30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 4392 participants (mean [SD] age, 68.2 [7.8] years; 2359 [53.7%] women), 723 (16.5%) were APOE ε4 heterozygotes and 33 (0.8%) were APOE ε4 homozygotes. 5 key findings →
Design: cohort study Participants: 4,392 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 413 477 All of Us participants, 2038 were eligible. 5 key findings →
Design: cohort study Participants: 26 Evidence: moderate
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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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The data do not support an association between serum total cholesterol or high density lipoprotein in late life and subsequent risk of dementia or Alzheimer disease (AD). 5 key findings →
Design: cohort study 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
Full summary, score breakdown and related studies → Original source Free full text
The study encompassed 479 723 participants (mean [SD] age, 56.5 [8.1] years; 260 730 females [54.4%]), including 271 690 in the YOD analyses and 334 939 in the LOD analyses. 5 key findings →
Design: cohort study Participants: 723 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) affects half the US population over the age of 85 and is universally fatal following an average course of 10 years of progressive cognitive disability. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although abnormal accumulation of amyloid in the brain is an early biomarker of Alzheimer's disease (AD), wide variation in cognitive trajectories during life can be seen in the setting of brain amyloidosis, ranging from maintenance of normal function to progression to dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mosaic loss of chromosome Y (LOY) is the most common somatic genetic aberration and is associated with increased risk for all-cause mortality, various forms of cancer and Alzheimer's disease, as well as other common human diseases. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. 1 key finding →
Design: cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This risk score could be used to identify persons at risk of LOAD, but can also be used to adjust for confounders in epidemiologic studies. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE epsilon4 carriers. 5 key findings →
Design: cohort study Participants: 907 Evidence: moderate
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Individuals with rapid progression were more likely to have at least one APOE ε4 allele (OR: 2.08 [95% CI: 1.16–3.74], p < 0.01), higher Braak stage (2.19 [1.20–3.98], p < 0.01), higher Thal phase (2.45 [1.24–4.83], p < 0.01), more severe white matter rarefaction (1.68 [1.21–2.35], p < 0.01), and in the final 24 months of life, more frequent untreated/undertreated hyperlipidemia (1.74 [1.35–5.56], p < 0.01) and less frequent untreated/undertreated depression (0.40 [0.17–0.91], p < 0.05). 3 key findings →
Design: cohort study Participants: 75 Evidence: moderate
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We identified rs13374761-A in SLAMF1 gene associated with less memory decline (MAF = 0.071, β= 0.0103, p = 4.14×10-8). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite differences in prevalence of APOE-ε4, its association with dementia risk was similar across Chinese, Japanese, Filipino, and non-Latino White participants. 2 key findings →
Design: cohort Participants: 46,325 Evidence: moderate
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High HDL-C levels in elderly individuals may be associated with a decreased risk of AD. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). 1 key finding →
Design: longitudinal study Participants: 96 Evidence: moderate
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MCI diagnosis frequencies are substantively affected by the stringency of the criteria, but the relative rankings of MCI subtype diagnoses are fairly consistent regardless of the stringency of the criteria. 5 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
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Education, occupation, premorbid intelligence, and brain size are surrogate markers for cognitive reserve. 1 key finding →
Design: longitudinal study Participants: 819 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study included 1,028 participants (mean age at baseline 76.4 years; 47.6% female): 521 with ADP, 96 with LBP, and 411 with mixed AD-LBP. 5 key findings →
Design: cohort study Participants: 1,028 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The role of the Alzheimer's Disease Neuroimaging Initiative Genetics Core is to facilitate the investigation of genetic influences on disease onset and trajectory as reflected in structural, functional, and molecular imaging changes; fluid biomarkers; and cognitive status. 5 key findings →
Design: longitudinal study 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →