Severe CAA confers a greater risk of VLs in AD, even within strata of APOE genotype. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The APOE ε4 allele segregated dose-dependently and selectively with CA1-SRLM thinning and worse episodic memory performance in a pool of older subjects across a cognitive spectrum. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular contributions to cognitive impairment and dementia (VCID) are a common cause of cognitive decline, yet limited therapies exist. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
49/100
Among 104 537 individuals, the absolute 10-year risk of Alzheimer disease in 3017 women and men who were carriers of the APOE ɛ44 genotype was, respectively, 7% and 6% at age 60-69 years, 16% and 12% at age 70-79 years, and 24% and 19% at age 80 years and older. 1 key finding →
Participants: 537 Evidence: low
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49/100
No frontal cognitive effects were as robust as memory decline. 2 key findings →
Participants: 27 Evidence: low
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In the HELIAD sample, among 618 cognitively healthy participants (mean age 73.37 years, 58.4% female), followed for 2.92 ± 0.80 years, 73 developed AD/aMCI. 5 key findings →
Participants: 142,637 Evidence: low
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We included 1179 CU subjects (n = 474 females (40%), 70.9 ± 4.5 years old) of European descent who had pTau217 and PACC. 5 key findings →
Design: longitudinal study Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
274 participants [average age 75.9 (SD 5.8); 57% women; 13% self-identified as Black] were offered their research results and 40% declined. 5 key findings →
Design: longitudinal study Participants: 274 Evidence: moderate
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The findings from the AHEAD Study screening process and longitudinal data from the LEARN Study are providing critical data to guide future prevention trial design. 5 key findings →
Design: longitudinal study Participants: 1,000 Evidence: moderate
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Among the 30 boxers, 11 were found to be normal (CBI score=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impaired (CBI score=3-4), and 3 showed signs of severe impairment (CBI score > 4). 3 key findings →
Evidence: low
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Inflammasomes are high molecular weight protein complexes that assemble in the cytosol upon pathogen encounter. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There has been great interest in the prospects of using single-nucleotide polymorphisms (SNPs) in the search for complex disease genes, and several initiatives devoted to the identification and mapping of SNPs throughout the human genome are currently underway. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Autosomal-dominant spinocerebellar ataxias (SCAs) are a heterogeneous group of neurodegenerative disorders. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
48/100
Intravitam PET and post-mortem studies revealed more pronounced cortical atrophy, elevated cortical and limbic Lewy pathologies (with APOE ε4), apart from higher prevalence of Alzheimer pathology in DLB than PDD. 2 key findings →
Evidence: low
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Epidemiologic studies indicate that elderly women are at higher risk for Alzheimer disease compared to men. 3 key findings →
Evidence: low
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Study objectives Emerging evidence suggests a role for sleep in contributing to the progression of Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
HIV produces a chronic viral infection of the central nervous system that elicits chronic glial activation and overexpression of glial cytokines that are also implicated in Alzheimer disease (AD) pathogenesis. 1 key finding →
Evidence: moderate
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Apolipoprotein (apo) E4 is the major genetic risk factor for late-onset Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD), the most common cause of dementia in the elderly, exists in both familial and sporadic forms. 3 key findings →
Evidence: low
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The most frequent human apolipoprotein (apo) E isoforms, E3 and E4, differentially affect Alzheimer's disease (AD) risk (E4 > E3) and age of onset (E4 < E3). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One of the pathological hallmarks of Alzheimer disease is the accumulation of amyloid plaques in the extracellular space in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
Inheritance of the APOE epsilon4 allele is associated with increased risk of late posttraumatic seizures. 5 key findings →
Participants: 106 Evidence: moderate
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48/100
Forty of 105 (38%) were classified as NC-low, and 65 (62%) as NC-high. 2 key findings →
Evidence: low
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Alzheimer's disease (AD), the most common form of dementia worldwide, is a mixed proteinopathy (β-amyloid, tau and other proteins). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →