The epsilon4 allele of apolipoprotein E (apoE) is associated with increased risk for Alzheimer's disease (AD) and poor outcome after brain injury. 3 key findings →
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.
It has been estimated that Alzheimer's disease (AD), the most common form of dementia, will affect approximately 81 million individuals by 2040. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E gene (APOE) alleles may shift the onset of Alzheimer's disease (AD) through apoE protein isoforms changing the probability of amyloid-β (Aβ) accumulation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
First recognized as a major determinant in lipoprotein metabolism and cardiovascular disease, apolipoprotein (apo) E has emerged as an important molecule in several biological processes not directly related to its lipid transport function, including Alzheimer's disease and cognitive function, immunoregulation, and possibly even infectious diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E is associated with age-related risk for Alzheimer's disease and plays critical roles in Abeta homeostasis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The premise of this review is that apolipoprotein (apo) E4 is much more than a contributing factor to neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Apolipoprotein (apo) E is a multifunctional protein with central roles in lipid metabolism, neurobiology, and neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood–brain barrier (BBB) limits the entry of neurotoxic blood-derived products and cells into the brain that is required for normal neuronal functioning and information processing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review examines the association between the apolipoprotein (apo) var epsilon gene polymorphism (or its protein product (apo E)), metabolic regulation of cholesterol, and cardiovascular disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the three human apolipoprotein E (apoE) isoforms, apoE4 increases the risk of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is unique in medicine in that millions of people suffer from what appears to be the same form of disease, and unlike most other late-onset diseases, the genetic etiologies have been well identified. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent evidence indicates that apolipoprotein E (ApoE) plays a central role in the hippocampal response to injury. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human apolipoprotein E (apoE) is a member of the family of soluble apolipoproteins. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Apolipoprotein (apo) E has roles beyond lipoprotein metabolism. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related macular degeneration (AMD) is a late-onset, multifactorial, neurodegenerative disease of the retina and the leading cause of irreversible vision loss in the elderly in the Western world. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E protein is strategically located at the same anatomic locus where drusen are situated, and the retinal pigmented epithelium is the most likely local biosynthetic source of apolipoprotein E at that location. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of amyloid-β (Aβ) metabolism is critical for Alzheimer's disease (AD) pathogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon4 genotype of apolipoprotein E (apoE4) is the most established predisposing factor in Alzheimer's disease (AD); however, it remains unclear how apoE4 contributes to the pathophysiology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipid-mediated signalling regulates a plethora of physiological processes, including crucial aspects of brain function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder, affecting millions of people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although an immense knowledge has accumulated concerning regulation of cholesterol homeostasis in the body, this does not include the brain, where details are just emerging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE = gene, apoE = protein) plays a central role in plasma lipoprotein metabolism and in lipid transport within tissues. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
From across this tag
10 of the 266 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.
- APOE2 protects against Aβ pathology by improving neuronal mitochondrial function through ERRα signaling
- A novel biochemical analysis for ApoE4 quantification in plasma and discrimination of homozygous and heterozygous APOE ε4 carriers
- The triggering receptor expressed on myeloid cells 2-apolipoprotein E signaling pathway in diseases
- Isoform-specific binding of apolipoprotein E to beta-amyloid
- Apolipoprotein E: the resilience gene
- APOE-Targeted Therapeutics for Alzheimer's Disease
- APOE4 impairs macrophage lipophagy and promotes demyelination of spiral ganglion neurons in mouse cochleae
- ABCA1 Is Required for Normal Central Nervous System ApoE Levels and for Lipidation of Astrocyte-secreted apoE
- APOE ɛ4 carriership determines a faster plasma p-tau217 progression in Aβ-positive individuals
- Apolipoprotein E lipoprotein particles inhibit amyloid-β uptake through cell surface heparan sulphate proteoglycan
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 →