Alzheimer's disease (AD) is the most common multifactorial neurodegenerative disease among elderly people. 2 key findings →
Design: meta-analysis Participants: 140 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Identifying ancestry-specific molecular profiles of late-onset Alzheimer's Disease (LOAD) in brain tissue is crucial to understand novel mechanisms and develop effective interventions in non-European, high-risk populations. 3 key findings →
Design: meta-analysis Participants: 731 Evidence: high
Full summary, score breakdown and related studies → Original source
This was, at the time, the largest genetic study of Alzheimer's disease ever done, comparing DNA from over 111,000 people with the disease (or a strong family history) to nearly 680,000 people without it. 4 key findings →
Design: meta-analysis Participants: 788,989 Evidence: high
Full summary, score breakdown and related studies → Original source
Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
72/100
Apolipoprotein E (ApoE) ε4 genotype was the main risk factor for both ARIA types; ARIA-E incidence was further associated with treatment dose, affecting the 55% of ApoE ε4 carriers in the high-dose aducanumab treatment group. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Over 10 years of close clinical dementia surveillance in this cohort study, loneliness was associated with increased dementia risk; this tripled in adults whose baseline risk would otherwise be relatively low on the basis of age and genetic risk, representing a majority of the US population. 5 key findings →
Design: cohort study Participants: 2,308 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The findings of the current study show that the longitudinal, cumulative trajectory of cardiovascular risk is predictive of dementia risk and associated with the emergence of memory decline. 4 key findings →
Design: prospective cohort Participants: 1,244 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Oligodendrocyte dysfunction has been implicated in the pathogenesis of neurodegenerative diseases, so understanding oligodendrocyte activation states would shed light on disease processes. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Our study indicates that changes in PVS-related MRI parameters occur in MCI and AD, possibly due to impairment of the glymphatic system. 3 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Improved insight into these pathomechanisms may allow to shed light on the role of Aβ deposition as a primary versus a secondary event in the complex pathogenesis of AD. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
To evaluate reverse causation, we assessed whether a polygenic risk score for AD is associated with HGS. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (ApoE) is a multifaceted secreted molecule synthesized in the CNS by astrocytes and microglia, and in the periphery largely by the liver. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
61/100
The established association of APOE*4 carriers with AD was confirmed in this community-based sample of older subjects (odds ratio (OR) = 2.22; p = 9.36E-14) and was stronger in females (OR = 2.72; p = 1.74E-10) than in males (OR = 1.88; p = 2.43E-05). 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus. 5 key findings →
Design: case-control Participants: 10,271 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sleep duration, psychiatric disorders and dementias are closely interconnected in older adults. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain arteriolosclerosis (B-ASC) is characterized by pathologically altered brain parenchymal arterioles. 3 key findings →
Participants: 3,382 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 1,261 participants from a Chinese community cohort were included and we identified 1 gene, PTPRT, for HV, with the top significant SNPs by whole genome-wide association study (GWAS). rs6030076 (p = 5.48 × 10-8, β = -0.092, SE 0.017) from WES and rs6030088 (p = 8.24 × 10-9, β = -105.22, SE 18.09) from SNP array data were both located in this gene. 5 key findings →
Participants: 1,261 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We retrospectively assessed the diagnostic accuracy of whole genome sequencing to detect the most common repeat expansion loci associated with neurological outcomes (AR, ATN1, ATXN1, ATXN2, ATXN3, ATXN7, C9orf72, CACNA1A, DMPK, FMR1, FXN, HTT, and TBP) using samples obtained within the National Health Service in England from patients who were suspected of having neurological disorders; previous PCR test results were used as the reference standard. 4 key findings →
Participants: 3,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia and a growing public health burden in the United States. 5 key findings →
Participants: 1,515 Evidence: low
Full summary, score breakdown and related studies → Original source
Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD). 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We propose a novel method to identify disease-related genetic variants enriched by imaging endophenotypes, which are the imaging traits associated with both genetic factors and disease status. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cortical neuron loss is a pathological hallmark of late-onset Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 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.
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 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 →