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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 401–425 of 1,002 studies in Risk genes beyond APOE marked Peer-reviewed (page 17 of 41) · 29,780 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.

Other subjects

Authors

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

Institutions

From OpenAlex; 15,255 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.

β-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Free radical biology & medicine 2010-10-26

Recent studies indicate that the deposition of β-amyloid peptide (Aβ) is related to the pathogenesis of Alzheimer disease (AD); however, the underlying mechanism is still not clear. 4 key findings →

Evidence: low

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

Reduction of brain beta-amyloid (Abeta) by fluvastatin, a hydroxymethylglutaryl-CoA reductase inhibitor, through increase in degradation of amyloid precursor protein C-terminal fragments (APP-CTFs) and Abeta clearance

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2010-05-14

Epidemiological studies suggest that statins (hydroxymethylglutaryl-CoA reductase inhibitors) could reduce the risk of Alzheimer disease. 4 key findings →

Evidence: low

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

Nicastrin is critical for stability and trafficking but not association of other presenilin/gamma-secretase components

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2005-02-11

gamma-Secretase, which is responsible for the intramembranous cleavage of Alzheimer beta-amyloid precursor protein and the signaling receptor Notch, is a multiprotein complex consisting of at least four components: presenilin (PS); nicastrin (Nct); APH-1 (anterior pharynx-defective-1); and presenilin enhancer-2 (PEN-2). 4 key findings →

Evidence: low

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

The purinergic receptor P2X7 triggers alpha-secretase-dependent processing of the amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2010-11-16

The amyloid precursor protein (APP) is cleaved by β- and γ-secretases to generate the β-amyloid (Aβ) peptides, which are present in large amounts in the amyloid plaques of Alzheimer disease (AD) patient brains. 4 key findings →

Evidence: low

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

The intracellular domain of the low density lipoprotein receptor-related protein modulates transactivation mediated by amyloid precursor protein and Fe65

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2003-07-29

Low density lipoprotein-related protein (LRP) is a transmembrane receptor, localized mainly in hepatocytes, fibroblasts, and neurons. 4 key findings →

Evidence: low

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

Amyloid-beta deposition is associated with decreased hippocampal glucose metabolism and spatial memory impairment in APP/PS1 mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuropathology and experimental neurology 2004-05-01

In Alzheimer disease (AD) patients, early memory dysfunction is associated with glucose hypometabolism and neuronal loss in the hippocampus. 4 key findings →

Evidence: low

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

γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2013-02-08

γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-04-24

Pathogenic generation of amyloid β-peptide (Aβ) by sequential cleavage of β-amyloid precursor protein (APP) by β- and γ-secretases is widely believed to causally underlie Alzheimer disease (AD). β-Secretase initially cleaves APP thereby generating a membrane-bound APP C-terminal fragment, from which γ-secretase subsequently liberates 37-43-amino acid long Aβ species. 4 key findings →

Evidence: low

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

Amyloid precursor protein in platelets of patients with Alzheimer disease: effect of acetylcholinesterase inhibitor treatment

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Archives of neurology 2001-03-01

All patients taking donepezil completed the 30 days of treatment without adverse effects. 3 key findings →

Design: clinical trial Participants: 30 Evidence: low

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

Beta-amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain research 2001-03-01

To elucidate the mechanisms involved in beta-amyloid-mediated inflammation in Alzheimer's disease, transgenic Tg2576 mice containing as transgene the Swedish double mutation of human amyloid precursor protein 695, were examined for the expression pattern of various cytokines using double immunocytochemistry and laser scanning microscopy. 4 key findings →

Evidence: low

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

Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2004-04-01

Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. 3 key findings →

Evidence: low

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

Lysosomal hydrolases of different classes are abnormally distributed in brains of patients with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1991-12-01

beta-Amyloid formation requires multiple abnormal proteolytic cleavages of amyloid precursor protein (APP), including one within its intramembrane domain. 4 key findings →

Evidence: low

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

Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretion

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of biological chemistry 2010-09-28

Epidemiological studies indicate that intake of statins decrease the risk of developing Alzheimer disease. 4 key findings →

Evidence: low

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

Biomarkers of Alzheimer disease in plasma

✓ Peer-reviewed alzhub usefulness score 43 out of 100. NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics 2004-04-01

Plasma and serum biochemical markers proposed for Alzheimer disease (AD) are based on pathophysiologic processes such as amyloid plaque formation [amyloid beta-protein (A beta), A beta autoantibodies, platelet amyloid precursor protein (APP) isoforms], inflammation (cytokines), oxidative stress (vitamin E, isoprostanes), lipid metabolism (apolipoprotein E, 24S-hydroxycholesterol), and vascular disease [homocysteine, lipoprotein (a)]. 2 key findings →

Evidence: low

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

The miR-124 regulates the expression of BACE1/β-secretase correlated with cell death in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Toxicology letters 2011-12-08

The role of miR-124 on the expression of β-site APP cleaving enzyme 1 (BACE1), an important cleavager of amyloid precursor protein that plays a pivotal role in the β-amyloid production, was studied in this paper using cellular models for Alzheimer' disease (AD) of cultured PC12 cell lines and primary cultured hippocampal neurons. 4 key findings →

Evidence: low

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

Cell cycle-dependent regulation of the phosphorylation and metabolism of the Alzheimer amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The EMBO journal 1994-03-01

Accumulation of the amyloid A beta peptide, which is derived from a larger precursor protein (APP), and the formation of plaques, are major events believed to be involved in the etiology of Alzheimer's disease. 4 key findings →

Evidence: low

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

Chemical characterization of A beta 17-42 peptide, a component of diffuse amyloid deposits of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of biological chemistry 1994-04-01

A peptide corresponding to the amino acid sequence of A beta 17-42 (LVFFAEDVGSNKGAIIGLMVGGVVIA) was isolated from Alzheimer Disease patient brains containing large deposits of diffuse-type amyloid. 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. 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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