Chronic glial activation and neuroinflammation induced by the amyloid‐β peptide (Aβ) contribute to Alzheimer's disease ( AD ) pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The lipids and proteins that comprise lipid droplets regulate several cellular functions including lipid storage, stress responses, and inflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →
Participants: 58,876 Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) genotype is theorised to influence dementia risk partly through effects on blood–brain barrier (BBB) function, but clinical studies examining APOE effects on BBB biomarkers report inconsistent results. 5 key findings →
Design: systematic review Participants: 5,375 Evidence: high
Full summary, score breakdown and related studies → Original source
16/100
Genetic variation in APOE , which encodes a lipid transporter apolipoprotein E (apoE), is the strongest risk factor for late-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Psychosis is a neuropsychiatric feature found across neurodegenerative conditions including Alzheimer’s disease (AD) and Parkinson’s disease (PD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks. 3 key findings →
Design: clinical trial Participants: 370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown. 1 key finding →
Participants: 413 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA), characterized by cerebrovascular amyloid deposition, is strongly associated with Alzheimer’s disease, ischemic injury, and lobar hemorrhages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified 27 phenotypes associated with APOE, mainly in neurological and lipid-related traits. 5 key findings →
Participants: 181,880 Evidence: moderate
Full summary, score breakdown and related studies → Original source
16/100
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, and its incidence is rising rapidly with population aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 ( APOE ε4) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet its associated protein changes across biofluids, brain regions, and cell types remain incompletely understood. 3 key findings →
Participants: 1,691 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
7 of the 269 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 7. The same 7 appear here every time.
- Apolipoprotein E polymorphisms and female fertility in a transgenic mouse model of Alzheimer's disease
- Deletion of Abca7 increases cerebral amyloid-β accumulation in the J20 mouse model of Alzheimer's disease
- Brain-targeting liposome-based APOE2 gene delivery exacerbates soluble amyloid-β accumulation in App NL-G-F mice
- Fatty Acid Binding Protein 3 (FABP3) and Apolipoprotein E4 (ApoE4) as Lipid Metabolism-Related Biomarkers of Alzheimer's Disease
- Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology
- Glial fibrillary acidic protein-apolipoprotein E (apoE) transgenic mice: astrocyte-specific expression and differing biological effects of astrocyte-secreted apoE3 and apoE4 lipoproteins
- APOE from astrocytes restores Alzheimer's Aβ-pathology and DAM-like responses in APOE deficient microglia
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →