27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). 1 key finding →
Evidence: low
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To avoid the problems that heterogeneity poses for genetic analysis, the researchers examined the cosegregation of Alzheimer's disease and markers along the long arm of chromosome 21 in a single family. 3 key findings →
Evidence: low
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Approximately 40% of dementia cases could be prevented or delayed by modifiable risk factors related to lifestyle and environment. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Rich data from large biobanks, coupled with increasingly accessible association statistics from genome-wide association studies (GWAS), provide great opportunities to dissect the complex relationships among human traits and diseases. 5 key findings →
Participants: 61,212 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and the most common form of dementia in the elderly. 2 key findings →
Design: case-control study Participants: 931 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Nineteen participants developed AD after a median of 60 months (interquartile range 30). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Through this approach, we identified 103 ARGs validated by various levels of pathobiological evidence in AD. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive impairment and neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nine female-specific associations were identified and replicated, involving ADGRV1, OR3A3, IFI27L1, LYRM1, STAP2, TSTD2, PDYN, and TMEM50B. We observed the preponderance of protective female-specific associations in neurons. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chronological age offers an imperfect estimate of the molecular changes that occur with aging. 4 key findings →
Participants: 4,000 Evidence: low
Full summary, score breakdown and related studies → Original source
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
Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE. 2 key findings →
Design: case-control study Participants: 753 Evidence: moderate
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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
If confirmed in longitudinal studies, these data would suggest circulating beta-amyloid peptide as a novel biomarker or risk factor for microvascular damage in these common diseases of the elderly. 2 key findings →
Design: cross-sectional Participants: 54 Evidence: moderate
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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
Patients with DLB had an increased risk of mortality vs patients with AD (hazard ratio [HR] 1.88, 95% CI: 1.4 to 2.5). 3 key findings →
Design: longitudinal study Participants: 315 Evidence: moderate
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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
Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level. 5 key findings →
Design: cross-sectional Participants: 1,079 Evidence: moderate
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Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
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 →