 

used MRI to measure changes in brain activity in healthy adults 

aged 58-78 before and after a 6-month program of brisk walking. 

The researchers found that improvements in the participants’ 

cardiovascular fitness were associated with increased functioning 

in certain regions of the brain. Compared to a physically inactive 

group, the walkers were able to pay attention better and focus more 

clearly on goals while disregarding unimportant information. 

In a second study, investigators studied the relationship of physical 

activity and mental function in nearly 6,000 healthy women 65 

years old and older over a period of up to 8 years. The investigators found that the women who were more physically active were 

less likely to experience a decline in their mental function than 

were inactive women. The NIA is currently funding several clinical 

trials that are studying the effects of physical activity programs on 

the cognitive abilities and brain function of healthy older adults 

and older adults with MCI.

Scientists have speculated about why physical activity may help 

our brains as much as our bodies. It may be that physical activity 

improves blood flow to the brain so that it responds better to a 

task. Or, it may activate cellular mechanisms that improve brain 

function. However, we still don’t know whether physical activity 

can actually prevent cognitive decline or postpone the development 

of AD, especially in people with a high genetic risk. 

Examining nonsteroidal anti-inflammatory drugs (NSAIDs).

Inflammation of tissues in the brain is a common feature of AD, 

but it is not clear whether it is a cause or effect of the disease. 

Some population studies suggest an association between a reduced 
Can Alzheimer’s Disease be Prevented?

page 20

risk of AD and commonly used NSAIDs, such as ibuprofen, 

naproxen, and indomethacin. 

Clinical trials thus far have not demonstrated a benefit for AD 

from these drugs or from the newer cyclooxygenase-2 (COX-2) 

inhibitors, such as rofecoxib and celecoxib. A trial testing whether 

naproxen or celecoxib could prevent AD in healthy older people at 

risk of the disease has been halted, but investigators are continuing to conduct follow-up examinations with participants and to 

examine data about cognitive changes and possible cardiovascular risk. Scientists continue to look for ways to test how antiinflammatory drugs targeting particular pathways might affect the 

development or progression of AD.

Learning about antioxidants and other interventions. Another 

promising area of research focuses on highly active molecules 

called free radicals. Damage from these free radicals during aging 

can build up in nerve cells and result in a loss of cell function, 

which could contribute to AD. Some population and laboratory 

studies suggest that antioxidants from dietary supplements or food 

may provide some protection against this damage (called oxidative 

damage), but other studies show no effect. 

Clinical trials may provide some answers. Several trials are investigating whether two antioxidants—vitamins E and C—can 

slow cognitive decline and development of AD in healthy older 

individuals. The NIA is conducting a clinical trial that will 

examine whether taking vitamin E and/or selenium supplements 

over a period of 7 to 12 years can help prevent memory loss and 

dementia. This trial has been added on to a prostate cancer prevention clinical trial funded by the National Cancer Institute. The NIA 


page 23

Can Alzheimer’s Disease be Prevented?

is also conducting a clinical trial to determine whether antioxidant 

supplements can prevent cognitive decline in healthy older women 

or older women at increased risk of dementia. 

Another just-completed study focused on the use of vitamin E 

supplements in people with MCI. This NIA study, the Memory 

Impairment Study, compared donepezil (Aricept), vitamin E 

supplements, or placebo (an inactive substance) in participants with 

MCI to see whether the drugs might delay or prevent progression 

to AD. The study found that taking the vitamin E had no effect on 

progression to AD at any time in the study when compared with 

placebo. It may be that this antioxidant may not help after memory 

declines have already started. Donepezil, however, did seem to delay 

progression to AD over the first year of treatment. Interestingly, 

there seemed to be an interaction between the genetic makeup of 

participants and their response to treatment: People carrying the risk 

factor APOE ε4 allele delayed the risk of developing AD for the 3 

years of the trial. Scientists caution, however, that people with MCI 

should not be tested to see whether they carry the APOE-ε4 allele 

because more research is still needed to understand how the drug 

works in the body and to answer other questions. 

Expanding knowledge about estrogen. This hormone is produced 

by a woman’s ovaries during her childbearing years. After this 

time, estrogen production declines dramatically. Over the past 

25 years, some laboratory and animal research, as well as observational studies in women, have suggested that estrogen used by 

women to treat the symptoms of menopause also protects the brain. 

Experts have wondered whether using estrogen could reduce the 

risk of AD or slow disease progression. 
Can Alzheimer’s Disease be Prevented?

page 24

A number of clinical trials have shown that estrogen does not slow 

the progression of already-diagnosed AD. Clinical trials testing 

whether estrogen might prevent AD in women who have already 

gone through menopause have also found that using estrogen to 

treat or prevent AD may not be effective, if treatment is begun in 

later life. A large trial found that women older than 65 who took 

estrogen (Premarin) alone or estrogen with a synthetic progestin 

were actually at increased risk of developing dementia, including 

AD. Some questions remain unanswered, however, such as 

whether some forms of estrogen might help if started somewhat 

earlier than the older ages tested in this trial. These questions are 

now being investigated. 

Researchers also are trying other ways to work with estrogen’s 

potentially positive effects for the brain. For example, scientists 

have developed estrogen-like molecules called SERMs (selective 

estrogen-receptor modulators) that protect against bone loss and 

other consequences of estrogen levels falling after menopause. 

These molecules may retain estrogen’s neuron-protecting ability 

but may not have some of its other harmful effects on the body. A 

large clinical trial tested a SERM called raloxifene, which is used 

in the prevention and treatment of osteoporosis. The study showed 

that this SERM lowered the risk of MCI among a group of postmenopausal women with osteoporosis. A newly-funded clinical 

trial is ongoing to test whether raloxifene can slow the rate of AD 

progression. 

Investigating ginkgo biloba. This readily available natural product 

has been proposed as a potential treatment or preventive agent for 

AD. A 1997 study in the U.S. suggested that a ginkgo extract may 

be of some help in treating the symptoms of AD and multi-infarct 


page 27

Can Alzheimer’s Disease be Prevented?

dementia, but no evidence exists that ginkgo biloba will prevent 

AD. At the NIH, the National Center for Complementary and 

Alternative Medicine and the NIA are currently supporting a large 

clinical trial to explore whether ginkgo has any effect on preventing AD or delaying cognitive decline in older adults.

Exploring immunization. Will a vaccine someday prevent AD? 

Early vaccine studies in mice were so successful in reducing 

deposits of beta-amyloid (the major component of the plaques 

that develop in the brains of people with AD) and improving brain 

performance on memory tests that investigators conducted preliminary clinical trials in humans with AD. These studies had to be 

stopped because of life-threatening inflammation that occurred in 

some participants. However, the pharmaceutical industry and NIHfunded scientists are continuing to refine this strategy in animal 

models of AD, hoping to find ways of maintaining the therapeutic 

effects while reducing the unwanted side effects. Several pharmaceutical companies have recently obtained permission from the 

FDA to test several of these new strategies for safety in early stage 

clinical trials. 

The Search for Other Clues That May 

Contribute to Prevention Strategies

Investigators are pursuing still other strategies that may eventually 

help to prevent or delay AD. For example, they are trying to 

discover whether changes in certain biological compounds in blood, 

urine, or cerebrospinal fluid could indicate early AD changes in the 

brain. Understanding more about these biological markers, how 

they work, and what causes their levels to change is important in 
Can Alzheimer’s Disease be Prevented?

page 28

helping scientists answer questions about what makes AD begin and 

develop. Learning more about these markers also may help scientists track whether certain medications are having their intended 

effects and may some day lead to new prevention strategies.

One major effort involves the use of imaging techniques, such as 

MRI and positron emission tomography (PET), to measure brain 

structure and function. An NIA public-private partnership—the 

AD Neuroimaging Initiative—is a large study that will determine 

whether MRI and PET scans or other imaging or biological 

markers can be used to identify early AD changes and disease 

progression. One day, these measurements may be able to identify 

those people who are at risk of AD before they develop symptoms. 

The measurements may also help physicians assess the response 

to treatment much more rapidly and less expensively than is 

possible today. To learn more about the Neuroimaging Initiative, 

visit the NIA’s Alzheimer’s Disease Education and Referral Center 

(ADEAR) at www.alzheimers.nia.nih.gov, or call the ADEAR 

Center toll-free at 1-800-438-4380. 

What Can You Do?

Our knowledge is growing rapidly as scientists expand their understanding of the many factors involved in the development of AD. 

Even though no treatments, drugs, or pills have yet been proven to 

prevent AD or even delay its development, people can take some 

actions that might reduce the effect of possible AD risk factors. 

