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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 376–400 of 847 studies in Risk genes beyond APOE (page 16 of 34) · 27,380 in the whole library · How the 0–100 score works

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; 12,859 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.

Ibuprofen effects on Alzheimer pathology and open field activity in APPsw transgenic mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of aging 2001-11-01

We previously showed the non-steroidal anti-inflammatory drug (NSAID) ibuprofen suppresses inflammation and amyloid in the APPsw (Tg2576) Tg2576 transgenic mouse. 4 key findings →

Design: post-hoc analysis Evidence: low

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

Inhibitors of cathepsin B improve memory and reduce beta-amyloid in transgenic Alzheimer disease mice expressing the wild-type, but not the Swedish mutant, beta-secretase site of the amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2008-01-09

Elucidation of Abeta-lowering agents that inhibit processing of the wild-type (WT) beta-secretase amyloid precursor protein (APP) site, present in most Alzheimer disease (AD) patients, is a logical approach for improving memory deficit in AD. 4 key findings →

Evidence: low

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

MicroRNA-339-5p down-regulates protein expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) in human primary brain cultures and is reduced in brain tissue specimens of Alzheimer disease subjects

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2013-12-18

Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ) peptide as neuritic plaques in the brain. 4 key findings →

Evidence: low

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

SorLA/LR11 regulates processing of amyloid precursor protein via interaction with adaptors GGA and PACS-1

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2007-09-12

SorLA has been recognized as a novel sorting receptor that regulates trafficking and processing of the amyloid precursor protein (APP) and that represents a significant risk factor for sporadic Alzheimer disease. 4 key findings →

Evidence: low

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

Identification of the Alzheimer beta/A4 amyloid precursor protein in clathrin-coated vesicles purified from PC12 cells

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 1993-01-01

The Alzheimer beta/A4 amyloid precursor protein (APP) can be proteolytically processed by at least two separate pathways in PC12 cells: chloroquine-insensitive secretory cleavage and chloroquine-sensitive intracellular degradation, presumably in the endosomal/lysosomal system. 4 key findings →

Evidence: low

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

The TspanC8 subgroup of tetraspanins interacts with A disintegrin and metalloprotease 10 (ADAM10) and regulates its maturation and cell surface expression

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-10-03

A disintegrin and metalloprotease 10 (ADAM10) is a ubiquitous transmembrane metalloprotease that cleaves the extracellular regions from over 40 different transmembrane target proteins, including Notch and amyloid precursor protein. 4 key findings →

Evidence: low

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

MAPK-activated protein kinase 2 deficiency in microglia inhibits pro-inflammatory mediator release and resultant neurotoxicity. Relevance to neuroinflammation in a transgenic mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2006-06-14

MAPK-activated protein kinase 2 (MAPKAP K2 or MK2) is one of several kinases directly regulated by p38 MAPK. 4 key findings →

Evidence: low

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

The amyloid precursor protein and its regulatory protein, FE65, in growth cones and synapses in vitro and in vivo

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2003-07-01

Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. 4 key findings →

Evidence: low

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

Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The American journal of pathology 2012-09-28

Lack of tau expression has been reported to protect against excitotoxicity and to prevent memory deficits in mice expressing mutant amyloid precursor protein (APP) identified in familial Alzheimer disease. 4 key findings →

Evidence: low

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

Scavenger receptor class B type I (SR-BI) regulates perivascular macrophages and modifies amyloid pathology in an Alzheimer mouse model

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2010-11-12

Scavenger receptor class B type I (SR-BI) is a high-density lipoprotein receptor that regulates cholesterol efflux from the peripheral tissues to the liver. 4 key findings →

Evidence: low

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

Conformation and fibrillogenesis of Alzheimer A beta peptides with selected substitution of charged residues

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of molecular biology 1994-11-01

A key pathological feature of Alzheimer's disease (AD) is the formation and accumulation of amyloid fibers within the neurophil as senile plaques and in the walls of cerebral and meningeal blood vessels. 4 key findings →

Evidence: low

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

Presenilin mutations in familial Alzheimer disease and transgenic mouse models accelerate neuronal lysosomal pathology

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuropathology and experimental neurology 2004-08-01

The neuronal lysosomal system is a major degradative pathway, induced by cell stress and closely linked to Alzheimer disease (AD) and other neurodegenerative diseases. 4 key findings →

Evidence: low

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

Amyloidogenic processing but not amyloid precursor protein (APP) intracellular C-terminal domain production requires a precisely oriented APP dimer assembled by transmembrane GXXXG motifs

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2008-01-16

The beta-amyloid peptide (Abeta) is the major constituent of the amyloid core of senile plaques found in the brain of patients with Alzheimer disease. 4 key findings →

Evidence: low

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

Multi-faced neuroprotective effects of Ginsenoside Rg1 in an Alzheimer mouse model

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Biochimica et biophysica acta 2011-10-12

There has been no extensive characterization of the effects of Ginsenoside Rg1, a pharmacological active component purified from the nature product ginseng, in an Alzheimer's disease mouse model. 4 key findings →

Evidence: low

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

Statins cause intracellular accumulation of amyloid precursor protein, beta-secretase-cleaved fragments, and amyloid beta-peptide via an isoprenoid-dependent mechanism

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2005-02-17

The use of statins, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors that block the synthesis of mevalonate (and downstream products such as cholesterol and nonsterol isoprenoids), as a therapy for Alzheimer disease is currently the subject of intense debate. 4 key findings →

Evidence: low

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

Intracellular and secreted Alzheimer beta-amyloid species are generated by distinct mechanisms in cultured hippocampal neurons

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01

Cerebral plaques containing beta-amyloid (beta A4) represent an invariant pathological feature of Alzheimer disease (AD). beta A4 is proteolytically generated from its parent molecule, amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

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

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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