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Research

31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 268 studies in Risk genes beyond APOE · free to read · tagged Brain Biology (page 1 of 11) · 31,780 in the whole library · How the 0–100 score works

Download bibliography of these 268 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; 17,251 studies have no institution on record and are not counted here.

What “Risk genes beyond APOE” covers

Risk genes beyond APOE — Genome-wide studies and individual genes other than APOE that shift Alzheimer's risk.

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.

The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice

✓ Peer-reviewed alzhub usefulness score 58 out of 100. The Journal of clinical investigation 2008-06-01

Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. 4 key findings →

Evidence: low

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

A genome-wide association meta-analysis of plasma Aβ peptides concentrations in the elderly

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Molecular psychiatry 2014-02-18

Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). 4 key findings →

Design: meta-analysis Evidence: high

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

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

Amyloidogenic processing of the Alzheimer beta-amyloid precursor protein depends on lipid rafts

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Journal of cell biology 2003-01-06

Formation of senile plaques containing the beta-amyloid peptide (A beta) derived from the amyloid precursor protein (APP) is an invariant feature of Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature medicine 2008-06-01

Alzheimer's disease is the most common dementia and is pathologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques, neuronal injury and low-level, chronic activation of brain immunity. 4 key findings →

Evidence: low

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

R47H Variant of TREM2 Associated With Alzheimer Disease in a Large Late-Onset Family: Clinical, Genetic, and Neuropathological Study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA neurology 2015-08-01

The R47H variant in the triggering receptor expressed on myeloid cells 2 gene (TREM2), a modulator of the immune response of microglia, is a strong genetic risk factor for Alzheimer disease (AD) and possibly other neurodegenerative disorders. 4 key findings →

Participants: 751 Evidence: low

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

The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature medicine 1996-10-01

Missense mutations in the presenilin 1 (PS1) gene cause the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated with increased levels of amyloid beta-peptides (A beta) ending at residue 42 (A beta 42) in plasma and skin fibroblast media of gene carriers. 4 key findings →

Evidence: low

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

Low cerebrospinal fluid concentration of mitochondrial DNA in preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of neurology 2013-09-04

Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). 4 key findings →

Participants: 282 Evidence: moderate

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

Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 1997-10-01

Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees. 3 key findings →

Evidence: low

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

Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2003-12-01

Converging evidence suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD) reflects an imbalance between the production and degradation of this self-aggregating peptide. 3 key findings →

Evidence: low

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

Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-11-01

Mutations in the amyloid precursor protein (APP) gene cause early-onset familial Alzheimer disease (AD) by affecting the formation of the amyloid beta (A beta) peptide, the major constituent of AD plaques. 4 key findings →

Evidence: low

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

Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of biological chemistry 2006-06-02

Nicotinamide adenine dinucleotide (NAD)+-dependent sirtuins have been identified to be key regulators in the lifespan extending effects of calorie restriction (CR) in a number of species. 4 key findings →

Evidence: low

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

Beta-amyloid precursor protein cleavage by a membrane-bound protease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-07-01

The principal component of amyloid plaques in Alzheimer disease is beta-amyloid protein, an approximately 4-kDa peptide derived from amyloid precursor proteins. 3 key findings →

Evidence: low

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

Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2005-09-01

Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by deposition of beta-amyloid (Abeta) peptides as senile plaques in the brain. 4 key findings →

Evidence: low

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

Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2012-12-07

Although amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer disease; soluble oligomeric Aβ has been hypothesized to more directly underlie impaired learning and memory in dementia of the Alzheimer type. 4 key findings →

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
  • Randomized / 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
  • Multicenter 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.

1,052 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events