The frequencies of individual ApoE genotypes did not differ between patients with ALS and ALS-free Caucasian populations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The frequencies of individual ApoE genotypes did not differ between patients with ALS and ALS-free Caucasian populations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have investigated the effect of genotypes of apolipoprotein E (ApoE) on the pathologies found in Alzheimer's disease (AD) and its related gene expression in 38 aged human brains obtained from consecutive autopsied cases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the discovery of the association of apolipoprotein E (apoE) 4 with Alzheimer's disease 17 years ago, numerous in vitro experiments with the apoE isoforms (apoE2, apoE3, and apoE4) have been performed to try to understand the basis for this association. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E (ApoE) epsilon4 allele is a major risk factor for neurodegenerative conditions, including Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronically activated glia associated with amyloid plaques might contribute to neuronal dysfunction in Alzheimer's disease (AD) through generation of neuroinflammatory molecules. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In humans, apolipoprotein E (apoE) has three major isoforms, E2 (Cys112, Cys158), E3 (Cys112, Arg158), and E4 (Arg112, Arg158). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein (apo) E plays an important role in lipid metabolism, and the major isoforms of apoE (apoE2, apoE3, and apoE4) have significantly different metabolic effects. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the accumulation and deposition of amyloid-beta (Aβ) peptides in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicated that 18p11.32 (rs1992269, P = 9.77 × 10(-7)), CNTNAP2 (rs802571, P = 1.26 × 10(-6)), and 12q24.23 (rs11613092, P = 6.85 × 10(-6)) were suggestive loci for susceptibility to LOAD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) are a powerful tool for understanding the genetic underpinnings of human disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large case/control genome-wide association studies (GWAS) often include groups of related individuals with known relationships. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Important methodological advancements in rare variant association testing have been made recently, among them collapsing tests, kernel methods and the variable threshold (VT) technique. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma SAH levels and atherosclerotic lesion size were significantly increased in adenosine dialdehyde and SAH hydrolase short hairpin RNA groups when compared with control group. 5 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
There is a substantial body of literature dealing with predictors of dementia in patients with MCI. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease (AD) polygenic risk scores (ADPRS) built from cell-type (ct) specific genetic variants can be used to infer cell-type contributions to AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the main cause of dementia and accounts for 60% of dementia syndromes in people older than 75 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We show that CD33M ectodomain dimerizes, enabling binding of large multi-sialylated molecules. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In UKB, PRS cancer was nominally associated with improved fluid intelligence ( β : 0.12, 95% CI: 0.01-0.22). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein ε4 allele (APOE4) is associated with decreased longevity and increased vulnerability to age-related declines and disorders across multiple systems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mineralized blood vessels (MBV) are a form of vascular pathology associated with cerebrovascular aging and neurodegeneration; however, their regional distribution and clinicopathological correlates in Alzheimer disease (AD) remain poorly characterized. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both 17αE2 and FMD independently reduced AD neuropathology in the EFAD mice, in an APOE-dependent manner. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
MR analysis identified phosphatidylinositol (PI) (16:0_20:4), phosphatidylcholine (PC) (16:0_22:4) and sterol ester (SE) (27:1/15:0) as risk factors for AD. 5 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Participants did not differ significantly based on sex. 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases (NDs) are common chronic diseases with unknown etiology, and the association between virus and its pathogenesis is not clear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BPSD severity was independent from cognitive impairment, vascular impairment, white matter lesions and ApoE status. 3 key findings →
Design: cross-sectional Participants: 92 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. 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 →