Claim: Pre and Post Testing Show Reversal of Memory Loss From Alzheimer’s Disease in Ten Patients
Verdict: REFUTES

Retrieved passages:
title: Memory and aging
text: years. There are four drugs currently approved by the FDA for the treatment of Alzheimer’s, and they all act on the cholinergic system: Donepezil, Galantamine, Rivastigmine, and Tacrine. Although these medications are not the cure for Alzheimer’s, symptoms may be reduced for up to eighteen months for mild or moderate dementia. These drugs do not forestall the ultimate decline to full Alzheimer's. Also, modality is important in determining the strength of the memory. For instance, auditory creates stronger memory abilities than visual. This is shown by the higher recency and primacy effects of an auditory recall test compared to that

title: Postmenopausal confusion
text: of Alzheimer's, as mentioned in "Causes". Women who had their uterus and ovaries removed for medical reasons and lost their gonadal hormones showed a decrease in short-term verbal (hippocampus) and working memories (pre-frontal cortex), yet with estrogen therapy the memory loss was prevented. Furthermore, those who have undertaken estrogen therapy have shown significantly higher scores on verbal memory, verbal fluency, and visual memory tasks as compared to those who did not undergo treatment. It is widely found that this treatment must be administered near to the onset of menopause as opposed to several years postmenopause, when hormone therapy can have

title: Memory error
text: errors. As noted above, memory errors may be due to the lack of cues that can trigger a memory trace and bring it to awareness. However, studies have shown that the opposite may be true for patients with Alzheimer’s, such that cues may actually decrease perform on priming tasks. Patients also demonstrate errors known as misattribution errors, otherwise known as source confusion. However, studies show that these misattribution errors are dependent on whether the task is a familiarity or recollection tas. Although patients tend to exhibit a higher level of false recognitions than control groups. researchers have shown that they

title: Avid Radiopharmaceuticals
text: with symptoms of Alzheimer's disease detected plaque in a PET scan in areas where it was typically found in the brain. Further tests found that the scans detected plaque in patients with Alzheimer's, didn't find it in those without the diagnosis and found intermediate amounts in patients with early signs of dementia. The tests found amyloid plaque in 20% of its test patients over age 60 that had been in the normal range, but had performed worse than a control group on tests of mental acuity. In order to confirm if the dye was accurate in detecting Alzheimer's, an advisory

title: Retrospective memory
text: activity (but no structural changes) in parahippocampal regions. However, when subject to associative memory tasks, users performed within normal ranges. This shows that a decrease in activation in these regions is associated with frequent marijuana use, but does not affect memory task performance. This is still a controversial issue, and more research is required to draw conclusive results. Alzheimer's disease accounts for 60 to 70 percent of cases of dementias. The brains of Alzheimer's patients have an abundance of plaques and tangles which begin in areas involved in memory, spreading to other areas, and eventually affecting most of the brain.

title: Alzheimer's Disease Neuroimaging Initiative
text: signs of the disease such as memory loss, preventive therapies are targeted to cognitively normal people. ADNI studies have focused on two aspects of clinical trials in particular: 1) how best to select trial participants who don't yet show any signs of cognitive impairment but who are at a high risk of developing AD (subject selection); and 2) how to detect the effect of a therapy (outcome measures). Subject selection ADNI studies have shown that people who are β-amyloid positive or have a small hippocampal volume, or carry an "APOE" ε4 allele are at a higher risk for AD. Therefore,

title: Apolipoprotein A1
text: trials the reversal of plaque build-up was measured over the course of five weeks. Lately, two novel susceptibility haplotypes i.e. P2-S2-X1 and P1-S2-X1 have been discovered in ApoAI-CIII-AIV gene cluster on chromosome 11q23, which confer approximately threefold higher risk of coronary heart disease in normal as well as in the patients having non-insulin diabetes mellitus. A G/A polymorphism in the promoter of the apo A1 gene has been associated with the age at which patients presented with Alzheimer disease. Protection from Alzheimer's disease by apo A1 may rely on a synergistic interaction with alpha-tocopherol. Amyloid deposited in the knee following

title: Protease-sensitive prionopathy
text: ataxia, parkinsonism, psychosis, aphasia and mood disorders). This is similar to what occurs in other spongiform encephalopathies, and the condition can be mistaken for Alzheimer's dementia. Contrary to what is the case in CJD, there were no cases with a positive 14-3-3 protein test in the cerebrospinal fluid, no periodic complexes on electroencephalography (EEG), and no pathognomonic changes on diffusion-weighted magnetic resonance images. The mean age of onset in the original 11 patients was 62 years. Patients progressed to death in 20 months on average. PSPr accounted for three percent of prion disease cases evaluated by the U.S. National Prion

title: Deficiency of RbAp48 protein and memory loss
text: from Alzheimer's disease (AD), a subregion of the hippocampal formation called the dentate gyrus (DG) was further studied, since it is thought to be targeted by aging. Human postmortem tissue was collected from both DG and entorhinal cortex (EC). Entorhinal cortex is a neighboring subregion unaffected by aging and known to be implicated in age-related memory loss. After normalizing the expression of EC, 17 genes were manifested due to age-related changes in the DG. Mice were used as the experimental subjects to test whether the decline of RbAp48 was also related to age-related memory loss. The results were consistent with

title: Alzheimer's disease
text: amyloid precursor protein (APP) and presenilins 1 and 2. Most mutations in the APP and presenilin genes increase the production of a small protein called Aβ42, which is the main component of senile plaques. Some of the mutations merely alter the ratio between Aβ42 and the other major forms—particularly Aβ40—without increasing Aβ42 levels. Most cases of Alzheimer's disease do not exhibit autosomal-dominant inheritance and are termed sporadic AD, in which environmental and genetic differences may act as risk factors. The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE). Between 40 and

title: Florbetapir (18F)
text: of Alzheimer's disease detected plaque in a PET scan in areas where it was typically found in the brain. Further tests found that the scans detected plaque in patients with Alzheimer's, didn't find it in those without the diagnosis and found intermediate amounts in patients with early signs of dementia. The tests found amyloid plaque in 20% of its test patients over age 60 that had been in the normal range, but had performed worse than a control group on tests of mental acuity. In order to confirm if the dye was accurate in detecting Alzheimer's, an advisory committee at

title: Peanut butter test
text: that processes it. Stamps cautioned that they can currently only use the test to confirm already-established diagnoses, but added that "...we plan to study patients with mild cognitive impairment to see if this test might be used to predict which patients are going to get Alzheimer's disease." NPR also reported that the study, at 94 patients, was "too small to be conclusive." In 2012, a systematic review had found that while there may be "an association between decreased olfaction and AD," "rigorously designed longitudinal cohort studies are necessary to clarify the value of olfactory identification testing in predicting the onset

title: Alzheimer's disease
text: has been placed on diagnosing the condition before symptoms begin. A number of biochemical tests have been developed to enable earlier detection. Some such tests involve the analysis of cerebrospinal fluid for beta-amyloid, total tau protein and phosphorylated tau protein concentrations. Because drawing CSF can be painful, repeated draws are avoided. A blood test for circulatory miRNA and inflammatory biomarkers is a potential alternative indicator. Alzheimer's disease Alzheimer's disease (AD), also referred to simply as Alzheimer's, is a chronic neurodegenerative disease that usually starts slowly and worsens over time. It is the cause of 60–70% of cases of dementia. The

title: Crenezumab
text: intravenous or subcutaneous crenezumab and placebo. In May 2012, it was announced that the efficacy of crenezumab will be tested in a five-year trial against early-onset Alzheimer's disease. The $100 million trial will be funded by Genentech, the Banner Alzheimer's Institute, and the National Institutes of Health. Participants in the study will be recruited from an extended family in and around Medellín, Colombia. Approximately one-third of the 5,000 family members carry an autosomal dominant allele of presenilin-1 (PSEN1) that causes the early-onset form of Alzheimer's disease. The trial will test the effect of the drug on 300 individuals who have

