Our results suggest that RAB10 could be a promising therapeutic target for AD prevention. 5 key findings →
Evidence: low
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.
This study provides empirical support for the suggestion that the APOE locus is the major susceptibility gene for late-onset AD in the human genome, with an OR significantly greater than any other locus in the human genome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genes play a strong role in Alzheimer's disease (AD), with late-onset AD showing heritability of 58-79% and early-onset AD showing over 90%. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Neuronal intranuclear inclusion disease (NIID) is a slowly progressing neurodegenerative disease characterized by eosinophilic intranuclear inclusions in the nervous system and multiple visceral organs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Linkage analysis was used to search the genome for chromosomal regions harboring familial Alzheimer's disease genes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Currently studies on the correlation between obesity and Alzheimer's disease (AD) are still unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) is a leading cause of ischaemic and haemorrhagic stroke and a major contributor to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The genetic locus containing the WWOX and MAF genes was implicated as a clinical Alzheimer's disease (AD) risk locus in two recent large meta-analytic genome wide association studies (GWAS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Eleven loci with GWAS hits for one disorder were also associated with one or both of the other disorders: one with all three disorders (the MAPT/KANSL1 locus), five with ADRD and PD (near LCORL, CLU, SETD1A/KAT8, WWOX, and GRN), three with ADRD and ALS (near GPX3, HS3ST5/HDAC2/MARCKS, and TSPOAP1), and two with PD and ALS (near GAK/TMEM175 and NEK1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Polygenic risk scores (PRS) are instrumental in genetics, offering insights into an individual level genetic risk to a range of diseases based on accumulated genetic variations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The high prevalence of Alzheimer's disease (AD) among the elderly population and its lack of effective treatments make this disease a critical threat to human health. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
ADVP V1.0 (February 2021) catalogs 6,990 associations related to disease-risk, expression quantitative traits, endophenotypes, or neuropathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In just over a decade, advances in genome-wide association studies (GWAS) have offered an approach to stratify individuals based on genetic risk for disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monogenic causes of complex diseases were more prevalent among individuals with a parental disease history than in the rest of the population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research into the genetic underpinnings of neuropsychiatric illness has occurred at many levels. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The success of genome-wide association studies (GWAS) completed in the last 15 years has reinforced a key fact: polygenic architecture makes a substantial contribution to variation of susceptibility to complex disease, including Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A multi-stage variable selection method is introduced for detecting association signals in structured brain-wide and genome-wide association studies (brain-GWAS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both social and genetic factors contribute to cognitive impairment and decline, yet genetic factors identified through genome-wide association studies (GWAS) explain only a small portion of trait variability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Genome-wide association studies (GWAS) have traditionally been undertaken in homogeneous populations from the same ancestry group. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is the most common type of dementia and is currently estimated to affect 6.2 million Americans. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with a complex genetic etiology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The treatment of complex and multifactorial diseases constitutes a big challenge in day-to-day clinical practice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is on the rise worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anorexia nervosa (AN) is a devastating disorder with evidence of underexplored heritability. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Late-onset Alzheimer's disease (LOAD), the most common cause of dementia, and a huge global health challenge, is a neurodegenerative disease of uncertain aetiology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 346 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Interpretation of risk loci from genome-wide association studies of Alzheimer's disease
- Evaluating pathogenicity of variants of unknown significance in APP, PSEN1, and PSEN2
- Common polygenic variation enhances risk prediction for Alzheimer's disease
- Metabolomic and lipidomic signatures in autosomal dominant and late-onset Alzheimer's disease brains
- Identification of common variants influencing risk of the tauopathy progressive supranuclear palsy
- Genome-wide association study of occupational attainment as a proxy for cognitive reserve
- Linkage disequilibrium fine mapping and haplotype association analysis of the tau gene in progressive supranuclear palsy and corticobasal degeneration
- Systematic validation of variants of unknown significance in APP, PSEN1 and PSEN2
- Machine learning suggests polygenic risk for cognitive dysfunction in amyotrophic lateral sclerosis
- FGWAS: Functional genome wide association analysis
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 →