30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Understanding the lifetime risk of dementia can inform public health planning and improve patient engagement in prevention. 1 key finding →
Design: cohort Participants: 15,043 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We found a significant association between GBA1 mutation carrier status and DLB, with an odds ratio of 8.28 (95% CI, 4.78-14.88). 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
New PRSs for dementia significantly improve risk-prediction performance, but still account for less risk than APOE genotype overall. 3 key findings →
Design: cohort Participants: 12,031 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Parkinson disease (PD) is a complex neurodegenerative disorder with largely unknown genetic mechanisms. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. 4 key findings →
Evidence: low
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Alzheimer's disease, a fatal neurodegenerative disorder of unknown aetiology, is usually considered to be a single disorder because of the general uniformity of the disease phenotype. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Population health research is increasingly focused on the genetic determinants of healthy ageing, but there is no public resource of whole genome sequences and phenotype data from healthy elderly individuals. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Analysis included a total of 121 145 patients in non-D-SNP plans with an enrollment of 173 662 patient-years (mean [SD] age, 81.8 [7.8] years; 122 565 female [70.6%]; 6078 Asian [3.5%], 34 150 Black [19.7%], 37 580 Hispanic [21.6%], 95 854 White [55.2%]) and 78 166 patients in D-SNP plans with an enrollment of 122 681 patient-years (mean [SD] age, 80.2 [8.0] years; 87 329 female [71.2%]; 10 530 Asian [8.6%], 33 280 Black [27.1%], 43 294 Hispanic [35.3%], 35 577 White [29.0%]). 5 key findings →
Design: cross-sectional Participants: 121 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Atherosclerosis is driven by the expansion of cholesterol-loaded 'foamy' macrophages in the arterial intima. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Trem2 (triggering receptor on myeloid cells 2), a surface lipid receptor, is expressed on foamy macrophages within atherosclerotic lesions and regulates cell survival, proliferation, and anti-inflammatory responses. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2), a receptor exclusively expressed by microglia in the brain, modulates microglial immune homeostasis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overexpression of Alzheimer amyloid precursor protein (APP) produces dramatically different phenotypes in transgenic mice depending on the genetic background. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The human and rat hippocampus is highly susceptible to iron deficiency (ID) during the late fetal, early neonatal time period which is a peak time of regulated brain iron uptake and utilization. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
TAR DNA binding protein 43 kDa (TDP-43), for instance, has been shown to cause frontotemporal dementia as well as some cases of familial ALS, and is associated with frontotemporal dysfunction in ALS. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Bệnh Alzheimer (AD) có căn nguyên không rõ ràng. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events