Alzheimer's disease is the world's most common dementing illness. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of the reference regions used, subcortical white matter, cerebellar white matter, and the pons, alone or in combination, generated the largest effect sizes. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Increasing cerebral Abeta deposition with age is the pathobiological phenotype of APOE4. 1 key finding →
Participants: 241 Evidence: low
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62/100
Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE. 2 key findings →
Design: case-control study Participants: 753 Evidence: moderate
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If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly. 2 key findings →
Design: cross-sectional Participants: 54 Evidence: moderate
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CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci. 3 key findings →
Evidence: low
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Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level. 5 key findings →
Design: cross-sectional Participants: 1,079 Evidence: moderate
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Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease. 3 key findings →
Design: systematic review Evidence: high
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There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →
Design: longitudinal study Participants: 1,075 Evidence: moderate
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Our results provide evidence supporting 25OHD as a causal risk factor for AD. 5 key findings →
Participants: 33,996 Evidence: high
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Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. 3 key findings →
Design: case-control study Participants: 10,578 Evidence: moderate
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Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →
Design: longitudinal study Participants: 193 Evidence: moderate
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This study questions the effect of statins on the processing of amyloid precursor protein in humans. 4 key findings →
Evidence: high
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Recently, several animal studies indicated that the 'gut-brain' axis might contribute to the amyloid deposition of AD. 5 key findings →
Design: cross-sectional Participants: 97 Evidence: low
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62/100
Levels of autolysosomal proteins in neurally derived blood exosomes distinguish patients with AD from case controls and appear to reflect the pathology of AD up to 10 years before clinical onset. 4 key findings →
Design: cross-sectional Participants: 26 Evidence: low
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All indicators of atherosclerosis were associated with dementia (odds ratios ranging from 1.3 to 1.9) and its major subtypes Alzheimer's disease (odds ratios 1.3-1.8) and vascular dementia (odds ratios 1.9-3.2). 4 key findings →
Participants: 284 Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord. 2 key findings →
Evidence: low
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Levels of P-S396-tau, P-T181-tau, and Aβ1-42 in extracts of neurally derived blood exosomes predict the development of AD up to 10 years before clinical onset. 2 key findings →
Participants: 57 Evidence: low
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Much of the genetic basis for Alzheimer disease (AD) is unexplained. 4 key findings →
Design: meta-analysis Evidence: high
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We present here both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of 15 patients with Alzheimer's disease and 9 neuropathologically normal subjects. 4 key findings →
Participants: 15 Evidence: low
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Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --> Asn, Met671 --> Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age. 4 key findings →
Evidence: low
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Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease.
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Analyzing postmortem brain pathology from over 3,200 people plus biomarker data from more than 10,000 more, researchers found that people who inherit two copies of the APOE4 gene variant (about 2-3% of the population) develop Alzheimer's brain changes almost universally and on a predictable timeline starting around age 55, much like known single-gene forms of Alzheimer's. The authors argue this makes APOE4 homozygosity itself a genetic form of Alzheimer's disease rather than just a risk factor. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source
61/100
Our results indicate that APOE ε4 is independently associated with a greater severity of LB pathology. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
61/100
Memory declined in APOE e4 carriers before the symptomatic presentation of MCI in a cohort whose mean age was 60 years over a median period of 33 months. 1 key finding →
Design: longitudinal study Participants: 212 Evidence: moderate
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From across this tag
10 of the 1,348 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.
- Cerebrovascular effects of apolipoprotein E: implications for Alzheimer disease
- Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene
- Apolipoprotein E (APOE) genotype has dissociable effects on memory and attentional-executive network function in Alzheimer's disease
- Diabetes and hypertension are related to amyloid-beta burden in the population-based Rotterdam Study
- Multi-omic comparison of Alzheimer's variants in human ESC-derived microglia reveals convergence at APOE
- Effects of sexual differentiation and APOE genotype on the development of Alzheimer-related pathology in female EFAD mice
- Characterization and Chromosomal Localization of a cDNA Encoding Brain Amyloid of Alzheimer's Disease
- MCI conversion to dementia and the APOE genotype: a prediction study with FDG-PET
- Association of residential neighborhood disadvantage with amyloid PET positivity among cognitively impaired individuals
- Amyloid Precursor Protein (APP) Metabolites APP Intracellular Fragment (AICD), Aβ42, and Tau in Nuclear Roles
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 →