27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Individuals with all types of mild cognitive impairment have an elevated risk of dementia over 3 years, more so in those with an APOE epsilon4 allele. 3 key findings →
Participants: 120 Evidence: low
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Unlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype. 3 key findings →
Participants: 312 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CST3 is a susceptibility gene for late-onset AD, especially in patients aged 75 years and older. 2 key findings →
Design: case-control study Participants: 260 Evidence: moderate
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The results showed different pattern of APOE contribution in PRS risk predictions of AD/MCI and amyloid deposition. 3 key findings →
Evidence: moderate
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The precise mechanism through which many of these genes are associated with AD remains unknown. 3 key findings →
Participants: 977 Evidence: low
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An a priori defined cutoff value of p-tau(231) yields relatively stable results across centers, suggesting a good feasibility of a standard criterion of p-tau(231) for the prediction of Alzheimer disease. 2 key findings →
Participants: 43 Evidence: low
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This enlarged study confirms earlier findings that statin therapy in early old age, but not in late age, may be associated with a lower risk of AD. 4 key findings →
Participants: 3,099 Evidence: moderate
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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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Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD. 2 key findings →
Design: cross-sectional Evidence: low
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The epsilon2 allele confers a protective effect, and women with DS have an increased risk for AD, as in the general population. 5 key findings →
Participants: 57 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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A total of 503 participants (mean [SD] age, 64.6 [2.8] years; 321 [63.8%] women; 305 [60.6%] Hispanic, 120 [23.9%] non-Hispanic Black, and 78 [15.5%] non-Hispanic White) with Aβ PET, MRI (n = 501), and tau PET (n = 355) data were studied. 5 key findings →
Design: cross-sectional Participants: 501 Evidence: moderate
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ObjectivesEmerging evidence suggests that the genetic architecture of Alzheimer disease (AD) and Parkinson disease (PD) risk varies across ancestries. 4 key findings →
Design: meta-analysis Evidence: high
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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
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Genome-wide association studies (GWAS) have identified several risk variants for late-onset Alzheimer's disease (LOAD). 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Numerous genetic susceptibility and protective markers for AD and disease biomarkers have been identified and replicated using ADNI data and have heavily implicated immune, mitochondrial, cell cycle/fate, and other biological processes. 2 key findings →
Design: longitudinal study Evidence: moderate
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Deposition of amyloid-β (Aβ) in the cerebral cortex is thought to be a pivotal event in Alzheimer's disease (AD) pathogenesis with a significant genetic contribution. 3 key findings →
Participants: 555 Evidence: low
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SPON1 has not been previously associated with AD risk, but is plausibly related because the gene product binds to the amyloid precursor protein and inhibits its cleavage by β-secretase. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglia, the tissue-resident macrophages of the central nervous system (CNS), play critical roles in immune defense, development and homeostasis. 1 key finding →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
Significant interactions were found between APOE ε4 status and mindfulness and social engagement on cognitive reserve, indicating stronger associations for APOE ε4 carriers. 5 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
APOE-ε4 carrier status appears to modify the cross-sectional association between cardiac output and neuropsychological performance such that lower cardiac output relates to poorer performances among carriers of the ε4 allele. 3 key findings →
Design: cross-sectional Participants: 306 Evidence: low
Full summary, score breakdown and related studies → Original source
Among all participants (mean age 66.7 ± 6.5 years, 100% non-Hispanic White), 451 (6.6%) were using statins at baseline. 5 key findings →
Participants: 564 Evidence: low
Full summary, score breakdown and related studies → Original source
The PRS using 131 SNPs had an effect independent of APOE. 5 key findings →
Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD). 2 key findings →
Design: case-control 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →