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Research

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

Find studies

Showing 701–725 of 847 studies in Risk genes beyond APOE (page 29 of 34) · 27,380 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; 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.

Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-amyloid plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology

✓ Peer-reviewed alzhub usefulness score 37 out of 100. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 2004-11-01

The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. 4 key findings →

Evidence: low

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

The aging brain. Changes in the neuronal insulin/insulin receptor signal transduction cascade trigger late-onset sporadic Alzheimer disease (SAD). A mini-review

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neural transmission (Vienna, Austria : 1996) 2002-07-01

Aging of the brain has been demonstrated to be the main risk factor for late-onset sporadic AD what is in contrast to early-onset familial AD in which mutations predominate the pathology. 4 key findings →

Evidence: low

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

Upregulation of BACE1 and beta-amyloid protein mediated by chronic cerebral hypoperfusion contributes to cognitive impairment and pathogenesis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neurochemical research 2009-01-04

Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain. 4 key findings →

Evidence: low

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

Effect of epigallocatechin-3-gallate (EGCG) on cognitive functioning and the expression of APP and BDNF in the hippocampus of rats with streptozotocin -induced Alzheimer-like disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Biochemistry and Biophysics Reports 2025-01-31

We aimed to investigate the potential therapeutic effects of the active substance of green tea, epigallocatechin-3-gallate (EGCG), on behavioral phenotypes and markers of neurogenesis in an Alzheimer disease (AD) rat model. 4 key findings →

Evidence: low

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

HIF‐1 Targeting Intervention Renders Protection From Alzheimer's‐Like Pathology in a Humanized Mice Model of HIV Infection

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of Extracellular Vesicles 2025-11-01

HIV-associated neurocognitive disorders (HAND) affect 30%-50% of individuals living with HIV on combination antiretroviral therapy, with Alzheimer 's-like pathology as a potent comorbidity of HAND. 2 key findings →

Evidence: low

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

Cerebral FURIN deficiency impairs astrocytic lipophagy through ITGAV maturation

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Autophagy 2025-12-11

: ACTB: actin, beta; AD: Alzheimer disease; ADAM10: a disintegrin and metallopeptidase domain 10; ADGGA: acyl diacylglyceryl glucuronide; AHexSIS: acylhexosyl sitosterol; AHexSTS: acylhexosyl stigmasterol; AIF1/IBA1: allograft inflammatory factor 1; APP: amyloid beta precursor protein; ATG5: autophagy related 5; Aβ: amyloid β-protein; BACE1: beta-site APP cleaving enzyme 1; BASulfate: bile acid sulfate; BMP: bismonoacylglycerophosphate; CAR: acylcarnitine; CE: cholesteryl ester; Cer_NS: ceramide non-hydroxyfatty acid-sphingosine; CL: cardiolipin; CMA: chaperone-mediated autophagy; DAPI: 4',6-diamidino-2-phenylindole; DCAE: esterified deoxycholic acid; DEP: differentially expressed protein; DG: diacylglycerol; DGCC: diacylglyceryl-3-O-carboxyhydroxymethylcholine; DLG4/PSD95: discs large MAGUK scaffold protein 4; ECM: extracellular matrix; EtherLPC: ether-linked lysophosphatidylcholine; EtherLPE: ether-linked lysophosphatidylethanolamine; EtherMGDG: ether-linked monogalactosyldiacylglycerol; EtherOxPC: ether-linked oxidized phosphatidylcholine; EtherPC: ether-linked phosphatidylcholine; EtherPE: ether-linked phosphatidylethanolamine; EtherPG: ether-linked phosphatidylglycerol; EtherSMGDG: semino lipid; EtherTG: ether-linked triacylglycerol; FA: fatty acyls; FA: free fatty acid; FAHFA: fatty acid ester of hydroxyl fatty acid; FJC: fluoro-Jade C; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GDCAE: esterified glycodeoxycholic acid; GFAP: glial fibrillary acidic protein; GL: glycerolipids; GP: glycerophospholipids; HBMP: hemibismonoacylglycerophosphate; HexCer_NS: hexosylceramide non-hydroxyfatty acid-sphingosine; HSPA8/HSC70: heat shock protein 8; IP-MS: immunoprecipitation-mass spectrometry; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDGCC: lysodiacylglyceryl-3-O-carboxyhydroxymethylcholine; LDs: lipid droplets; LNAPE: N-acyl-lysophosphatidylethanolamine; LNAPS: N-acyl-lysophosphatidylserine; LPA: lysophosphatidic acid; LPC: lyso-phophatidylcholine; LPE: lysophosphatidylethanolamine; LPG: lysophosphatidylglycerol; LPI: lysophosphatidylinositol; LPS: lysophosphatidylserine; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MGDG: monogalactosyldiacylglycerol; MWM: Morris Water Maze; OA: oleic acid; OFT: Open Field Test; OxPC: oxidized phosphatidylcholine; OxPG: oxidized phosphatidylglycerol; OxPI: oxidized phosphatidylinositol; OxPS: oxidiz 1 key finding →

Evidence: low

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

Plasma levels of Abeta42 and Abeta40 in Alzheimer patients during treatment with the acetylcholinesterase inhibitor tacrine

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Dementia and geriatric cognitive disorders 2002-01-01

Deregulation of amyloid precursor protein (APP) processing with increased production of amyloid beta-peptide (Abeta) is considered to be a key pathogenic event in Alzheimer's disease (AD). 4 key findings →

Design: clinical trial Evidence: low

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

Degeneration in vivo of rat hippocampal neurons by wild-type Alzheimer amyloid precursor protein overexpressed by adenovirus-mediated gene transfer

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1998-04-01

In an attempt to elucidate the pathological implications of intracellular accumulation of the amyloid precursor protein (APP) in postmitotic neurons in vivo, we transferred APP695 cDNA into rat hippocampal neurons by using a replication-defective adenovirus vector. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Characterization of endothelin-converting enzyme 1 as a key enzyme in the multienzyme Aβ degradation pathway

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences 2025-10-27

Altered β-amyloid (Aβ) homeostasis is a critical event triggering the shift from healthy aging to Alzheimer disease (AD) through the overproduction and impaired clearance of Aβ peptides. 2 key findings →

Evidence: low

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

Amyloid precursor protein processing and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Annual review of neuroscience 2011-01-01

Alzheimer's disease (AD), the leading cause of dementia worldwide, is characterized by the accumulation of the β-amyloid peptide (Aβ) within the brain along with hyperphosphorylated and cleaved forms of the microtubule-associated protein tau. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

A beta oligomers - a decade of discovery

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2007-02-05

Converging lines of evidence suggest that progressive accumulation of the amyloid beta-protein (A beta) plays a central role in the genesis of Alzheimer's disease, but it was long assumed that A beta had to be assembled into extracellular amyloid fibrils to exert its cytotoxic effects. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease--is this type 3 diabetes?

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2005-02-01

The neurodegeneration that occurs in sporadic Alzheimer's disease (AD) is consistently associated with a number of characteristic histopathological, molecular, and biochemical abnormalities, including cell loss, abundant neurofibrillary tangles and dystrophic neurites, amyloid-beta deposits, increased activation of pro-death genes and signaling pathways, impaired energy metabolism/mitochondrial function, and evidence of chronic oxidative stress. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Alzheimer's disease beta-amyloid peptides are released in association with exosomes

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-07-12

Although the exact etiology of Alzheimer's disease (AD) is a topic of debate, the consensus is that the accumulation of beta-amyloid (Abeta) peptides in the senile plaques is one of the hallmarks of the progression of the disease. 1 key finding →

Evidence: low

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 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