28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The Apolipoprotein E ε4 (ApoE ε4) allele, encoding ApoE4, is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
ApoE is the major lipid and cholesterol carrier in the CNS. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) is the single greatest genetic risk factor for late onset Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a common feature in neurodegenerative diseases, modulated by the Alzheimer's disease risk factor, apolipoprotein E (APOE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (ApoE)'s ϵ4 alle is the most important genetic risk factor for late onset Alzheimer's Disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently studies on the correlation between obesity and Alzheimer's disease (AD) are still unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE germline variants impact melanoma progression through disparate mechanisms, such as the protein synthesis-promoting function of the APOE2 variant, indicating that germline genetic variants are causal contributors to metastatic outcomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the identification of the apolipoprotein E (apoE) *ε4 allele as a major genetic risk factor for late-onset Alzheimer's disease, significant efforts have been aimed at elucidating how apoE4 expression confers greater brain amyloid-β (Aβ) burden, earlier disease onset and worse clinical outcomes compared to apoE2 and apoE3. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A preponderance of evidence obtained from genetically modified mice and human population studies reveals the association of apolipoprotein E (apoE) deficiency and polymorphisms with pathogenesis of numerous chronic diseases, including atherosclerosis, obesity/diabetes, and Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Obesity was associated with cognitive decline in early elderly cognitively normal individuals without APOE4, especially those with APOE2. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the brains of Apoeshl mice, the levels of apoM were lower, while those of ceramides were higher. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common type of dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ε4-allele variant of apolipoprotein E (ApoE4) is the strongest genetic risk factor for Alzheimer's disease, although it only differs from its neutral counterpart ApoE3 by a single amino acid substitution. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related macular degeneration (AMD) is a multifactorial retinal disorder that is a major global cause of severe visual impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (apoE) is associated with lipoproteins in the cerebrospinal fluid (CSF). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aberrant low γ-secretase activity is associated with most of the presenilin mutations that underlie familial Alzheimer's disease (fAD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human apolipoprotein E (ApoE) is a 299-amino acid secreted glycoprotein that binds cholesterol and phospholipids. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Though apolipoprotein E ε4 (APOE ε4) is a major genetic risk factor for late-onset Alzheimer's disease, its association with depression remains controversial. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Here, we report that the acute exposure of primary cortical neurons or synaptoneurosomes to APOE4 leads to a significant decrease in global protein synthesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A key hallmark of Alzheimer's disease (AD) is the accumulation of hyperphosphorylated tau in neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mean coverage of the amino acid sequence of full-length ApoE was 91.6% in the protein resequence. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein (APOE) is a major risk factor of Alzheimer's disease (AD), with the E2, E3 and E4 isoforms differentially regulating the burden of AD-associated neuropathologies, such as amyloid β and tau. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E gene (APOE) confers the greatest genetic risk factor for Alzheimer's disease (AD), wherein the ε4 allele confers an elevated risk compared with the ε3 allele. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As predicted, we observed a differential impact of CBE status on cognition as a function of APOE ε4 status, in which CBE ε4 carriers displayed significantly worse neuropsychological performance, specifically in the domain of memory. 3 key findings →
Evidence: low
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 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.
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 →