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Find studies

Showing 1,551–1,575 of 1,616 studies in Genetics (page 63 of 65) · 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.

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.

Pathway-specific polygenic risk scores reveal underlying mechanisms of cerebral small vessel disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-14

White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia. 5 key findings →

Participants: 46,944 Evidence: moderate

Genetically Predicted Blood DNA Methylation Reveals Putative Regulatory Signals Associated with ALS Risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-20

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder whose genetic architecture and underlying molecular mechanisms remain incompletely understood, particularly in sporadic disease. 5 key findings →

Evidence: low

Associations of menopause hormone therapy with late-life cognition and brain health vary by formulation and APOEε4 presence

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-20

Implications of menopause hormone therapy (MHT) for cognitive aging remain unclear despite decades of research. 3 key findings →

Participants: 8,741 Evidence: low

INTRODUCTIONMultimodal lifestyle interventions can delay or slow Alzheimers disease (AD) in at-risk older adults, and plasma pTau217, a blood-based biomarker, now enables scalable AD risk stratification. 3 key findings →

Evidence: moderate

Genetic Associations with Alzheimer's, Lewy Body and Vascular Neuropathology Reveal Shared and Distinct Biological Pathways

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-22

INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia. 5 key findings →

Evidence: moderate

Integrated genomic meta-analysis identifies cell-type-specific signatures and targets in early Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-23

Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data. 5 key findings →

Design: systematic review Evidence: high

The lipids and proteins that comprise lipid droplets regulate several cellular functions including lipid storage, stress responses, and inflammation. 1 key finding →

Evidence: low

To better characterize the genetic architecture underlying Alzheimer's disease (AD) and related dementia (ADRD), we performed a meta-analysis of European ancestry genome-wide association studies in 128,681 cases or proxy cases of ADRD and 849,833 (proxy) controls. 3 key findings →

Design: meta-analysis Evidence: high

Genetic drivers of progression in Alzheimer's disease are distinct from disease risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-11-19

Established AD risk factors, including APOE ε4 dosage and polygenic risk scores, were not associated with disease progression amyloid positive individuals who are actively declining. 5 key findings →

Design: meta-analysis Participants: 222 Evidence: high

Pervasive biases in proxy GWAS based on parental history of Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2023-10-17

Almost every recent Alzheimer's disease (AD) genome-wide association study (GWAS) has performed meta-analysis to combine studies with clinical diagnosis of AD with studies that use proxy phenotypes based on parental disease history. 2 key findings →

Design: meta-analysis Evidence: high

Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research square 2024-12-24

The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults. 4 key findings →

Evidence: low

Human brain single nucleus cell type enrichments in neurodegenerative diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2023-07-01

Single cell RNA sequencing has opened a window into clarifying the complex underpinnings of disease, particularly in quantifying the relevance of tissue- and cell-type-specific gene expression. 1 key finding →

Evidence: low

Single-nucleus multiome analysis of human cerebellum in Alzheimer's disease-related dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research square 2024-08-16

Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. 2 key findings →

Evidence: low

Spatial Multi-Omics Workflow and Analytical Guidelines for Alzheimer's Neuropathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-11-17

Spatial biology technologies enable high-dimensional profiling within intact tissues, revealing how molecular and cellular organization drives function and disease. 5 key findings →

Evidence: low

Phenotype Scoring of Population Scale Single-Cell Data Dissects Alzheimer's Disease Complexity

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2024-11-02

The complexity of Alzheimer's disease (AD) manifests in diverse clinical phenotypes, including cognitive impairment and neuropsychiatric symptoms (NPSs). 5 key findings →

Evidence: low

Single-nucleus transcriptomic studies have revealed glial cell states associated with Alzheimer's disease; however, these nuclei are dissociated from the complex architecture of the human neocortex. 2 key findings →

Evidence: low

Brain Region-Specific Epigenomic Reorganization and Altered Cell States in Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-09-30

Alzheimer's disease (AD) is the most common neurodegenerative disorder, yet the molecular mechanisms underlying its region- and cell-type-specific pathogenesis remain poorly defined. 5 key findings →

Evidence: low

The full cohort included 1044 participants, of whom 779 comprised the proteomics cohort. 5 key findings →

Design: longitudinal study Participants: 674 Evidence: moderate

Genetic susceptibility to Lewy body disease and the distribution of Lewy pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-24

Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →

Design: meta-analysis Participants: 1,362 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 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