Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. 2 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.
The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The identification of subjects at high risk for Alzheimer's disease is important for prognosis and early intervention. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A genome-wide, whole brain approach to investigate genetic effects on neuroimaging phenotypes for identifying quantitative trait loci is described. 4 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source
We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1 , ATXN2/BRAP , FURIN/FES , ZW10 , PSORS1C3 , and 13q21.31, and identify and replicate novel findings near ABO , ZC3HC1 , and IGF2R . 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia in Alzheimer's disease progresses alongside neurodegeneration 1-4 , but the specific events that cause neuronal dysfunction and death remain poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
The apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer's disease (AD). 5 key findings →
Participants: 641 Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Genome-wide association studies (GWAS) originally identified ATP-binding cassette, sub-family A, member 7 (ABCA7), as a novel risk gene of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic association studies have identified 44 common genome-wide significant risk loci for late-onset Alzheimer's disease (LOAD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With a rapidly aging global human population, finding a cure for late onset neurodegenerative diseases has become an urgent enterprise. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein aggregation is the hallmark of neurodegeneration, but the molecular mechanisms underlying late-onset Alzheimer's disease (AD) are unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epigenetic dysregulation of gene expression is thought to be critically involved in the pathophysiology of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe a human single-nuclei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approximately 17,000 nuclei from matched cortical and SN samples. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (ApoE) mediates the bidirectional transport of lipids between cells. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that TDP-43 overexpression induced motor function deficits, neuronal loss, and gliosis in the motor cortex, especially in APOE2 mice, with much milder or absent effects in APOE3, APOE4, or Apoe-KO mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4 is a strong genetic risk factor for Alzheimer's disease and Dementia with Lewy bodies; however, how its expression impacts pathogenic pathways in a human-relevant system is not clear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Liver-generated plasma apolipoprotein E (apoE) does not enter the brain but nonetheless correlates with Alzheimer's disease (AD) risk and AD biomarker levels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Alzheimer's disease (AD) are at an increased risk of bone fracture, while osteoporosis in women is one of the earliest predictors of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified APOE2 allele as linked to exceptional longevity, with carriers exhibiting a reduced risk of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Alzheimer's disease risk gene apolipoprotein E epsilon 4 (APOE ε4) is associated with increased cerebral amyloid. 4 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source
As the size of genome-wide association studies increase, the number of associated trait loci identified inevitably increase. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has a strong genetic predisposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
AD was associated with lower PRS for premorbid cognitive performance, intelligence, and educational attainment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Seventeen variants were significantly associated with AD within five genomic regions implicating the genes OARD1/NFYA/TREML1, JAZF1, FERMT2, and SLC24A4. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →