30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Epigenome-wide association studies of Alzheimer's disease have highlighted neuropathology-associated DNA methylation differences, although existing studies have been limited in sample size and utilized different brain regions. 3 key findings →
Design: meta-analysis Participants: 1,453 Evidence: high
Full summary, score breakdown and related studies → Original source
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD). 5 key findings →
Design: meta-analysis Participants: 12,017 Evidence: high
Full summary, score breakdown and related studies → Original source
Progressive loss of neurons in a specific brain area is one of the manifestations of Alzheimer's disease (AD). 2 key findings →
Design: meta-analysis Participants: 33,992 Evidence: high
Full summary, score breakdown and related studies → Original source
Narcolepsy type 1 is strongly associated with human leukocyte antigen (HLA)-DQB1*06:02; however, no significant associations between IH and HLA alleles have been reported. 4 key findings →
Design: meta-analysis Participants: 414 Evidence: high
Full summary, score breakdown and related studies → Original source
In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified. 4 key findings →
Design: meta-analysis Participants: 2,784 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A key driver of patients' well-being and clinical trials for Parkinson's disease (PD) is the course that the disease takes over time (progression and prognosis). 5 key findings →
Design: longitudinal study Participants: 3,821 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The APOE ε4 allele remains the strongest genetic risk factor for sporadic Alzheimer's disease and the APOE ε2 allele the strongest genetic protective factor after multiple large scale genome-wide association studies and genome-wide association meta-analyses. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have discovered numerous genomic loci associated with Alzheimer's disease (AD); yet the causal genes and variants are incompletely identified. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Psychotic symptoms, defined as the occurrence of delusions or hallucinations, are frequent in Alzheimer disease (AD with psychosis, AD + P). 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Genetic discoveries of Alzheimer's disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. 2 key findings →
Design: case-control study Participants: 409,435 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Previous genome-wide association studies have identified dozens of susceptibility loci for sporadic Alzheimer's disease, but few of these loci have been validated in longitudinal cohorts. 4 key findings →
Design: longitudinal study Participants: 3,913 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has no cure, but early detection and risk prediction could allow earlier intervention. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CSF NPTX2 concentration is a strong prognostic biomarker candidate of accelerated cognitive decline with potential use as a therapeutic target. 2 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that longitudinal changes in cognitive function measured by the cognitive composite decreased at low and high values of total sleep time (P < 0.001), time in non-REM (P < 0.001) and REM sleep (P < 0.001), sleep efficiency (P < 0.01) and <1 Hz and 1-4.5 Hz non-REM slow wave activity (P < 0.001) even after adjusting for age, CSF total tau/amyloid-β42 ratio, APOE ε4 carrier status, years of education and sex. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (APOE) ε4 is the single most important genetic risk factor for cognitive impairment and Alzheimer disease (AD), while lifestyle factors such as smoking, drinking, diet, and physical activity also have impact on cognition. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The 4417 participants in the study included 2618 women (59%) and had a mean (SD) age of 71.3 (4.7) years. 5 key findings →
Design: cross-sectional Participants: 2,618 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. 2 key findings →
Design: cross-sectional Participants: 512 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Worldwide, the prevalence of dementia is increasing and diet as a modifiable factor could play a role. 3 key findings →
Participants: 493,888 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In cross-sectional analyses at baseline, there was no association between DNAm age acceleration and cognitive function scores. 5 key findings →
Design: cross-sectional Participants: 266 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We have generated a controlled and manipulable resource that captures genetic risk for Alzheimer's disease: iPSC lines from 53 individuals coupled with RNA and proteomic profiling of both iPSC-derived neurons and brain tissue of the same individuals. 2 key findings →
Design: longitudinal study Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified polymorphism in the Apolipoprotein E gene (APOE) to be the most prominent risk factor for Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Sporadic Alzheimer's disease (AD) exclusively affects elderly people. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Diabetes was associated with shorter lifespan in APOE3 carriers (n = 12,415, HR = 1.29, 95%CI = 1.17-1.42, p < 0.001) and APOE2 carriers (n = 2,390, HR = 1.37, 95%CI = 1.10-1.69, p = 0.016), while such associations were weaker and not significant in APOE4 carriers (n = 9,490, HR = 1.11, 95%CI = 0.99-1.24, p = 0.162). 5 key findings →
Participants: 12,415 Evidence: low
Full summary, score breakdown and related studies → Original source
The PRS for AD was significantly higher in APOE ε4 homozygote AD cases compared to older cognitively healthy APOE ε4/ε4 controls (odds ratio [OR] 8.39; confidence interval [CI] 2.0-35.2; P = .003). 4 key findings →
Participants: 213 Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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