27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma biomarkers of AD neuropathology, neuronal injury, and astrogliosis increase with age and are associated with known dementia risk factors. 5 key findings →
Design: cohort Participants: 1,525 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Midlife p-tau181 was associated with faster 11-year memory decline beginning 20 years later in the ARIC cohort, which underscores a potentially long prodromal phase of cognitive decline that could precede dementia onset. 5 key findings →
Design: prospective cohort Participants: 920 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The mean (SD) baseline age of 758 participants was 61.5 (6.1) years, and 424 participants [55.9%] were female. 4 key findings →
Design: cohort study Participants: 758 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Analyses measured the associations between predictor variables and the memory score, and whether AT(N) biomarker profiles significantly improved prediction of memory z score rates of change beyond a model with clinical and genetic variables only. 3 key findings →
Design: cohort study Participants: 480 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These were compared with the prevalence of 3 clinically defined diagnostic groups (mild cognitive impairment or dementia, dementia, and clinically defined probable Alzheimer disease). 4 key findings →
Design: cohort study Participants: 4,660 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Out of the 664 studies screened, five studies met eligibility criteria. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
High cholesterol in late life was associated with decreased dementia risk, which is in contrast to previous studies suggesting high cholesterol in mid-life is a risk factor for later dementia. 5 key findings →
Design: longitudinal study Participants: 392 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 2766 participants (mean [SD] age, 69.9 [3.8] years; 486 [17.9%] Black, 196 [7.1%] Hispanic, and 2007 [73.9%] White), 1311 developed the combined end point of MCI or dementia (849 participants with MCI and 752 participants with dementia). 5 key findings →
Design: cohort Participants: 2,766 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 1430 cognitively normal participants included, the mean (SD) age was 79.5 (5.3) years, 49.4% were men, the mean duration of education was 14.3 years, and 25.4% were APOE ε4 carriers. 5 key findings →
Design: longitudinal study Participants: 1,630 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Baseline EDS was associated with increased longitudinal Aβ accumulation in elderly persons without dementia, suggesting that those with EDS may be more vulnerable to pathologic changes associated with Alzheimer disease. 5 key findings →
Design: longitudinal study Participants: 283 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuropsychiatric symptoms in MCI are associated with significantly an increased risk of incident dementia and AD. 5 key findings →
Design: cohort study Participants: 1,821 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease. 3 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
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In persons selected from a population-based study, elevated amyloid levels at baseline were associated with worse cognition and imaging biomarkers at baseline and with greater clinical decline and neurodegeneration. 5 key findings →
Design: longitudinal study Participants: 286 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A diagnosis of COPD is associated with an increased risk for MCI, particularly NA-MCI. 5 key findings →
Design: cross-sectional Participants: 1,425 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Twenty-seven (27.3%) of the 99 women developed incident dementia. 5 key findings →
Design: longitudinal study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this largely presymptomatic population, these results suggest subtle differences across plasma p-tau species and platforms for the prediction of amyloid and tau PET and magnetic resonance imaging measures of cerebrovascular and Alzheimer-related pathology. 5 key findings →
Participants: 1,329 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The utility of plasma total tau level as a prognostic marker for cognitive decline and dementia is not well understood. 4 key findings →
Design: cohort study Participants: 458 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Protection from these ADP factors may be important for aging without significant ADP. 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition. 3 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →
Design: cross-sectional Participants: 1,246 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These factors should be investigated in longitudinal studies for their role in detecting onset of symptoms in AD. 1 key finding →
Design: longitudinal study Participants: 749 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitively normal elderly individuals who engage in specific mentally stimulating activities even in late life have a decreased risk of incident MCI. 3 key findings →
Design: cohort study Participants: 973 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Over a median follow-up of 5.1 years, 153 of 534 participants (28.7%) with prevalent or incident MCI progressed to dementia (71.3 per 1,000 person-years). 2 key findings →
Participants: 534 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There were minimal effects of lifestyle enrichment on AD biomarker trajectories (specifically rates). 5 key findings →
Design: longitudinal study Participants: 393 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. 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →