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Find studies

Showing 26–50 of 125 studies in Genetics of type systematic review or meta-analysis (page 2 of 5) · 29,780 in the whole library · How the 0–100 score works

Download bibliography of these 125 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.

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.

These results provide new insight into the genetic basis of habitual PA, and the genetic links connecting PA with other traits and diseases. 5 key findings →

Design: meta-analysis Participants: 8,556 Evidence: high

Genome-wide association study of idiopathic hypersomnia in a Japanese population

✓ Peer-reviewed alzhub usefulness score 79 out of 100. Sleep and biological rhythms 2021-10-12

Narcolepsy type 1 is strongly associated with human leukocyte antigen (HLA)-DQB1*06:02; however, no significant associations between IH and HLA alleles have been reported. 4 key findings →

Design: meta-analysis Participants: 414 Evidence: high

The aims of this study were to identify candidate single nucleotide polymorphisms (SNPs) and mechanisms of Alzheimer's disease (AD) and to generate SNP to gene to pathway hypotheses. 5 key findings →

Design: meta-analysis Participants: 370,542 Evidence: high

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

UK Biobank: opportunities for cardiovascular research

✓ Peer-reviewed alzhub usefulness score 79 out of 100. European Heart Journal 2017-04-24

The need for large sample sizes has led to collaborative efforts, such as the Prospective Studies Collaboration (an individual participant meta-analysis of data from 61 studies and more than a million participants11) that has demonstrated conclusively that a continuous increase in blood pressure corresponds with an increased risk of vascular death across all age groups (see Figure 1 that illustrates the importance of a large sample size (about 500 000 participants) for detecting this association).12 Sample size is also of particular importance in the current era of genome-wide association studies, where many investigations are aiming to detect either small effects from common variants or large effects from rare variants.13 Absolute risk of ischaemic heart disease mortality by usual systolic blood pressure and age at risk in 5000, 50 000, and 500 000 participants. 5 key findings →

Design: meta-analysis Participants: 5,200 Evidence: high

GWAS for executive function and processing speed suggests involvement of the CADM2 gene

✓ Peer-reviewed alzhub usefulness score 79 out of 100. Molecular psychiatry 2015-04-14

To identify common variants contributing to normal variation in two specific domains of cognitive functioning, we conducted a genome-wide association study (GWAS) of executive functioning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium. 3 key findings →

Design: meta-analysis Participants: 32,070 Evidence: high

Recent genome-wide association studies have identified 5 loci (BIN1, CLU, CR1, EXOC3L2, and PICALM) as genetic determinants of Alzheimer's disease (AD). 2 key findings →

Design: meta-analysis Participants: 2,816 Evidence: high

Our results underscore the importance of international efforts combining GWAS datasets to isolate genetic loci for complex diseases. 4 key findings →

Design: meta-analysis Participants: 10,181 Evidence: high

Genome-wide significance in fully adjusted models (sex, age, APOE genotype, population stratification) was observed for a SNP in ABCA7 (rs115550680, allele = G; frequency, 0.09 cases and 0.06 controls; odds ratio [OR], 1.79 [95% CI, 1.47-2.12]; P = 2.2 × 10(-9)), which is in linkage disequilibrium with SNPs previously associated with Alzheimer disease in Europeans (0.8 Conclusions and relevance In this meta-analysis of data from African American participants, Alzheimer disease was significantly associated with variants in ABCA7 and with other genes that have been associated with Alzheimer disease in individuals of European ancestry. 4 key findings →

Design: meta-analysis Participants: 5,896 Evidence: high

In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified. 4 key findings →

Design: meta-analysis Participants: 2,784 Evidence: high

The effect of genome-wide significant variants at the GFRA2 locus on expression of GFRA2 was assessed using mRNA expression studies in cerebellar tissue samples from the Mayo Clinic brain bank. 4 key findings →

Design: meta-analysis Participants: 382 Evidence: high

New insights into the genetic etiology of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 77 out of 100. Nature Genetics 2022-04

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

Genome-wide association analysis of age-at-onset in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 77 out of 100. Molecular psychiatry 2011-10-18

The risk of Alzheimer's disease (AD) is strongly determined by genetic factors and recent genome-wide association studies (GWAS) have identified several genes for the disease risk. 4 key findings →

Design: meta-analysis Participants: 2,222 Evidence: high

Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database

✓ Peer-reviewed alzhub usefulness score 76 out of 100. Nature genetics 2007-01-01

The past decade has witnessed hundreds of reports declaring or refuting genetic association with putative Alzheimer disease susceptibility genes. 1 key finding →

Design: meta-analysis Evidence: high

Polygenic risk scores (PRSs) have been used to combine the effects of variants with small effects identified by genome-wide association studies. 4 key findings →

Design: meta-analysis Participants: 1,200 Evidence: high

Whole-exome sequencing of individuals with mild cognitive impairment, combined with genotype imputation, was used to identify coding variants other than the apolipoprotein E (APOE) ε4 allele associated with rate of hippocampal volume loss using an extreme trait design. 4 key findings →

Design: meta-analysis Participants: 315 Evidence: high

HPA axis genes implicated in glucocorticoid regulation play an important role in regulating the physiological impact of social and environmental stress, and have become a focal point for investigating the role of glucocorticoid regulation in the etiology of disease. 1 key finding →

Design: systematic review Participants: 32 Evidence: high

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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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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