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Find studies

Showing 1–25 of 103 studies in Risk factors · tagged Genetics (page 1 of 5) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Risk factors” covers

Risk factors — Conditions, exposures and habits linked to a higher or lower chance of dementia, and how strong each link is.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →

Design: meta-analysis Participants: 94,437 Evidence: high

Hearing loss is one of the top contributors to years lived with disability and is a risk factor for dementia. 3 key findings →

Design: meta-analysis Participants: 723,266 Evidence: high

Decades of research have revealed numerous risk factors for mental disorders beyond genetics, but their consistency and magnitude remain uncer-tain. 1 key finding →

Design: meta-analysis Participants: 176 Evidence: high

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified. 3 key findings →

Design: meta-analysis Participants: 985 Evidence: high

Age-related hearing loss is linked to loneliness and poorer cognitive health, but it remains unclear whether loneliness helps explain associations between hearing difficulties and cognitive performance or dementia, and whether these patterns reflect causal pathways or shared underlying liability. 4 key findings →

Design: longitudinal study Participants: 10,375 Evidence: moderate

Evidence on the association between air pollution and dementia is accumulating but still inconclusive, and the potential effect modification by genetics is unclear. 2 key findings →

Design: cohort study Participants: 227,840 Evidence: moderate

The eMERGE (electronic MEdical Records and GEnomics) Network is an NHGRI-supported consortium of five institutions to explore the utility of DNA repositories coupled to Electronic Medical Record (EMR) systems for advancing discovery in genome science. eMERGE also includes a special emphasis on the ethical, legal and social issues related to these endeavors. 2 key findings →

Design: meta-analysis Evidence: high

Evaluating Genomic and Clinical Risk Factors for Alzheimer's Disease in Individuals with Hypertension

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Biomedicines 2025-06-26

Obesity and Area Deprivation Index, a measure of socioeconomic status, were significantly associated with elevated AD risk within the hypertensive cohort. 4 key findings →

Design: retrospective cohort Participants: 1,862 Evidence: moderate

Patterns of brain activation in people at risk for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. The New England journal of medicine 2000-08-01

Both the magnitude and the extent of brain activation during memory-activation tasks in regions affected by Alzheimer's disease, including the left hippocampal, parietal, and prefrontal regions, were greater among the carriers of the APOE epsilon4 allele than among the carriers of the APOE epsilon3 allele. 1 key finding →

Participants: 30 Evidence: low

Our results suggest that the TREM2 p.R47H substitution is a risk factor for frontotemporal dementia and Parkinson's disease in addition to Alzheimer's disease. 4 key findings →

Participants: 609 Evidence: low

During a median of 10.8 years follow-up, sleeping more or fewer than 7 hours was associated with a higher dementia risk (hazard ratio [HR] for 5 vs 7 hours: 1.35, 95% confidence interval [CI] 1.11-1.64; HR for 9 vs 7 hours: 1.59; 95% CI 1.37-1.85) as was daytime napping (HR for often/all of the time vs never/rarely: 1.67; 95% CI 1.37-2.03). 4 key findings →

Design: longitudinal study Evidence: moderate

ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2022-03-16

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →

Evidence: low

The observed relation between high triglycerides, diabetes, and vascular dementia emphasizes the need for detection and treatment of vascular risk factors in older individuals in order to prevent the likelihood of clinical dementia. 3 key findings →

Evidence: moderate

In late middle age, cognitively normal subjects who are homozygous for the epsilon 4 allele for apolipoprotein E have reduced glucose metabolism in the same regions of the brain as in patients with probable Alzheimer's disease. 3 key findings →

Evidence: low

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has been recently reported as a cause of stroke. 5 key findings →

Evidence: low

A prospective analysis of risk factors for Alzheimer's disease was a major objective of the Canadian Study of Health and Aging, a nationwide, population-based study. 3 key findings →

Participants: 194 Evidence: low

Patients with Alzheimer's disease (AD) have elevations of fasting plasma insulin that are hypothesized to be associated with disrupted brain insulin metabolism. 2 key findings →

Participants: 25 Evidence: low

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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 →

Newest studies, as a dated timeline →    Atom feed