Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →
Participants: 85 Evidence: moderate
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We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures. 3 key findings →
Participants: 734 Evidence: moderate
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Late-life dementia has a strong heritable component. 1 key finding →
Evidence: low
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The first SVD component accounted for 21.56%, 12.93%, 11.91% of the total co-variability between the pairs (cortical thickness, tau), (relative GM density, tau) and (absolute GM density, tau), respectively. 5 key findings →
Design: cross-sectional Participants: 222 Evidence: low
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The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. 2 key findings →
Evidence: low
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Amyloid precursor protein (APP) has an important function in the generation of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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We suggest that the APP23 Tg mouse may develop an earlier blockage in A beta clearance than the Tg2576 mice, resulting in a more severe accumulation of A beta in the perivascular drainage pathways and in the brain. 4 key findings →
Evidence: low
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> 0.95) and is present in all African ancestry tested. 5 key findings →
Evidence: low
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Overall SNP‐based heritability estimates using this restricted set of variants varied: AA ( h 2 = 0.13, SE=0.05), NHW ( h 2 = 0.14, SE=0.01), AsA ( h 2 = 0.29, SE=0.09) and HL ( h 2 = 0.48, SE=0.17). 2 key findings →
Participants: 6,343 Evidence: low
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Finally, at the RHOJ locus, the rare allele was associated with increased tTau ( p ‐value=4.74×10 ‐05 ) and pTau181 ( p ‐value=4.07×10 ‐07 ), and decreased Aβ42/40 ratio ( p ‐value=4.32×10 ‐05 ). 2 key findings →
Participants: 91 Evidence: moderate
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Identity-by-descent (IBD) mapping provides complementary signals to genome-wide association studies (GWASs) when multiple causal haplotypes or variants are present but not directly tested. 5 key findings →
Evidence: low
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CAD did not differ across biomarker groups (Kruskal–Wallis H(2) = 0.17, p = 0.91). 5 key findings →
Participants: 140 Evidence: low
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The distribution of apolipoprotein E (APOE) genotypes as a function of age and sex has been examined in a French population of 417 Alzheimer disease (AD) patients and 1,030 control subjects. 1 key finding →
Evidence: low
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Neurexins (NRXNs) are synaptic cell adhesion molecules having essential roles in the assembly and maturation of synapses into fully functional units. 1 key finding →
Evidence: low
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We observed that GSK-3β activity was significantly upregulated in ApoE4 mice, accompanied by disruption of the insulin signaling pathway. 5 key findings →
Evidence: low
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In analyses of APOE ε4 carriers, dosage, and genetic risk score, APOE ε4 was associated with lower odds of fluctuating cognition and parkinsonism and higher odds of visual hallucinations. 5 key findings →
Evidence: low
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Peruvian GWAS identified Amerindian ancestry specific exonic AD susceptibility variant p.H157Y. This variant has been previously reported as AD marker in Han Chinese populations with extreme effect size, but its rarity and contradictory findings in other groups suggest a potential ancestry‐specific effect. 4 key findings →
Participants: 567 Evidence: low
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Early and accurate prognosis of Alzheimer’s disease (AD) remains limited by current biomarkers, which are often invasive, require expensive equipment, or fail to predict individual trajectories of cognitive decline. 2 key findings →
Participants: 459 Evidence: moderate
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At the between-person level, no associations were observed between sleep and cognition. 5 key findings →
Participants: 319 Evidence: low
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Employing the random-effects IVW approach, we found that, as indicated by GrimAge, EAA was associated with an increased risk of AD (Odds Ratio [OR] = 1.025, 95% Confidence Interval [CI]: 1.006-1.044, p = 0.009). 5 key findings →
Participants: 63,926 Evidence: low
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Using a 2-sample Mendelian randomization (MR) approach, we evaluated MR evidence for genetically proxied effects of 10 pre-specified gut bacterial classes on type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD), and assessed MR evidence for a direct genetically proxied effect of T2DM on AD. 5 key findings →
Evidence: low
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There is significant evidence that microglia contribute to neuroinflammation and neurotoxicity in AD 1,2 , yet there is also evidence to the contrary. 5 key findings →
Participants: 89 Evidence: low
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Alzheimer disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for senile dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1). 5 key findings →
Evidence: low
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →