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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 426–450 of 1,593 studies · free to read · tagged Genetics (page 18 of 64) · 28,180 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.

Subjects

Authors

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

Institutions

From OpenAlex; 13,658 studies have no institution on record and are not counted here.

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.

Mitochondrial dysfunction gene expression, DNA methylation, and inflammatory cytokines interaction activate Alzheimer's disease: a multi-omics Mendelian randomization study

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Journal of translational medicine 2024-10-03

This study highlighted that the AD-causal MD genes could be regulated by epigenetic changes and interact with inflammatory cytokines, providing evidence for AD prevention and intervention. 3 key findings →

Design: meta-analysis Evidence: high

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

A multiancestry polygenic risk score for Alzheimer's disease is associated with cognitive decline and neuropathological hallmarks in diverse populations

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature genetics 2026-08-27

Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →

Design: cohort Evidence: high

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

Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature Aging 2026-05-15

The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. 1 key finding →

Design: cohort Evidence: moderate

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

Autosomal dominant and sporadic late onset Alzheimer's disease share a common in vivo pathophysiology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2022-10-01

The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →

Participants: 559 Evidence: low

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

Improved discrimination of AD patients using beta-amyloid(1-42) and tau levels in CSF

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 1999-05-01

The combined measure of CSF Abeta42 and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders. 4 key findings →

Participants: 84 Evidence: low

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

Conversion of amyloid positive and negative MCI to AD over 3 years: an 11C-PIB PET study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2009-07-08

PIB-positive subjects with mild cognitive impairment (MCI) are significantly more likely to convert to AD than PIB-negative patients, faster converters having higher PIB retention levels at baseline than slower converters. 4 key findings →

Evidence: low

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

Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2015-01-07

The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). 2 key findings →

Participants: 201 Evidence: low

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

Dementia revealed: novel chromosome 6 locus for late-onset Alzheimer disease provides genetic evidence for folate-pathway abnormalities

✓ Peer-reviewed alzhub usefulness score 56 out of 100. PLoS genetics 2010-09-23

Genome-wide association studies (GWAS) of late-onset Alzheimer disease (LOAD) have consistently observed strong evidence of association with polymorphisms in APOE. 5 key findings →

Design: case-control study Evidence: moderate

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

Trajectory of the MAPT-PACC-Preclinical Alzheimer Cognitive Composite in the Placebo Group of a Randomized Control Trial: Results from the MAPT Study: Lessons for Further Trials

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The journal of prevention of Alzheimer's disease 2018-01-01

Defining the primary cognitive endpoint is a major decision for Alzheimer's disease preventive trials. 1 key finding →

Design: randomized controlled trial Evidence: high

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

An update on genetic frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Journal of neurology 2019-05-22

Grey matter changes on MRI and hypometabolism on FDG-PET are seen at least 10 years before symptom onset with white matter abnormalities seen earlier, but the pattern and exact timing of changes differ between different genetic groups. 5 key findings →

Evidence: low

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

Multimorbidity burden and dementia risk in older adults: The role of inflammation and genetics

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-01-06

Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. 3 key findings →

Participants: 2,478 Evidence: low

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

Choroid Plexus Volume and Permeability at Brain MRI within the Alzheimer Disease Clinical Spectrum

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Radiology 2022-05-17

Among patients with cognitive symptoms, larger choroid plexus volume was associated with severity of cognitive impairment in the Alzheimer disease spectrum. 5 key findings →

Participants: 532 Evidence: low

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

Pathological combinations in neurodegenerative disease are heterogeneous and disease-associated

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2023-06-01

The presence of multiple additive pathologies associated with older age, increasing disease duration, APOE e4 allele and presence of dementia across the clinical groups. 2 key findings →

Evidence: low

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

Controversies and priorities in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2013-03-01

Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were linked to mutations in the superoxide dismutase-1 (SOD1) gene, a substantial proportion of the remainder of cases of familial ALS have now been traced to an expansion of the intronic hexanucleotide repeat sequence in C9orf72. 1 key finding →

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.

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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 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