These actions include:

♦ lowering cholesterol and homocysteine levels
page 29

Can Alzheimer’s Disease be Prevented?

lowering high blood pressure levels

controlling diabetes

exercising regularly

engaging in social and intellectually stimulating activities

All of these strategies are good to do anyway because they lower 

risk of other diseases and help maintain and improve overall health 

and well-being. However, it is important to remember that pursuing 

any of these strategies will not necessarily prevent or delay AD in 

any one individual. Even if the strategies were eventually proven 

to be effective, they might not offset a person’s individual genetic 

and other risk factors enough to prevent AD from developing.

Another important action a person can take is to volunteer for the 

Genetics Study, the Neuroimaging Initiative, or an AD clinical 

trial. People who participate in these studies say that the biggest 

benefit is having regular contact with experts on AD who have 

lots of practical experience and a broad perspective on the disease. 

They also feel they are making a valuable contribution to future 

knowledge that will help scientists, people with AD, and their 

families. Families interested in participating in the Genetics Study 

can call the National Cell Repository for Alzheimer’s Disease 

(NCRAD) toll-free at 1-800-526-2839. Information may also be 

requested through its website at http://ncrad.iu.edu. People who 

are interested in joining the Neuroimaging Initiative or an AD 

clinical trial should contact the ADEAR Center at www.alzheimers.

nia.nih.gov, or call the ADEAR Center toll-free at 1-800-438-4380 

for a referral to the nearest participating study site.

♦

♦

♦

♦
Can Alzheimer’s Disease be Prevented?

page 30

A Final Word of Caution

Because AD is such a devastating disease, caregivers and patients 

may be tempted by untried, unproven, and unscientific cures, 

supplements, or prevention strategies. Before trying pills or 

anything else that promises to prevent AD, people should check 

with their doctor first. These purchases might be unsafe or a waste 

of money. They might even interfere with other medical treatments 

that have been prescribed.

For More Information

Becoming well informed is another important thing that people can 

do to protect their health. Thousands of Internet websites provide 

health-related information, including information on AD.

Some of the information on these websites is reliable, but some 

is not. Health websites sponsored by the Federal Government are 

good sources of information, as are websites of large professional 

organizations and well-known medical schools. Some excellent 

Internet sources of AD and other health-related information for 

consumers are:
page 31

Can Alzheimer’s Disease be Prevented?

Alzheimer’s Disease Education and Referral 

(ADEAR) Center

P.O. Box 8250

Silver Spring, MD 20907-8250

1-800-438-4380

www.alzheimers.nia.nih.gov

This service of the NIA offers information and publications on 

diagnosis, treatment, patient care, caregiver needs, long-term 

care, education and training, and research related to AD. The 

ADEAR Center provides several easy-to-understand publications 

that explain memory loss and AD, highlight ongoing research, 

and describe efforts to support AD caregivers. Other publications, 

including the Progress Report on Alzheimer’s Disease, provide a 

more comprehensive update on NIH’s AD research effort. These 

and other ADEAR publications can be previewed and ordered on 

the website. Staff at the ADEAR Center also respond to information requests and make referrals to local and national resources. 

The Center also maintains a database of AD clinical trials and 

studies and can answer questions about where particular ones are 

being conducted. 
Can Alzheimer’s Disease be Prevented?

page 32

Alzheimer’s Association

225 N. Michigan Avenue, Suite 1700

Chicago, IL 60601-7633

1-800-272-3900

www.alz.org

This nonprofit association supports families and caregivers of 

patients with AD and funds AD research. Chapters nationwide 

provide referrals to local resources and services, and sponsor 

support groups and educational programs.

National Institute on Aging Information Center

P.O. Box 8057

Gaithersburg, MD 20898-8057

1-800-222-2225

1-800-222-4225 (TTY)

www.nia.nih.gov

Visit: www.nia.nih.gov/HealthInformation to order publications (in 

English or Spanish) or sign up for regular email alerts. 

Visit NIHSeniorHealth.gov (www.nihseniorhealth.gov), a seniorfriendly website from the National Institute on Aging and the 

National Library of Medicine. This simple-to-use website features 

popular health topics for older adults. It has large type and a 

“talking” function that reads the text out loud.
For additional copies of this publication or further information 

on Alzheimer’s disease, please contact:

Alzheimer’s Disease Education and 

Referral (ADEAR) Center

P.O. Box 8250

Silver Spring, MD 20907-8250

1-800-438-4380

www.alzheimers.nia.nih.gov

National Institutes of Health

National Institute on Aging

Alzheimer’s Disease Education and Referral (ADEAR) Center
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

PUBLIC HEALTH SERVICE

National Institutes of Health

National Institute on Aging

NIH Publication No. 06-5503

June 2006