27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The genotype KL-VSHET+ is associated with reduced AD risk and Aβ burden in individuals who are aged 60 to 80 years, cognitively normal, and carrying APOE4. 5 key findings →
Design: case-control study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families. 2 key findings →
Design: cohort study Participants: 173 Evidence: moderate
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Among the 183 study participants, mean (SD) age was 85.5 (3) years, 76 were women (41.5%), and 177 were white (96.7%). 4 key findings →
Design: cross-sectional Participants: 183 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This preliminary report suggests that CETP V405 valine homozygosity is associated with slower memory decline and lower incident dementia and AD risk. 5 key findings →
Design: cohort study Participants: 523 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ARIA-E can also occur spontaneously in cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with increased CSF levels of anti-Aβ autoantibodies. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We hypothesized that telomere length might thus relate to increased risk for dementia and mortality. 2 key findings →
Design: case-control study Participants: 257 Evidence: moderate
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We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD). 4 key findings →
Design: case-control study Participants: 113 Evidence: moderate
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Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The neuropathologic changes underlying Alzheimer disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes. 4 key findings →
Design: cross-sectional Participants: 217 Evidence: moderate
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A candidate gene for the chromosome 1 Alzheimer's disease (AD) locus was identified (STM2).
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Using Fisher's exact test, there was significant association of both ABI3_rs616338-T (OR = 1.41, p = 0.044) and PLCG2_rs72824905-G (OR = 0.56, p = 0.008) with AD. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The results of this preliminary case-control study suggest that estradiol levels may decline significantly in women in whom AD develops. 5 key findings →
Design: case-control study Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We characterized the world's second case with ascertained extreme resilience to autosomal dominant Alzheimer's disease (ADAD). 5 key findings →
Evidence: preliminary
Full summary, score breakdown and related studies → Original source Free full text
Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus. 5 key findings →
Design: case-control Participants: 10,271 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma β-synuclein demonstrated discriminative properties for Aβ PET positive and negative subjects. 3 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. 3 key findings →
Participants: 75,708 Evidence: low
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The APOE epsilon4 allele acts as a potent risk factor for AD by accelerating onset. 1 key finding →
Design: longitudinal study Participants: 3,308 Evidence: moderate
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A population-based longitudinal study in Sweden, the Kungsholmen Project A random sample of 370 nondemented persons, aged 75 years and older and not treated with B(12) and folate, was followed for 3 years to detect incident AD cases. 1 key finding →
Design: longitudinal study Evidence: moderate
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Even in elderly subjects without dementia, the apolipoprotein E genotype is related to the degree of deposition of beta-amyloid protein in the cerebral cortex. 2 key findings →
Participants: 271 Evidence: moderate
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Alzheimer's disease (AD) is the most common cause of progressive intellectual failure in aged humans. 4 key findings →
Evidence: low
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Microglia are central players in Alzheimer's disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathogenic mutations in APP, PSEN1, PSEN2, MAPT and GRN have previously been linked to familial early onset forms of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are the principal immune cells of the brain. 4 key findings →
Evidence: low
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Among 2157 older adults without dementia (mean [SD] age 71.2 [9.2] years; 1337 female [62.0%]), 1680 participants had longitudinal cognition data and 569 participants (26.4%) had APOE34/44 genotypes. 5 key findings →
Design: cohort study Participants: 1,680 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the first of five phases in the evolution of beta-amyloidosis Abeta deposits are found exclusively in the neocortex. 5 key findings →
Design: clinical trial Evidence: low
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10 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →