Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Aging with and without DAT is associated with weight loss; however, weight loss may accelerate before the diagnosis of DAT.
Why it matters
Among 449 older adults, those who developed Alzheimer's disease weighed about 8 pounds less at enrollment and their weight loss doubled about 1 year before diagnosis. This describes a change that may precede diagnosis and gives no information on treating, curing or preventing Alzheimer's disease.
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If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly.
Why it matters
In this cross-sectional study, higher plasma beta-amyloid 40 was linked to more white matter hyperintensity on MRI in people with Alzheimer disease, mild cognitive impairment, or cerebral amyloid angiopathy. The authors say that if this is confirmed in longitudinal studies, circulating beta-amyloid could serve as a biomarker or risk factor for microvascular damage, but it does not yet show a way to treat or prevent the disease.
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There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans.
Why it matters
In this population, higher cholesterol and LDL were linked to higher Alzheimer risk only in people without the APOE-epsilon4 allele, not in those with it. Triglycerides showed no significant link to Alzheimer risk in people without APOE-epsilon4.
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These data suggest that AD pathology is more likely to be clinically expressed as dementia in women than in men.
Why it matters
In 141 older Catholic clergy members who had yearly check-ups and a brain autopsy after death, women had more Alzheimer pathology than men, mainly more neurofibrillary tangles. Sex on its own was not linked to a dementia diagnosis (OR 1.35, 95% CI 0.56-3.25). But each extra unit of pathology went with much higher odds of clinical Alzheimer's in women (OR 22.67) than in men (OR 2.82), so the authors conclude that pathology "is more likely to be clinically expressed as dementia in women than in men." It is an observational autopsy study in a selected group and reports no treatment or prevention.
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62/100
Based on analysis of prospective and nonprospective studies, NSAID exposure was associated with decreased risk of Alzheimer's disease.
Why it matters
This meta-analysis of observational studies found that nonaspirin NSAID exposure was associated with decreased risk of Alzheimer's disease. The evidence comes from observational studies, which cannot prove that NSAIDs prevent Alzheimer's disease, and the review does not establish a treatment or cure.
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This study questions the effect of statins on the processing of amyloid precursor protein in humans.
Why it matters
In 39 patients with high cholesterol, statin treatment lowered cholesterol but did not change plasma levels of beta-amyloid 1-40, beta-amyloid 1-42, or total beta-amyloid. This suggests that statins do not affect amyloid metabolism in the blood, and the study did not test whether statins prevent or treat Alzheimer's disease.
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Alzheimer's disease is associated with progressive cerebral atrophy, which can be seen on MRI with high resolution.
Why it matters
This commentary discusses how serial MRI tracking of cerebral atrophy could detect neurodegenerative disease earlier and help assess treatments that slow atrophy. It reports on imaging as a potential tool and does not itself test any treatment or cure.
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The consistency of MRI measurements obtained across sites, and the consistency between the multisite milameline data and that obtained in prior single-site studies, demonstrate the technical feasibility of using structural MRI measures as a surrogate endpoint of disease progression in therapeutic trials.
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The data suggest that engagement in leisure activities may reduce the risk of incident dementia, possibly by providing a reserve that delays the onset of clinical manifestations of the disease.
Why it matters
Among 1,772 adults aged 65 and older in northern Manhattan, New York, without dementia at the start and followed for a mean of 2.9 years, those reporting high leisure activity had a lower risk of developing dementia (relative risk 0.62, 95% CI 0.46 to 0.83), and the link held after accounting for baseline thinking skills, health limits on activity, cerebrovascular disease and depression. The study measured dementia overall rather than Alzheimer's disease specifically, and as an observational study it shows an association; the authors suggest only that leisure activities 'may' reduce risk, possibly by building a mental reserve.
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The transition of microglia from the normal resting state to the activated state is associated with an increased expression of receptors known as peripheral benzodiazepine binding sites, which are abundant on cells of mononuclear phagocyte lineage.
Why it matters
Using brain imaging, this study measured peripheral benzodiazepine binding sites, a marker of activated microglia, in 15 normal individuals, eight patients with Alzheimer's disease and one patient with minimal cognitive impairment. It demonstrates a way to measure microglial activation in dementia but reports no treatment, cure or prevention.
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Rivastigmine administration during open-label extension therapy benefited patients who had progressed slowly and those who had progressed rapidly during initial double-blind placebo treatment.
Why it matters
In this open-label extension study, 187 patients with mild to moderate Alzheimer's disease who had previously received placebo were treated with rivastigmine, and both slowly and rapidly progressing patients benefited. However, more rapidly progressive patients had a smaller response, suggesting that the rate of disease progression may predict how well patients respond to this treatment.
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62/100
We report the first detailed population-based maps of cortical gray matter loss in Alzheimer's disease (AD), revealing prominent features of early structural change.
Why it matters
This study used magnetic resonance imaging and a population-based brain atlas to map cortical gray matter loss in mild to moderate Alzheimer's disease compared with normal elderly controls. It is an imaging study of structural change, not a treatment, cure, or prevention study.
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Both the magnitude and the extent of brain activation during memory-activation tasks in regions affected by Alzheimer's disease, including the left hippocampal, parietal, and prefrontal regions, were greater among the carriers of the APOE epsilon4 allele than among the carriers of the APOE epsilon3 allele.
Why it matters
This study found that cognitively normal APOE epsilon4 carriers had greater brain activation during memory tasks in regions affected by Alzheimer's disease than non-carriers. It examines brain responses related to genetic risk, not treatment, cure, or prevention.
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Donepezil has been shown to be well tolerated and to improve cognition and global function in patients with mild to moderately severe Alzheimer's disease (AD).
Why it matters
In this 30-week randomized trial, both 5 and 10 mg/day of donepezil produced statistically significant improvements in cognitive and global function compared with placebo in mild to moderately severe Alzheimer's disease. The study confirms donepezil is effective and well tolerated for symptoms, not that it cures or prevents the disease.
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We hypothesized that LBV patients would have a faster cognitive decline and shorter survival compared with patients with pure AD.
Why it matters
This study quantified the rate of cognitive decline on the Mini-Mental State Examination in autopsy-diagnosed Lewy body variant of Alzheimer's disease compared with pure Alzheimer's disease. It describes how fast cognition declines in these groups and does not test any treatment, cure or prevention.
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Levels of CSF Abeta42 decrease and levels of CSF tau increase in AD.
Why it matters
In this cohort study, spinal fluid amyloid beta42 was significantly lower and tau significantly higher in probable Alzheimer's disease than in normal controls or those with other neurological disorders, and a classification tree distinguished the groups with 90% sensitivity and 80% specificity. The authors note that autopsy follow-up is needed to decide whether some results are false positives, and the study does not test any treatment, cure, or prevention.
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These findings suggest that cerebrovascular disease may play an important role in determining the presence and severity of the clinical symptoms of AD.
Why it matters
This study found that among women who met the brain tissue criteria for Alzheimer's disease, those who also had small brain infarcts had poorer thinking and a higher rate of dementia. It suggests that vascular brain damage may add to the effects of Alzheimer's disease, but it did not test any treatment or prevention.
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All indicators of atherosclerosis were associated with dementia (odds ratios ranging from 1.3 to 1.9) and its major subtypes Alzheimer's disease (odds ratios 1.3-1.8) and vascular dementia (odds ratios 1.9-3.2).
Why it matters
In this Rotterdam population study of 284 people with dementia (207 with Alzheimer's disease) and 1,698 without, signs of hardened arteries, measured by neck-artery ultrasound and an ankle-arm blood-pressure ratio, were more common in those with dementia. People with severe atherosclerosis had about three times the odds of having Alzheimer's disease as people with none (odds ratio 3.0, 95% CI 1.5–6.0). Dementia was more common still in people who carried the APOE ε4 gene variant and had moderate-to-severe atherosclerosis (odds ratio 4.5 for all dementia). The study looked at people at one point in time, so it shows a link, not that atherosclerosis causes Alzheimer's or that treating it would prevent the disease.
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62/100
In the 852 subjects without dementia, depressed mood was more common in individuals with greater cognitive impairment.
Why it matters
In this community study, depressed mood at baseline was associated with an increased risk of incident dementia, primarily Alzheimer's disease. It reports an association only and does not show that treating depression prevents or cures Alzheimer's disease.
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The prevalence of dementia increases exponentially with age.
Why it matters
In a survey of 7,528 people aged 55 and over in a Rotterdam suburb, 6.3% had dementia. That rose from 0.4% at ages 55–59 to about one third of those 85 and over, and Alzheimer's disease accounted for 72% of cases. Dementia, especially Alzheimer's, was more common in people with less education, and this was not explained by cardiovascular disease. This was a one-time snapshot: it shows a link with education, not that education protects against dementia, and it tested no treatment.
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We present here both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of 15 patients with Alzheimer's disease and 9 neuropathologically normal subjects.
Why it matters
In this study of 15 Alzheimer's disease patients and 9 normal subjects, synapse density in the neocortex showed very strong correlations with cognitive tests, while plaques and tangles showed only weak correlations. It suggests synapse loss is a major correlate of cognitive impairment in Alzheimer's disease.
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61/100
A total of 621 participants (aged 69.9 ± 3.8, 71% female) had available data for the main analyses and 355 had PET Centiloid data available.
Why it matters
People with younger-appearing brains showed a weaker link between Alzheimer's pathology (p-tau217) and poorer cognition across several domains, supporting the idea that brain reserve may buffer the cognitive effects of pathology. The authors note longitudinal studies are needed to confirm this, and it does not show that reserve prevents or cures the disease.
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Our findings suggest a higher prevalence of Alzheimer’s disease dementia in older individuals and a lower prevalence of preclinical Alzheimer’s disease in younger groups than previously estimated 2 .
Why it matters
Using plasma p-tau217 as a surrogate marker, the estimated prevalence of Alzheimer's disease neuropathological changes rose with age, from less than 8% in people aged 58–69.9 to 65.2% in those over 90. The findings suggest a higher prevalence of Alzheimer's disease dementia in older individuals and a lower prevalence of preclinical Alzheimer's disease in younger groups than previously estimated.
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Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %).
Why it matters
This longitudinal modeling study found four progression pathways and showed that severe brain glucose hypometabolism on FDG-PET was linked to a 7.4-fold faster direct conversion to dementia compared with preserved metabolism. It does not test a treatment or cure, but it suggests FDG-PET may help stratify people for pathway-specific prevention approaches.
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Researchers at the University of Pittsburgh developed a new plasma p-tau217 test (using a different antibody than existing commercial tests) and validated it in 363 people, including some with genetic early-onset Alzheimer's mutations and community-dwelling older adults.
Why it matters
A newly developed plasma p-tau217 test distinguished genetic mutation carriers from non-carriers very accurately and separated amyloid-positive from amyloid-negative cognitively normal adults reasonably well, performing comparably to an established commercial assay. This is a cross-sectional diagnostic validation, so it addresses detection rather than treatment or prevention.
From across this topic
10 of the 5,374 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Association of Elevated Amyloid and Tau Positron Emission Tomography Signal With Near-Term Development of Alzheimer Disease Symptoms in Older Adults Without Cognitive Impairment
- Effect of Cognitive Reserve on Age-Related Changes in Cerebrospinal Fluid Biomarkers of Alzheimer Disease
- Independent and interactive contributions of white matter hyperintensities and Alzheimer’s disease imaging and plasma biomarkers to cognitive decline in older adults without dementia
- Small-Data Deep Learning for Alzheimer-Spectrum Classification from Structural MRI: A Feasibility Study Using OASIS
- Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease
- The number of trait loci in late-onset Alzheimer disease
- Increased immunoreactivity for Jun- and Fos-related proteins in Alzheimer's disease: association with pathology
- Visit-to-Visit Blood Pressure Variability and CSF Alzheimer Disease Biomarkers in Cognitively Unimpaired and Mildly Impaired Older Adults
- Outcome associations of CSF total tau in suspected non-Alzheimer pathophysiology
- The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias