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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 176–200 of 1,301 studies in Genetics · tagged Genetics (page 8 of 53) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

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

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 13,259 studies have no institution on record and are not counted here.

What “Genetics” covers

Genetics — Inherited risk: APOE and the other risk genes, and what they do and don't tell you.

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.

Guidelines for bioinformatics of single-cell sequencing data analysis in Alzheimer's disease: review, recommendation, implementation and application

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Molecular neurodegeneration 2022-03-02

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

Candidate single-nucleotide polymorphisms from a genomewide association study of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Archives of neurology 2007-11-12

Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE. 2 key findings →

Design: case-control study Participants: 753 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Rapidly progressive Alzheimer's disease features distinct structures of amyloid-β

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain : a journal of neurology 2015-02-15

Genetic and environmental factors that increase the risk of late-onset Alzheimer disease are now well recognized but the cause of variable progression rates and phenotypes of sporadic Alzheimer's disease is largely unknown. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Plasma apolipoprotein E and Alzheimer disease risk: the AIBL study of aging

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2011-03-01

Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level. 5 key findings →

Design: cross-sectional Participants: 1,079 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

APOE-[epsilon]2 allele associated with higher prevalence of sporadic Parkinson disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2004-06-01

Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease. 3 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Odor identification as a biomarker of preclinical AD in older adults at risk

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2017-06-28

These findings from healthy high-risk older individuals suggest that OI reflects degree of preclinical AD pathology, while its relationships with age and cognition result from the association of these latter variables with such pathology. 3 key findings →

Design: cross-sectional Participants: 101 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →

Design: longitudinal study Participants: 1,075 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis

✓ Peer-reviewed alzhub usefulness score 62 out of 100. PLoS medicine 2014-09-16

Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. 3 key findings →

Design: case-control study Participants: 10,578 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Association Between Mentally Stimulating Activities in Late Life and the Outcome of Incident Mild Cognitive Impairment, With an Analysis of the APOE ε4 Genotype

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA neurology 2017-03-01

Cognitively normal elderly individuals who engage in specific mentally stimulating activities even in late life have a decreased risk of incident MCI. 3 key findings →

Design: cohort study Participants: 973 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Clinical predictors of severe cerebral amyloid angiopathy and influence of APOE genotype in persons with pathologically verified Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA neurology 2014-07-01

Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →

Design: longitudinal study Participants: 193 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Hippocampal atrophy as a quantitative trait in a genome-wide association study identifying novel susceptibility genes for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. PloS one 2009-08-07

Using hippocampal atrophy as a quantitative phenotype in a genome-wide scan, we have identified candidate risk genes for sporadic Alzheimer's disease that merit further investigation. 1 key finding →

Design: case-control study Participants: 381 Evidence: moderate

Full summary, score breakdown and related studies → Original source

APOE4 homozygosity represents a distinct genetic form of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature Medicine 2024-05

Analyzing postmortem brain pathology from over 3,200 people plus biomarker data from more than 10,000 more, researchers found that people who inherit two copies of the APOE4 gene variant (about 2-3% of the population) develop Alzheimer's brain changes almost universally and on a predictable timeline starting around age 55, much like known single-gene forms of Alzheimer's. The authors argue this makes APOE4 homozygosity itself a genetic form of Alzheimer's disease rather than just a risk factor. 3 key findings →

Design: cohort Evidence: high

Full summary, score breakdown and related studies → Original source

Genetic risk for Alzheimer disease is distinct from genetic risk for amyloid deposition

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Annals of Neurology 2019

This study asked whether the genes that raise Alzheimer's risk are the same genes that cause amyloid plaques to build up in the brain, and found they are not quite the same thing. 5 key findings →

Design: case-control Participants: 770 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Transferability of European-derived Alzheimer's disease polygenic risk scores across multiancestry populations

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature genetics 2025-06-18

A polygenic score (PGS) for Alzheimer's disease (AD) was derived recently from data on genome-wide significant loci in European ancestry populations. 4 key findings →

Design: cohort Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Head injury and the risk of AD in the MIRAGE study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2000-03-01

Comparison of probands with their unaffected spouses yielded odds ratios for AD of 9.9 (95% CI, 6.5 to 15.1) for head injury with loss of consciousness and 3.1 (2.3 to 4.0) for head injury without loss of consciousness. 3 key findings →

Participants: 2,233 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Longitudinal changes in cognition and behavior in asymptomatic carriers of the APOE e4 allele

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2004-06-01

Memory declined in APOE e4 carriers before the symptomatic presentation of MCI in a cohort whose mean age was 60 years over a median period of 33 months. 1 key finding →

Design: longitudinal study Participants: 212 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

APOE genotype, cholesterol level, lipid-lowering treatment, and dementia: the Three-City Study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2005-05-01

This observational study provides further evidence that lipid-lowering agents are associated with decreased risk of dementia, whereas hyperlipidemia is associated with increased odds for non-Alzheimer-disease-type dementia. 5 key findings →

Participants: 9,294 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Elevated serum pesticide levels and risk for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA neurology 2014-03-01

Levels of DDE were 3.8-fold higher in the serum of those with AD (mean [SEM], 2.64 [0.35] ng/mg cholesterol) when compared with control participants (mean [SEM], 0.69 [0.1] ng/mg cholesterol; P Conclusions and relevance Elevated serum DDE levels are associated with an increased risk for AD and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE. 2 key findings →

Design: case-control study Participants: 20 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Impaired insulin secretion increases the risk of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2008-04-09

In this longitudinal study, impaired acute insulin response at midlife was associated with an increased risk of Alzheimer disease (AD) up to 35 years later suggesting a causal link between insulin metabolism and the pathogenesis of AD. 4 key findings →

Design: longitudinal study Participants: 2,322 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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