APOE2 is associated with less cognitive decline during aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
APOE2 is associated with less cognitive decline during aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The degree of coronary artery disease is independently associated with the cardinal neuropathological lesions of Alzheimer disease. 3 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD), a progressive and neurodegenerative disease, is the most common form of dementia with high incidence in elderly people. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Higher phosphatidylcholine intake was associated with lower risk of incident dementia and better cognitive performance in men in eastern Finland. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE affects microstructural properties of the brain WM from early adulthood, but the specific allelic effects do not directly reflect the associated risk of developing Alzheimer disease. 4 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Polygenic risk scores (PRSs) predict an individual's genetic risk for complex diseases, yet their utility in elucidating disease biology remains limited. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Stroke interacts with APOE ε4 to influence dementia, with the association being more pronounced in APOE ε4 non‐carriers. 4 key findings →
Design: cohort study Participants: 336 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Genome-wide association studies of neurological diseases have identified thousands of variants associated with disease phenotypes. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Age-related cognitive decline is likely promoted by accumulated brain injury due to chronic conditions of aging, including neurodegenerative and vascular disease. 4 key findings →
Participants: 749 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. 3 key findings →
Participants: 700 Evidence: low
Full summary, score breakdown and related studies → Original source
The neocortex is disproportionately expanded in human compared with mouse 1,2 , both in its total volume relative to subcortical structures and in the proportion occupied by supragranular layers composed of neurons that selectively make connections within the neocortex and with other telencephalic structures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This transcriptomic network analysis of 19 brain regions provides a comprehensive assessment of the critical molecular pathways associated with AD pathology and offers new insights into molecular mechanisms underlying selective regional vulnerability to AD at different stages of the progression of cognitive compromise and development of the canonical neuropathological lesions of AD. 5 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with Alzheimer's disease (AD) and Parkinson's disease (PD) often have overlap in clinical presentation and brain neuropathology suggesting that these two diseases share common underlying mechanisms. 1 key finding →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies indicate that the adaptive immune system plays a role in Lewy body dementia (LBD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
Functional phenotypes (e.g., subcortical surface representation), which commonly arise in imaging genetic studies, have been used to detect putative genes for complexly inherited neuropsychiatric and neurodegenerative disorders. 2 key findings →
Participants: 708 Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical models of Alzheimer's disease (AD) suggest APOE modulates brain function in structures vulnerable to AD pathophysiology. 5 key findings →
Participants: 608 Evidence: low
Full summary, score breakdown and related studies → Original source
Gene-based PRS identified 389 genes with 164 of them not previously reported as AD-associated. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglia are central mediators of neuroinflammation in Alzheimer's disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia and cognitive disorders are major aging-associated pathologies. 4 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) is linked to a higher risk of premature aging, but the mechanisms underlying this association remain unclear. 5 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →