27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →
Design: meta-analysis Participants: 1,362 Evidence: high
Full summary, score breakdown and related studies → Original source
How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study represents the largest PD AAO meta-analysis in European-ancestry populations to date. 5 key findings →
Design: meta-analysis Participants: 50,859 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer’s disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
According to the AT(N) framework, Alzheimers disease (AD) can be biologically characterised by amyloid deposition, tau pathology, and neurodegeneration, yet how these processes relate to whole-brain dynamics remains unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The rs28834970 regulatory variant was identified as the most functionally relevant in our model, with the C risk allele promoting transcription factor C/EBPβ binding within a cis-regulatory element. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings identify microglia as the immune population most strongly remodeled by Ms4a4a loss in the setting of amyloid pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenic risk scores (PRSs) have improved substantially in predictive performance, yet results remain difficult to compare across studies that differ in cohorts, phenotype definitions, and evaluation procedures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape. 1 key finding →
Participants: 3,202 Evidence: low
Full summary, score breakdown and related studies → Original source
Sequence models predict the molecular effects of genetic variation, yet their contribution to interpreting Alzheimer’s disease (AD) association signals remains uncertain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetically predicted BP raises WMH in European and Japanese ancestry. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identifying early life biomarkers of suboptimal aging trajectories could help design interventions to delay or even prevent the onset of pathological conditions in older adulthood. 1 key finding →
Participants: 522 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic studies have identified thousands of variants associated with brain-related traits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inverse-variance weighted MR indicated that genetically predicted focal epilepsy with hippocampal sclerosis was associated with increased odds of AD (OR=3.99, 95% CI 1.17–13.61; P=0.027). 5 key findings →
Participants: 803 Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic pain and cognitive impairment are rising ageing-related burdens. 4 key findings →
Design: longitudinal study Participants: 387,649 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Butyrate, a 4-carbon fatty acid produced from insoluble starch by the gut microbiome, plays key roles in mitochondrial respiration, activation of cell-surface G-protein-coupled receptors, and protein acetylation by inhibiting histone deacetylases (HDACs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing. 1 key finding →
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 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 →