Overall, cumulative incidence was uniformly higher in NACC than in the population-based cohorts. 3 key findings →
Participants: 5,073 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variants within the VCAN gene may play a role in the mechanisms underlying microstructural integrity of the white matter in the brain measured as FA and MD. 4 key findings →
Design: cohort study Participants: 8,448 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a total of 602 autopsy cases (median [IQR] age at death, 78 [71-85] years; 328 male [54.5%] and 274 female [45.5%]), higher PM2.5 exposure prior to death was associated with increased odds of more severe Alzheimer disease neuropathologic change (ADNC) (odds ratio, 1.19; 95% CI, 1.11-1.28). 5 key findings →
Design: cohort study Participants: 602 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 3414 included individuals, the mean (SD) age was 68.8 (6.0) years and 2116 (62%) were female. 5 key findings →
Design: cohort study Participants: 1,184 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Increasing cerebral Abeta deposition with age is the pathobiological phenotype of APOE4. 1 key finding →
Participants: 241 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We used Kaplan-Meier survival analysis to examine the distribution of incident ARIA-E from the start of bapineuzumab treatment and proportional hazards regression models to assess risk factors associated with ARIA. 3 key findings →
Design: clinical trial Participants: 262 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
During the 17-year follow-up period, 164 participants developed dementia; 136 of these cases were AD. 5 key findings →
Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genetic and environmental factors that increase the risk of late-onset Alzheimer disease are now well recognized but the cause of variable progression rates and phenotypes of sporadic Alzheimer's disease is largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This should be considered when designing protocols for amyloid-modifying clinical trials. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings from healthy high-risk older individuals suggest that OI reflects degree of preclinical AD pathology, while its relationships with age and cognition result from the association of these latter variables with such pathology. 3 key findings →
Design: cross-sectional Participants: 101 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →
Design: longitudinal study Participants: 1,075 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results provide evidence supporting 25OHD as a causal risk factor for AD. 5 key findings →
Participants: 33,996 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. 3 key findings →
Design: case-control study Participants: 10,578 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
Cognitively normal elderly individuals who engage in specific mentally stimulating activities even in late life have a decreased risk of incident MCI. 3 key findings →
Design: cohort study Participants: 973 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →
Design: longitudinal study Participants: 193 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
62/100
Disturbing dreams were reported by 24.2% overall and all-cause dementia, and AD incidence was 10.8 and 5.3 per 1000 person-years, respectively. 5 key findings →
Design: cohort study Participants: 10,238 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A polygenic score (PGS) for Alzheimer's disease (AD) was derived recently from data on genome-wide significant loci in European ancestry populations. 4 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
61/100
Our results indicate that APOE ε4 is independently associated with a greater severity of LB pathology. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Levels of DDE were 3.8-fold higher in the serum of those with AD (mean [SEM], 2.64 [0.35] ng/mg cholesterol) when compared with control participants (mean [SEM], 0.69 [0.1] ng/mg cholesterol; P Conclusions and relevance Elevated serum DDE levels are associated with an increased risk for AD and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE. 2 key findings →
Design: case-control study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To evaluate reverse causation, we assessed whether a polygenic risk score for AD is associated with HGS. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD. 5 key findings →
Design: cohort study Participants: 3,601 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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.
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 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.
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 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 →