Collecting cases for case-control genetic association studies can be time-consuming and expensive. 1 key finding →
Design: meta-analysis Participants: 116,196 Evidence: high
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Collecting cases for case-control genetic association studies can be time-consuming and expensive. 1 key finding →
Design: meta-analysis Participants: 116,196 Evidence: high
Full summary, score breakdown and related studies → Original source
Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). 3 key findings →
Design: meta-analysis Participants: 24,000 Evidence: high
Full summary, score breakdown and related studies → Original source
In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. 2 key findings →
Design: meta-analysis Participants: 1,743 Evidence: high
Full summary, score breakdown and related studies → Original source
The need for large sample sizes has led to collaborative efforts, such as the Prospective Studies Collaboration (an individual participant meta-analysis of data from 61 studies and more than a million participants11) that has demonstrated conclusively that a continuous increase in blood pressure corresponds with an increased risk of vascular death across all age groups (see Figure 1 that illustrates the importance of a large sample size (about 500 000 participants) for detecting this association).12 Sample size is also of particular importance in the current era of genome-wide association studies, where many investigations are aiming to detect either small effects from common variants or large effects from rare variants.13 Absolute risk of ischaemic heart disease mortality by usual systolic blood pressure and age at risk in 5000, 50 000, and 500 000 participants. 5 key findings →
Design: meta-analysis Participants: 5,200 Evidence: high
Full summary, score breakdown and related studies → Original source
An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. 5 key findings →
Design: cohort study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Contrary to long-standing views, men and women with the APOE ε3/ε4 genotype have nearly the same odds of developing AD from age 55 to 85 years, but women have an increased risk at younger ages. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
More than 20 genetic loci have been associated with risk for Alzheimer's disease (AD), but reported genome-wide significant loci do not account for all the estimated heritability and provide little information about underlying biological mechanisms. 5 key findings →
Design: case-control study Participants: 3,146 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuous variables, and results are reported per SD increase of each lipid fraction. 5 key findings →
Design: cohort study Participants: 9,294 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We undertook a genome-wide association study (GWAS) of parental longevity in European descent UK Biobank participants. 4 key findings →
Design: longitudinal study Participants: 1,181 Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a frequent problem encountered in advanced stages of Parkinson disease (PD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Protection from these ADP factors may be important for aging without significant ADP. 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4. 5 key findings →
Design: case-control study Participants: 346 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
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
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
Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 183 study participants, mean (SD) age was 85.5 (3) years, 76 were women (41.5%), and 177 were white (96.7%). 4 key findings →
Design: cross-sectional Participants: 183 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous estimates of the utility of polygenic risk score analysis for the prediction of Alzheimer disease have given area under the curve (AUC) estimates of <80%. 1 key finding →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher GRS predicted mortality (hazard ratio = 1.05; 95% confidence interval: 1.00-1.10, P = .04). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Identifying individuals at risk for developing Alzheimer disease (AD) is of utmost importance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanisms underlying phenotypic heterogeneity in young onset Alzheimer disease (YOAD) are poorly understood. 1 key finding →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease. 4 key findings →
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 →