title: Biochemistry of Alzheimer's disease
text: the posterior cingulate, parietal, temporal, and prefrontal cortices. These brain regions are believed to control multiple aspects of memory and cognition. This metabolic pattern is reproducible and has even been proposed as a diagnostic tool for Alzheimer’s disease. Moreover, diminished cerebral glucose metabolism (DCGM) correlates with plaque density and cognitive deficits in patients with more advanced disease. Diminished cerebral glucose metabolism (DCGM) may not be solely an artifact of brain cell loss since it occurs in asymptomatic patients at risk for Alzheimer’s disease, such as patients homozygous for the epsilon 4 variant of the apolipoprotein E gene (APOE4, a genetic

title: HIV-associated neurocognitive disorder
text: Melrose et al. (2008) examined the integrity of the fronto-striatal circuitry that underlies executive functioning in HIV. Participants in the study were diagnosed with HIV three months to sixteen years before the study. Ten out of eleven patients were on antiretroviral medication and none scored within the demented range on the HIV Dementia Scale. It was found that HIV+ patients showed less activity within the ventral prefrontal cortex (PFC) and left dorsolateral PFC. There was reduced connectivity between the left caudate and ventral PFC and between the left caudate and dorsolateral PFC compared to healthy controls. Additionally, there was hypoactivation

title: Short-term memory
text: study which compiled normative French data for three short-term memory tasks (Verbal, visual and spatial). They found impairments present in participants between the ages of 55 and 85 years of age. Memory distortion in Alzheimer's disease is a very common disorder found in older adults. Performance of patients with mild to moderate Alzheimer's disease was compared with the performance of age matched healthy adults. Researchers concluded the study with findings that showed reduced short-term memory recall for Alzheimer's patients. Episodic memory and semantic abilities deteriorate early in Alzheimer's disease. Since the cognitive system includes interconnected and reciprocally influenced neuronal networks,

title: Giovanna Mallucci
text: over-activated a natural defence mechanism, ‘switching off’ the vital production of new proteins in brain cells. Switching protein production back on with an experimental drug halted neurodegeneration but the drug tested was toxic to the pancreas and not suitable for testing in humans. But in a study published in Brain, the researchers revealed how they identified a number of suitable candidates after testing 1,040 compounds from the National Institute for Neurological Disorders and Stroke, initially in worms, which have a functioning nervous system. Testing on mice with prion disease and a form of familial tauopathy or frontotemporal dementia (FTD) identified

title: Steroid dementia syndrome
text: compatible with early dementia. When the steroid treatment ended after a year, the patent's confusion and disorganized appearance stopped immediately. Within several weeks, testing showed strong improvement in almost all cognitive functions. His doctors were surprised at the improvement, since the results were inconsistent with a diagnosis of dementia or Alzheimer's. Testing after 14 months showed a large jump in Full Scale IQ from 87 to 124, but mild dysfunction in executive function, memory, attentional control, and verbal/nonverbal memory remained. Steroid dementia syndrome Steroid dementia syndrome describes the signs and symptoms of hippocampal and prefrontal cortical dysfunction, such as deficits

title: Dementia
text: several hours, to determine functional patterns of decline associated with varying types of dementia. Tests of memory, executive function, processing speed, attention, and language skills are relevant, as well as tests of emotional and psychological adjustment. These tests assist with ruling out other etiologies and determining relative cognitive decline over time or from estimates of prior cognitive abilities. Routine blood tests are also usually performed to rule out treatable causes. These tests include vitamin B, folic acid, thyroid-stimulating hormone (TSH), C-reactive protein, full blood count, electrolytes, calcium, renal function, and liver enzymes. Abnormalities may suggest vitamin deficiency, infection, or other