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Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 376–400 of 1,528 studies in Genetics marked Peer-reviewed (page 16 of 62) · 28,580 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; 14,058 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.

Whole-genome Sequence Analysis Revealed Novel Subjective Cognitive Decline-associated Genes in 10,763 Chinese

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Genomics, proteomics & bioinformatics 2025-10-28

Subjective cognitive decline (SCD) is widely regarded as a potential preclinical stage of Alzheimer's disease (AD), yet its genetic basis remains poorly understood. 5 key findings →

Participants: 9,284 Evidence: moderate

Full summary, score breakdown and related studies → Original source

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

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

Alpha-2 macroglobulin is genetically associated with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature genetics 1998-08-01

Alpha-2-macroglobulin (alpha-2M; encoded by the gene A2M) is a serum pan-protease inhibitor that has been implicated in Alzheimer disease (AD) based on its ability to mediate the clearance and degradation of A beta, the major component of beta-amyloid deposits. 3 key findings →

Evidence: low

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

Evaluation of CSF-tau and CSF-Abeta42 as diagnostic markers for Alzheimer disease in clinical practice

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Archives of neurology 2001-03-01

Cerebrospinal fluid tau and CSF-Abeta42 have so far been studied in research settings, under conditions providing data on the optimal performance. 1 key finding →

Participants: 105 Evidence: low

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

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

Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2018-02-27

The amyloid β subgroups did not differ for any psychobehavioural, cognitive, actigraphy, and structural and functional neuroimaging results after adjustment for age, sex, and level of education More participants positive for amyloid β deposition had the APOE ε4 allele (33 [38%] vs 29 [13%], p 1-42 concentration in CSF significantly correlated with mean 18 F-florbetapir uptake at baseline (r=-0·62, p 1-42 to amyloid β 1-40 (r=-0·61, p 18 F-florbetapir uptake at baseline (mean standard uptake value ratio 1·46 [SD 0·16] vs 1·02 [SD 0·20]), and more were carriers of the APOE ε4 allele (three [75%] of four vs 33 [39%] of 83). 1 key finding →

Participants: 318 Evidence: low

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

Amyloid precursor protein metabolism and inflammation markers in preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2015-07-15

Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD. 2 key findings →

Design: cross-sectional Evidence: moderate

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

Associations between cerebral small-vessel disease and Alzheimer disease pathology as measured by cerebrospinal fluid biomarkers

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2014-07-01

Microbleed presence was associated with lower CSF Aβ42 in AD and vascular dementia (standardized beta = -0.09, P = .003; standardized beta = -0.30, P = .01), and higher CSF tau in controls (standardized beta = 0.10, P = .03). 4 key findings →

Design: cross-sectional Participants: 914 Evidence: moderate

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

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

APOE genotype, family history of dementia, and Alzheimer disease risk: a 6-year follow-up study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Archives of neurology 2004-12-01

Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE epsilon4 carriers. 5 key findings →

Design: cohort study Participants: 907 Evidence: moderate

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

Longitudinal assessment of cognitive decline and resilience in high-level Alzheimer disease neuropathologic change

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Alzheimer s Research & Therapy 2025-12-03

Individuals with rapid progression were more likely to have at least one APOE ε4 allele (OR: 2.08 [95% CI: 1.16–3.74], p < 0.01), higher Braak stage (2.19 [1.20–3.98], p < 0.01), higher Thal phase (2.45 [1.24–4.83], p < 0.01), more severe white matter rarefaction (1.68 [1.21–2.35], p < 0.01), and in the final 24 months of life, more frequent untreated/undertreated hyperlipidemia (1.74 [1.35–5.56], p < 0.01) and less frequent untreated/undertreated depression (0.40 [0.17–0.91], p < 0.05). 3 key findings →

Design: cohort study Participants: 75 Evidence: moderate

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

Chromosome 9p21 in sporadic amyotrophic lateral sclerosis in the UK and seven other countries: a genome-wide association study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2010-10-01

In this analysis, two single nucleotide polymorphisms in a locus on chromosome 9p21.2 were associated with ALS: rs3849942 (p=2·22×10(-6); odds ratio [OR] 1·39, 95% CI 1·21-1·59) and rs2814707 (p=3·32×10(-6); 1·38, 1·20-1·58). 5 key findings →

Participants: 599 Evidence: moderate

Full summary, score breakdown and related studies → Original source

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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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