The study population consisted of 194 patients (123 AD and 71 non-AD). 5 key findings →
Participants: 194 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer's dementia (AD) capitalizing on National Alzheimer's Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed. 3 key findings →
Participants: 389 Evidence: low
Full summary, score breakdown and related studies → Original source
This study demonstrated that APOE4 carrier status was associated with lower MoCA-INA scores in this small VaD cohort. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
For the purpose of studying the potential neurobehavioral effects of different human apolipoprotein E (apoE) isoforms produced within the brain, transgenic (TG) mice were generated in which human apoE3 or apoE4 isoforms were under control of an astrocyte-specific, glial fibrillary acidic protein promoter and these TG mice were bred back to apoE knockout (KO) mice. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Several genetic risk factors for Alzheimer's disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 . 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although APOE ε2 is known to be protective against Alzheimer's disease, it has also been shown to increase risk for hemorrhage with cerebral amyloid angiopathy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pleiotropic nature of the apolipoprotein E (APOE) gene is associated with complex diseases in different populations. 2 key findings →
Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular deposition of the amyloid beta-peptide, leading to intracerebral hemorrhage in severe cases. 4 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TT genotype of rs688 in the LDLR gene was not found to be associated with elevated levels of total cholesterol or LDL-C. 4 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE) is associated with Alzheimer's neurofibrillary tangles and beta-amyloid protein in senile plaques. 3 key findings →
Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Apolipoprotein E (APOE) plays a pivotal role in lipid including cholesterol metabolism. 2 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes are critical for maintaining blood-brain barrier (BBB) integrity and have emerged as key contributors to Alzheimer's disease (AD) pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ApoE-4 was strongly associated with AD in this sample (allele frequency = 0.46 vs. 0.14 in controls, p < 0.000001). 5 key findings →
Participants: 679 Evidence: low
Full summary, score breakdown and related studies → Original source
An association between the 19q13.2 chromosomal region and Alzheimer's disease (AD) has been reported in AD families and for sporadic AD. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
The mean age was 51 ± 12 years. Forty-two of the patients had OSAS. 5 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Higher HOMA-IR was associated with higher sAβPPβ and Aβ42 . 4 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
CSF-sLR11 concentrations were higher in patients with AD than controls (adjusted for sLR11 using phospholipid). 3 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
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
The pathway analysis of six major cell types revealed a strong association between APOE2 and cellular stress and energy metabolism, particularly in excitatory and inhibitory neurons, which was found to be more pronounced in the presence of beta-amyloid (Aβ). 5 key findings →
Evidence: moderate
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
From across this tag
9 of the 268 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 9. The same 9 appear here every time.
- Peripheral TREM2 mRNA levels in early and late-onset Alzheimer disease's patients
- How proteomic ApoE serotyping could impact Alzheimer's disease risk assessment: genetic testing by proteomics
- APOE4 impairs autophagy and Aβ clearance by microglial cells
- Apolipoprotein E affects amyloid formation but not amyloid growth in vitro: mechanistic implications for apoE4 enhanced amyloid burden and risk for Alzheimer's disease
- Apolipoprotein E2 Stimulates Protein Synthesis and Promotes Melanoma Progression and Metastasis
- Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease
- APOE4 Increases Energy Metabolism in APOE-Isogenic iPSC-Derived Neurons
- Association of human, rat, and rabbit apolipoprotein E with beta-amyloid
- Cerebral amyloid angiopathy-related hemorrhage. Interaction of APOE epsilon2 with putative clinical risk factors
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 →