27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
ApoE4-CLEAR interactions may account for suppressed autophagy in APOE ɛ4/ɛ4 carriers and, in this way, contribute to earlier AD onset. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apoE epsilon 4 allele may be associated with decreased cognitive function in discordant twin pairs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that neuronal injury markers such as VLP-1 may have utility as biomarkers for AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The preliminary findings from this study support the possibility that aerobic fitness is positively associated with the memory performance of those individuals at most genetic risk for Alzheimer disease. 3 key findings →
Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of AD associated with this region. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration. 5 key findings →
Participants: 1,542 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified sex differences for several classes of metabolites, such as glycerophospholipids, sphingolipids, and amino acids. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer's disease (AD) risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF levels of apoE2, apoE3, and apoE4 were significantly higher (all nominal P < 10 × 10-5 , false discovery rate < 0.001) and those of tumor necrosis factor-α (TNF-α) were significantly lower (nominal P = 1.39 × 10-6 , false discovery rate < 0.001) in APOE-ε4 carriers than in noncarriers. 3 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic Alzheimer's disease (sAD) is marked by dysregulated lipid metabolism, prominently involving apolipoprotein E (ApoE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical outcomes of severe acute respiratory syndrome 2 (SARS-CoV-2) infection are highly heterogeneous, ranging from asymptomatic infection to lethal coronavirus disease 2019 (COVID-19). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In humans, apolipoprotein E (apoE) is a polymorphic protein of which three common isoforms can be distinguished, designated apoE2, apoE3, and apoE4. 3 key findings →
Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4-KI mice showed impaired retinal structure, vasculature, function, vision, increased gliosis and neuroinflammation, and downregulation of synaptogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our analysis of common SNVs and indels confirmed known genetic loci at MAPT, MOBP, STX6, SLCO1A2, DUSP10, and SP1, and further uncovered novel signals in APOE, FCHO1/MAP1S, KIF13A, TRIM24, TNXB, and ELOVL1. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found a significant genetic overlap between hearing impairment and AD and a polygenic risk score for AD was able to significantly predict hearing loss in an independent cohort. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The data processing pipelines, research-ready imputed genetic data, and PRS scores are now available on the DPUK platform and can be accessed upon request though the DPUK application process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We calculated a PRS for LOY in 5131 men aged 70 years and older. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia, a collective term for neurodegenerative disorders marked by cognitive decline, affects millions worldwide, and is expected to rise significantly in prevalence. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Seventeen variants were significantly associated with AD within five genomic regions implicating the genes OARD1/NFYA/TREML1, JAZF1, FERMT2, and SLC24A4. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Some viruses, such as varicella zoster virus, are associated with severe dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of Alzheimer's disease (AD) depends on environmental and heritable factors, with its molecular etiology still unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The emergence of single nucleus RNA sequencing (snRNA-seq) offers to revolutionize the study of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This molecular genetics study found that several TREM2 gene variants previously thought to work only by altering the TREM2 protein itself, also disrupt how the TREM2 gene's RNA message is spliced together, sometimes producing dysfunctional protein versions. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →