31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. 4 key findings →
Design: longitudinal study Evidence: moderate
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Preclinical AD is associated with rest-activity rhythm fragmentation, independent of age or sex. 5 key findings →
Design: cross-sectional Participants: 205 Evidence: moderate
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MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone. 3 key findings →
Participants: 399 Evidence: low
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Level of conscientiousness is a risk factor for Alzheimer disease. 5 key findings →
Design: cohort study Participants: 176 Evidence: moderate
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The TICS has high diagnostic validity for identification of dementia among ethnically diverse older adults, especially when supported by the DQ and prior visit data. 2 key findings →
Design: longitudinal study Participants: 256 Evidence: moderate
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In this diverse community-based cohort, cross-sectional data revealed significant race/ethnic disparities in the prevalence of MCI and dementia. 3 key findings →
Design: cross-sectional Participants: 989 Evidence: moderate
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Compared with individuals classed as normal, participants with preclinical Alzheimer's disease had an increased risk of death after adjusting for covariates (hazard ratio 6·2, 95% CI 1·1-35·0; p=0·040). 2 key findings →
Participants: 311 Evidence: low
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In a large community-based sample of middle-aged adults, BI predicted an increased risk of stroke and dementia independent of vascular risk factors. 5 key findings →
Participants: 1,694 Evidence: moderate
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Key message Extensive variation was observed in conversion rates due to the population sampled, diagnostic criteria, and duration, and because many studies did not account for loss to follow-up. 5 key findings →
Design: systematic review Evidence: high
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Gut microbiota composition was associated with amyloid and p-tau status. 5 key findings →
Participants: 170 Evidence: moderate
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Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
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Late-onset NPS improve the specificity of MCI as an at-risk state for progression to dementia. 4 key findings →
Participants: 409 Evidence: low
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Depressive symptoms in MCI appear to be predictors for progression to AD. 3 key findings →
Design: longitudinal study Participants: 74 Evidence: moderate
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Pooling data across 4 cohort studies, 814 cognitively normal participants (mean baseline age = 59.6 years) were classified into 8 ATN groups using baseline CSF levels of β-amyloid 1-42 as a measure of amyloid (A), phosphorylated tau 181 as a measure of tau (T), and total tau as a measure of neurodegeneration (N). 4 key findings →
Design: cohort study Evidence: moderate
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This study evaluated longitudinal CSF biomarker measures collected when participants were cognitively normal to determine the magnitude and time course of biomarker changes before the onset of clinical symptoms in subjects with mild cognitive impairment (MCI). 4 key findings →
Design: longitudinal study Participants: 265 Evidence: moderate
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Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
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Patients with Alzheimer's Disease (AD) exhibit decreased retinal blood flow and vessel density (VD). 4 key findings →
Design: case-control study Participants: 16 Evidence: moderate
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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 . 1 key finding →
Evidence: moderate
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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 %). 5 key findings →
Design: longitudinal study Participants: 1,136 Evidence: moderate
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →
Evidence: low
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It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm. 5 key findings →
Design: phase-3-trial Participants: 598 Evidence: null result
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This cross-sectional evaluation of the NIA-AA criteria for preclinical AD indicates that the 1-3 staging criteria coupled with stage 0 and SNAP categories classify 97% of CN subjects from a population-based sample, leaving only 3% unclassified. 2 key findings →
Design: cross-sectional Evidence: moderate
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Higher adherence to the MeDi is associated with a trend for reduced risk of developing MCI and with reduced risk of MCI conversion to AD. 4 key findings →
Participants: 482 Evidence: moderate
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This advantage may represent a sex-specific form of cognitive reserve delaying verbal memory decline until more advanced disease stages. 1 key finding →
Design: cross-sectional Participants: 379 Evidence: low
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While prior work reliably demonstrates that the APOE ɛ4 allele has deleterious group level effects on Alzheimer disease pathology, the homogeneity of its influence across the lifespan and spatially in the brain remains unknown. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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.
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events