27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
While genome wide association studies (GWASs) of Alzheimer's Disease (AD) in European (EUR) ancestry cohorts have identified approximately 83 potentially independent AD risk loci, progress in non-European populations has lagged. 5 key findings →
Design: meta-analysis Participants: 4,385 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Non-Hispanic white and NHB Health and Retirement Study (HRS) participants provided genetic information and either a composite memory score (n = 10,401) or a dementia probability score (n = 7690). 1 key finding →
Design: meta-analysis Participants: 10,401 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. 5 key findings →
Design: longitudinal study Participants: 329 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In patients with sporadic ALS, we identified the repeat expansion in 236 (7·0%) of 3377 white individuals from the USA, Europe, and Australia, two (4·1%) of 49 black individuals from the USA, and six (8·3%) of 72 Hispanic individuals from the USA. 1 key finding →
Participants: 4,448 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ϵ4 prevalence in Black (46%) and White participants (46%) was almost double that of Latino participants (24%). ϵ4 was associated with poorer baseline episodic memory only in White participants (p = .001), but had a moderately strong association with episodic memory change across all racial/ethnic groups (Blacks= -.061 SD/year, Latinos = -.055,Whites= -.055). ϵ4 association with semantic memory change was strongest in White participants (-.071), intermediate in Latino participants (-.041), and weakest in Black participants (-.022). 4 key findings →
Design: longitudinal study Participants: 297 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Limited evidence suggests that the APOEε4 allele may confer risk for CTE, but previous studies were small with limited scope. 5 key findings →
Design: cross-sectional Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although APOE ε4 carriers are at high risk for cognitive decline, our findings suggest possible intervention targets, including the enhancement of cognitive reserve and improvement of other psychosocial and health factors, to promote cognitive resilience among black and white APOE ε4 carriers. 5 key findings →
Design: prospective cohort Participants: 2,487 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The ASDIR for ADRD was higher for women (17.0 per 1000 person-years) than for men (15.3) and varied across African Americans (22.9 in women, 21.5 in men), Native Hawaiians (19.3, 19.4), Latinos (16.8, 14.7), Whites (16.4, 15.5), Japanese Americans (14.8, 13.8), and Filipinos (12.5, 9.7). 5 key findings →
Participants: 16,410 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We hypothesized that telomere length might thus relate to increased risk for dementia and mortality. 2 key findings →
Design: case-control study Participants: 257 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In this study, we report the experience of the only reference clinical next-generation sequencing lab in Saudi Arabia with the first 1000 families who span a wide-range of suspected Mendelian phenotypes. 1 key finding →
Participants: 1,019 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study confirms the association between genetic variants in SORL1 and AD. 5 key findings →
Design: case-control study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (APO-E) binds to the beta-amyloid peptide and is present in senile neuritic plaques in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion. 2 key findings →
Design: cross-sectional Participants: 397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genetic risk modeling for dementia offers significant benefits, but studies based on real-world data, particularly for underrepresented populations, are limited. 3 key findings →
Participants: 610 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results add to the body of evidence on the adverse impact of ambient air pollution on cognitive aging and brain health and provide new insights into the genetic and behavioral factors that may impact individual susceptibility. 4 key findings →
Participants: 4,821 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As indicated by Cox regression modeling, dementia risk of low-educated individuals was not significantly different between ethnic groups but was related to having an APOE e4 allele (hazard ratio [HR] 1.89), depression (HR 1.67), stroke (HR 1.60), and smoking (HR 1.32). 3 key findings →
Participants: 819 Evidence: low
Full summary, score breakdown and related studies → Original source
CAG trinucleotide expansion is the molecular basis of Huntington's disease worldwide and is a highly sensitive and specific marker for inheritance of the disease mutation. 4 key findings →
Participants: 1,007 Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) is a clinical syndrome with a heterogeneous molecular basis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fine particulate matter, known as PM 2.5, is recognized as a risk factor for dementia. 1 key finding →
Participants: 217,336 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Early identification of younger, non-demented adults at elevated risk for Alzheimer's disease (AD) is crucial because the pathological process begins decades before dementia onset. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The findings support the pathological evidence that underlying variations in MAPT could contribute to disease pathogenesis by subtle effects on gene expression and/or splicing. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
To better characterize the potential biological mechanisms underlying insulin resistance (IR) and dementia, we derive cross-population and population specific polygenic scores [PSs] for fasting insulin and IR-related partitioned PSs [pPSs]. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia, a heterogeneous neurodegenerative disorder, is a common cause of young onset dementia (i.e. dementia developing in midlife or earlier). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The purpose of the study was to provide characterization of Mexican Americans who meet criteria for Alzheimer's disease (AD) and mild cognitive impairment (MCI). 3 key findings →
Participants: 633 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →