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Research

30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 351–375 of 448 studies in Risk genes beyond APOE · free to read (page 15 of 18) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of these 448 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; 16,054 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.

Pomegranate polyphenols and extract inhibit nuclear factor of activated T-cell activity and microglial activation in vitro and in a transgenic mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of nutrition 2013-03-06

Alzheimer disease (AD) brain is characterized by extracellular plaques of amyloid β (Aβ) peptide with reactive microglia. 4 key findings →

Evidence: low

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

PCSK9 is required for the disposal of non-acetylated intermediates of the nascent membrane protein BACE1

✓ Peer-reviewed alzhub usefulness score 41 out of 100. EMBO reports 2008-07-25

We have recently identified a new form of post-translational regulation of BACE1 (beta-site amyloid precursor protein (APP)-cleaving enzyme 1), a membrane protein that acts as the rate-limiting enzyme in the generation of the Alzheimer disease amyloid beta-peptide (Abeta). 4 key findings →

Evidence: low

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

Two endoplasmic reticulum (ER)/ER Golgi intermediate compartment-based lysine acetyltransferases post-translationally regulate BACE1 levels

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2008-11-14

We have recently identified a novel form of post-translational regulation of BACE1 (beta-site amyloid precursor protein-cleaving enzyme 1), a membrane protein that acts as the rate-limiting enzyme in the generation of the Alzheimer disease amyloid beta-peptide. 4 key findings →

Evidence: low

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

Calcium-mediated transient phosphorylation of tau and amyloid precursor protein followed by intraneuronal amyloid-beta accumulation

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2006-11-03

Intraneuronal accumulation of hyperphosphorylated protein tau in paired helical filaments together with amyloid-beta peptide (Abeta) deposits confirm the clinical diagnosis of Alzheimer disease. 4 key findings →

Evidence: low

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

BRI2 interacts with amyloid precursor protein (APP) and regulates amyloid beta (Abeta) production

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2005-07-18

Transmembrane proteins BRI2 and amyloid precursor protein (APP) co-localize with amyloid beta (Abeta) lesions in sporadic Alzheimer disease and mutations in both precursor proteins are linked to early-onset familial cases of cerebral amyloidosis associated with dementia and/or cerebral hemorrhage. 4 key findings →

Evidence: low

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

Hyperphosphorylation of Tau induced by naturally secreted amyloid-β at nanomolar concentrations is modulated by insulin-dependent Akt-GSK3β signaling pathway

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2012-08-21

Alzheimer disease (AD) is neuropathologically characterized by the formation of senile plaques from amyloid-β (Aβ) and neurofibrillary tangles composed of phosphorylated Tau. 4 key findings →

Evidence: low

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

Ubiquitin regulates GGA3-mediated degradation of BACE1

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2010-05-18

BACE1 (beta-site amyloid precursor protein-cleaving enzyme 1) is a membrane-tethered member of the aspartyl proteases, essential for the production of beta-amyloid, a toxic peptide that accumulates in the brain of subjects affected by Alzheimer disease. 4 key findings →

Evidence: low

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

Genetic targeting aromatase in male amyloid precursor protein transgenic mice down-regulates beta-secretase (BACE1) and prevents Alzheimer-like pathology and cognitive impairment

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2010-05-01

As brain testosterone plays both androgenic and estrogenic actions due to its conversion into estrogen via aromatase naturally, it is unclear that the age-related reduction of testosterone increased risk of Alzheimer's disease (AD) in men is mediated through androgen alone or both androgen and estrogen mechanisms. 4 key findings →

Evidence: low

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

Induced dimerization of the amyloid precursor protein leads to decreased amyloid-beta protein production

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2009-07-13

The amyloid precursor protein (APP) plays a central role in Alzheimer disease (AD) pathogenesis because sequential cleavages by beta- and gamma-secretase lead to the generation of the amyloid-beta (Abeta) peptide, a key constituent in the amyloid plaques present in brains of AD individuals. 4 key findings →

Evidence: low

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

Soluble oligomers of amyloid-β peptide disrupt membrane trafficking of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor contributing to early synapse dysfunction

✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of biological chemistry 2011-06-10

β-Amyloid (Aβ), a peptide generated from the amyloid precursor protein, is widely believed to underlie the pathophysiology of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Autoantibodies to amyloid beta-peptide (Abeta) are increased in Alzheimer's disease patients and Abeta antibodies can enhance Abeta neurotoxicity: implications for disease pathogenesis and vaccine development

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neuromolecular medicine 2003-01-01

Studies of amyloid precursor protein transgenic mice suggest that immune responses to amyloid beta peptide (Abeta) may be instrumental in the removal of plaques from the brain, but the initial clinical trial of an Abeta vaccine in patients with Alzheimer s disease (AD) was halted as the result of serious neurological complications in some patients. 4 key findings →

Evidence: low

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

apl-1, a Caenorhabditis elegans gene encoding a protein related to the human beta-amyloid protein precursor

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-12-01

The major component of senile plaques found in the brains of Alzheimer disease patients is the beta-amyloid peptide, which is derived from a larger amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Multi-target-directed coumarin derivatives: hAChE and BACE1 inhibitors as potential anti-Alzheimer compounds

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Bioorganic & medicinal chemistry letters 2007-10-04

The complex etiology of Alzheimer's disease (AD) prompts scientists to develop multifunctional compounds to combat causes and symptoms of such neurodegeneration. 2 key findings →

Evidence: low

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

Hyperhomocysteinemia increases beta-amyloid by enhancing expression of gamma-secretase and phosphorylation of amyloid precursor protein in rat brain

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The American journal of pathology 2009-03-05

Hyperhomocysteinemia and beta-amyloid (Abeta) overproduction are critical etiological and pathological factors in Alzheimer disease, respectively; however, the intrinsic link between them is still missing. 4 key findings →

Evidence: low

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

Interactions between age, stress and insulin on cognition: implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2010-02-24

There is much interest in understanding the mechanisms responsible for interactions among stress, aging, memory and Alzheimer's disease. 4 key findings →

Evidence: low

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

The neurodegeneration mutant löchrig interferes with cholesterol homeostasis and Appl processing

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The EMBO journal 2002-12-01

The novel Drosophila mutant löchrig (loe) shows progressive neurodegeneration and neuronal cell death, in addition to a low level of cholesterol ester. loe affects a specific isoform of the gamma-subunit of AMP-activated protein kinase (AMPK), a negative regulator of hydroxymethylglutaryl (HMG)-CoA reductase and cholesterol synthesis in vertebrates. 4 key findings →

Evidence: low

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

CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature Communications 2026-07-17

We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD). 2 key findings →

Evidence: low

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

A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain pathology (Zurich, Switzerland) 2003-10-01

Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. 4 key findings →

Evidence: low

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

Molecular basis of neuroprotective activities of rasagiline and the anti-Alzheimer drug TV3326 [(N-propargyl-(3R)aminoindan-5-YL)-ethyl methyl carbamate]

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cellular and molecular neurobiology 2001-12-01

Rasagiline (N-propargyl-1-(R)-aminoindan) is a selective, irreversible monoamine oxidase B (MAO B) inhibitor which has been developed as an anti-Parkinson drug. 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
  • 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% 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    Where this research is being discussed: events