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Research

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

Find studies

Showing 1,401–1,425 of 1,593 studies · free to read · tagged Genetics (page 57 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.

HHV-6A infection induces amyloid-beta expression and activation of microglial cells

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer's research & therapy 2019-12-12

The control of viral infections in the brain involves the activation of microglial cells, the macrophages of the brain that are constantly surveying the central nervous system, and the production of amyloid-beta (Aβ) as an anti-microbial molecule. 4 key findings →

Evidence: low

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

Both Targeted Mass Spectrometry and Flow Sorting Analysis Methods Detected the Decreased Serum Apolipoprotein E Level in Alzheimer's Disease Patients

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular & Cellular Proteomics 2013-12-08

Apolipoprotein E (ApoE) polymorphism has been appreciated as a valuable predictor of Alzheimer disease (AD), and the associated ε4 allele has been recognized as an indicator of susceptibility to this disease. 4 key findings →

Evidence: moderate

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

O4–04–05: Geographical variation in dementia prevalence in Swedish twins: Using Bayesian inference to separate genetic and environmental effects

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2013-07-01

There is evidence of geographical variation in dementia[1], not all of which can be ascribed to genetic factors[2]. 1 key finding →

Participants: 568 Evidence: low

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

Does Neighborhood Disadvantage Moderate the Relationship between Apolipoprotein E Status and Cognitive Functioning?

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

Environmental factors like neighborhood disadvantage are also associated with cognitive decline, however, few studies have integrated this with APOE research. 5 key findings →

Participants: 190 Evidence: low

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

APOE ε4 linked effects on clinical features and neuropathology in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-10-01

In analyses of APOE ε4 carriers, dosage, and genetic risk score, APOE ε4 was associated with lower odds of fluctuating cognition and parkinsonism and higher odds of visual hallucinations. 5 key findings →

Evidence: low

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

Peruvian Population Empowers Discovery of a TREM2 Missense Variant in Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

Peruvian GWAS identified Amerindian ancestry specific exonic AD susceptibility variant p.H157Y. This variant has been previously reported as AD marker in Han Chinese populations with extreme effect size, but its rarity and contradictory findings in other groups suggest a potential ancestry‐specific effect. 4 key findings →

Participants: 567 Evidence: low

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

Predicting Alzheimer progression using EEG-based digital twins

✓ Peer-reviewed alzhub usefulness score 39 out of 100. npj Digital Medicine 2026-08-03

Early and accurate prognosis of Alzheimer’s disease (AD) remains limited by current biomarkers, which are often invasive, require expensive equipment, or fail to predict individual trajectories of cognitive decline. 2 key findings →

Participants: 459 Evidence: moderate

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

Frontotemporal dementia as a consequence of GRN mutations: From disease cause to models to therapies

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Pharmacological Research 2025-09-17

Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →

Evidence: low

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

Ethics of disclosure of onset‐predictive biomarker test results for genetic frontotemporal dementia in the research context

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring 2025-04-01

Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →

Evidence: low

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

Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production

✓ Peer-reviewed alzhub usefulness score 39 out of 100. eLife 2025-02-11

Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →

Evidence: low

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

Ethanol induces neuroimmune dysregulation and soluble TREM2 generation in a human iPSC neuron, astrocyte, microglia triculture model

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alcohol 2025-11-07

Alcohol use disorders (AUDs) affect substantial populations worldwide and increase the risk of developing cognitive impairments and alcohol-associated dementia. 2 key findings →

Evidence: low

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

Frontotemporal dementia patient-derived iPSC neurons show cell pathological hallmarks and evidence for synaptic dysfunction and DNA damage

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular Psychiatry 2025-09-26

Frontotemporal dementia (FTD) is the second most common cause of dementia in patients under 65 years, characterized by diverse clinical symptoms, neuropathologies, and genetic background. 5 key findings →

Evidence: low

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

Inflammation, cytokines, immune response, apolipoprotein E, cholesterol, and oxidative stress in Alzheimer disease: therapeutic implications

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Rejuvenation research 2010-04-01

Alzheimer disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for senile dementia. 5 key findings →

Evidence: low

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

A combination of long- and short-read genomics reveals frequent p-arm breakpoints within chromosome 21 complex genomic rearrangements

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Genetics in medicine open 2024-06-28

Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes. 3 key findings →

Evidence: low

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

Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Alzheimer's disease reports 2017-09-28

Diverse pathogens are detected in Alzheimer's disease (AD) brains. 4 key findings →

Evidence: low

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

The Association Between Polygenic Risk for Alzheimer's, Objective Sleep Architecture, and Plasma Neurofilament Light Chain in Midlife

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Health Wellness and Community Research 2026-01-15

PRS correlated positively with log-NFL (r = 0.31, p = 0.004) and inversely with N3 duration (r = −0.26, p = 0.017). 5 key findings →

Design: cross-sectional Participants: 84 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