This situation presents difficulties for experimental studies, drug development, and other future research. 5 key findings →
Design: meta-analysis Participants: 94 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We identified 2 core dimensions of heterogeneity: typicality and severity. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The primary genetic risk factor for late onset Alzheimer's disease (LOAD) is the APOE4 allele of Apolipoprotein E (APOE) gene. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
DNA methylation differences in Alzheimer's disease (AD) have been reported. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Approximately 30% of older adults exhibit the neuropathological features of Alzheimer's disease without signs of cognitive impairment. 5 key findings →
Design: cohort study Participants: 5,108 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Developing Alzheimer's disease (AD) is influenced by multiple genetic variants that are involved in five major AD-pathways. 5 key findings →
Design: longitudinal study Participants: 1,895 Evidence: moderate
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
70/100
A one standard deviation increase in AD-PGS was associated with an accelerated time to dementia diagnosis by 4.8 months. 5 key findings →
Design: prospective cohort Participants: 7,039 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The availability of high-quality RNA-sequencing and genotyping data of post-mortem brain collections from consortia such as CommonMind Consortium (CMC) and the Accelerating Medicines Partnership for Alzheimer's Disease (AMP-AD) Consortium enable the generation of a large-scale brain cis-eQTL meta-analysis. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
This study shows that PUTG component scores were significantly associated with diagnostic group and AD biomarkers, a finding that was more pronounced in APOE ε4 carriers. 5 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher educational level (standardized β = 0.23, P Conclusions and relevance Results of this study suggest that women and young patients with AD have relative preservation of brain structure when exposed to neocortical pathological tau. 3 key findings →
Design: cross-sectional Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, the clinical presentation, associated factors, frequency in community-based cohorts, genetic characteristics, and cognitive trajectories associated with the quadruple misfolded proteins phenotype are not well understood. 5 key findings →
Design: cohort study Participants: 375 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
66/100
Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
66/100
Amyotrophic lateral sclerosis (ALS) is a multi-system disease characterized primarily by progressive muscle weakness. 2 key findings →
Design: longitudinal study Participants: 327 Evidence: moderate
Full summary, score breakdown and related studies → Original source
66/100
Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. 3 key findings →
Design: longitudinal study Participants: 1,087 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These protein signals may represent novel targets for the maintenance of cognition in old age. 4 key findings →
Design: longitudinal study Participants: 391 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining human cohort data (over 24,000 people) with mouse models, this study found that carrying the APOE2 gene variant is linked to a longer lifespan, and that this benefit holds even when accounting for Alzheimer's diagnosis and brain pathology. 4 key findings →
Design: cohort Participants: 24,661 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher dietary intakes of flavonols may be associated with reduced risk of developing Alzheimer dementia. 5 key findings →
Design: prospective cohort Participants: 691 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
All synaptic biomarkers tested had a good discriminatory power to distinguish patients with AD abnormal CSF from those with non-AD disorders. 4 key findings →
Design: cross-sectional Participants: 81 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Variants in GBA, encoding the enzyme glucocerebrosidase, are associated with Lewy body diseases such as Parkinson's disease and Lewy body dementia. 5 key findings →
Design: case-control study Participants: 165 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
After correction for multiple testing, PheWAS analyses identified associations with 37 outcomes, representing 18 distinct diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that AD may causally influence sleep patterns. 4 key findings →
Participants: 446,118 Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we test whether AD pathogenesis is associated with dysregulation in brain transmethylation and polyamine pathways. 5 key findings →
Design: cross-sectional Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Insomnia in cognitively unimpaired adults at increased risk for AD is associated to poorer performance in some executive functions and volume changes in cortical and subcortical gray matter, including key areas involved in Alzheimer's disease, as well as decreased white matter diffusivity. 4 key findings →
Design: cross-sectional Participants: 366 Evidence: low
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. Show only studies that are free to read
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% 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 →