28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →
Design: cohort study Participants: 624 Evidence: moderate
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Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →
Design: case-control study Participants: 338 Evidence: moderate
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Simultaneous consideration of previous knowledge regarding potentially AD-related nutrients and multiple food groups can aid in identifying food combinations that are associated with AD risk. 3 key findings →
Design: cohort study Evidence: moderate
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Older patients with a college education who present with complaints of cognitive decline (reported by themselves or others) and score less than 27 on the MMSE are at a greater risk of being diagnosed with dementia and should be referred for a comprehensive dementia evaluation, including formal neuropsychological testing. 2 key findings →
Participants: 307 Evidence: moderate
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This study confirms the association between genetic variants in SORL1 and AD. 5 key findings →
Design: case-control study Participants: 296 Evidence: moderate
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Optimal ranges of CDR-SOB scores corresponding to the global CDR scores were 0.5 to 4.0 for a global score of 0.5, 4.5 to 9.0 for a global score of 1.0, 9.5 to 15.5 for a global score of 2.0, and 16.0 to 18.0 for a global score of 3.0. 2 key findings →
Participants: 1,577 Evidence: moderate
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Study objective To describe a population that was categorized as "cognitively impaired not demented" (CIND) and to examine the utility of some of the proposed criteria for describing this degree of cognitive impairment. 4 key findings →
Design: longitudinal study Participants: 2,914 Evidence: moderate
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Early and accurate diagnosis of Alzheimer's disease (AD) has a major impact on the progress of research on dementia. 5 key findings →
Participants: 37 Evidence: low
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Apolipoprotein E epsilon4 led to increased risk of AD among white subjects but not black subjects. 5 key findings →
Participants: 6,158 Evidence: low
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Our findings suggest that APOE epsilon4-mediated risk for Alzheimer disease is associated with widespread decline in rCBF over time that precedes the onset of dementia. 3 key findings →
Design: longitudinal study Evidence: moderate
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In women, increased plasma adiponectin levels are an independent risk factor for the development of both all-cause dementia and AD. 3 key findings →
Design: cohort study Participants: 159 Evidence: moderate
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Our genome-wide search of Caribbean Hispanic individuals identified several novel genetic variants associated with LOAD and replicated these associations in a white cohort. 3 key findings →
Design: case-control study Evidence: moderate
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Biomarker trajectory shapes by MMSE score were complex and were affected by interactions with age and APOE status. 3 key findings →
Design: cross-sectional Participants: 343 Evidence: moderate
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APOE epsilon4 carrier status was associated with conversion to AD in older outpatients after controlling for known demographic and clinical risk factors, and APOE epsilon4 homozygosity was associated with increased risk of conversion to AD. 3 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
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Obesity at midlife is associated with an increased risk of dementia and AD later in life. 3 key findings →
Participants: 1,449 Evidence: low
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Elevated CSF tau levels are associated with AD pathology and can help discriminate AD from other dementing disorders. 3 key findings →
Participants: 74 Evidence: moderate
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In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →
Design: longitudinal study Evidence: moderate
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Older age and vascular disease, particularly among African Americans, are associated with increased brain atrophy and WMH burden. 4 key findings →
Design: cross-sectional Participants: 769 Evidence: moderate
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Longitudinal clinicopathologic cohort study. 1 key finding →
Design: cohort study Evidence: moderate
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The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD. 5 key findings →
Participants: 53 Evidence: moderate
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In a prospective longitudinal study with death as the end point in 17 middle-aged patients with Down's syndrome, dementia was clinically diagnosed in 15 patients, by means of careful observations in daily circumstances. 2 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
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As ascertained by several operational definitions, MCI is a heterogeneous entity at the population level but progresses to dementia at rates higher than in normal elderly individuals. 1 key finding →
Participants: 1,982 Evidence: moderate
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Our results indicate that altered tau and Abeta42 concentrations may be detectable in subjects who are clinically diagnosed as having MCI but demonstrate the pathological changes of AD. 5 key findings →
Design: longitudinal study Participants: 28 Evidence: moderate
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Imaging and postmortem studies suggest that frontal lobe white matter (FLWM) volume expands until about the age of 44.6 years and then declines. 4 key findings →
Design: cross-sectional Participants: 34 Evidence: low
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Occipital predominance of microbleeds with corresponding parietooccipital leukoaraiosis has not been well described in prior imaging studies of AD. 3 key findings →
Design: case-control study Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →