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Research

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

Find studies

Showing 476–500 of 1,301 studies in Genetics · tagged Genetics (page 20 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.

Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2000-05-01

The major known genetic risk for Alzheimer's disease (AD), apolipoprotein E-4 (APOE-4), is associated with lowered parietal, temporal, and posterior cingulate cerebral glucose metabolism in patients with a clinical diagnosis of AD. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Resistance to autosomal dominant Alzheimer's disease in an APOE3 Christchurch homozygote: a case report

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature medicine 2019-11-04

We identified a PSEN1 (presenilin 1) mutation carrier from the world's largest autosomal dominant Alzheimer's disease kindred, who did not develop mild cognitive impairment until her seventies, three decades after the expected age of clinical onset. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Herpes simplex virus type 1 in brain and risk of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Lancet (London, England) 1997-01-01

By multiple logistic regression, the APOE-epsilon 4 allele frequency was significantly higher in the patients positive for HSV1 in brain than in the HSV1-negative AD group, the HSV1-positive non-AD group, or the HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%, respectively). 3 key findings →

Participants: 40 Evidence: low

Full summary, score breakdown and related studies → Original source

Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N=112 151) and 24 GWAS consortia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2016-01-26

Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. 4 key findings →

Participants: 112 Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E Alleles and Motor Signs in Older Adults with Alzheimer's Dementia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. International journal of molecular sciences 2025-09-03

We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer's dementia (AD) capitalizing on National Alzheimer's Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed. 3 key findings →

Participants: 389 Evidence: low

Full summary, score breakdown and related studies → Original source

Polygenic score for Alzheimer's disease identifies differential atrophy in hippocampal subfield volumes

✓ Peer-reviewed alzhub usefulness score 52 out of 100. PloS one 2022-07-13

Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer's disease. 3 key findings →

Participants: 1,086 Evidence: low

Full summary, score breakdown and related studies → Original source

Clinical impact of whole-genome sequencing in patients with early-onset dementia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Journal of neurology, neurosurgery, and psychiatry 2022-07-29

Clinical genetic diagnosis was achieved in 7 of 50 (14%) of the patients, with a further 8 patients (16%) found to have established risk factors which may have contributed to their EOD. 5 key findings →

Participants: 50 Evidence: moderate

Full summary, score breakdown and related studies → Original source

A Genome-Wide Association Study of 2304 Extreme Longevity Cases Identifies Novel Longevity Variants

✓ Peer-reviewed alzhub usefulness score 52 out of 100. International journal of molecular sciences 2022-12-21

We performed a genome-wide association study (GWAS) of human extreme longevity (EL), defined as surviving past the 99th survival percentile, by aggregating data from four centenarian studies. 4 key findings →

Participants: 2,304 Evidence: low

Full summary, score breakdown and related studies → Original source

Polygenic risk score of Alzheimer's disease is associated with cognitive trajectories and phenotypes of cerebral organoids

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-09

OptPRS predicted AD dementia and Aβ positivity, independent of apolipoprotein E (APOE). 5 key findings →

Participants: 1,634 Evidence: low

Full summary, score breakdown and related studies → Original source

Genome-wide association and interaction studies of CSF T-tau/Aβ42 ratio in ADNI cohort

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurobiology of aging 2017-05-15

The pathogenic relevance in Alzheimer's disease (AD) presents a decrease of cerebrospinal fluid amyloid-ß42 (Aß42) burden and an increase in cerebrospinal fluid total tau (T-tau) levels. 3 key findings →

Participants: 843 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Genome-Wide association study of quantitative biomarkers identifies a novel locus for alzheimer's disease at 12p12.1

✓ Peer-reviewed alzhub usefulness score 52 out of 100. BMC genomics 2022-01-28

Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →

Participants: 1,576 Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Cold Spring Harbor perspectives in medicine 2012-03-01

Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective. 5 key findings →

Evidence: low

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

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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