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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 25 studies in Risk genes beyond APOE with an author at Mayo Clinic in Florida (US) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 25 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.

Other institutions

From OpenAlex; 13,658 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.

Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Nature Genetics 2011-04-03

The authors sought to identify new susceptibility loci for Alzheimer's disease through a staged association study and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium in a companion paper. 2 key findings →

Evidence: low

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

γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)

✓ Peer-reviewed alzhub usefulness score 63 out of 100. The Lancet. Neurology 2024-07-26

A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses. 3 key findings →

Design: cross-sectional Participants: 190 Evidence: moderate

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

The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature genetics 2007-01-14

The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. 4 key findings →

Evidence: low

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

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 1998-01-01

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. 4 key findings →

Evidence: low

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

C9orf72 hexanucleotide repeat expansions in clinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2013-06-01

Hexanucleotide repeat expansions in the chromosome 9 open reading frame 72 (C9orf72) gene underlie a significant fraction of frontotemporal dementia and amyotrophic lateral sclerosis. 4 key findings →

Design: case-control study Evidence: moderate

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

17beta-estradiol reduces plasma Abeta40 for HRT-naïve postmenopausal women with Alzheimer disease: a preliminary study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2003-03-01

These results provide preliminary clinical evidence to support an effect of estradiol on Abeta-processing for AD women who are HRT-naïve. 4 key findings →

Design: randomized controlled trial Evidence: high

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

Location of pathogenic variants in PSEN1 impacts progression of cognitive, clinical, and neurodegenerative measures in autosomal-dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Aging cell 2023-06-08

Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →

Design: cross-sectional Evidence: moderate

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

Estimation of the genetic contribution of presenilin-1 and -2 mutations in a population-based study of presenile Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Human molecular genetics 1998-01-01

Two closely related genes, the presenilins ( PS ), located at chromosomes 14q24.3 and 1q42.1, have been identified for autosomal dominant Alzheimer disease (AD) with onset age below 65 years (presenile AD). 4 key findings →

Evidence: low

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

15 years of longitudinal genetic, clinical, cognitive, imaging, and biochemical measures in DIAN

✓ Peer-reviewed alzhub usefulness score 50 out of 100. npj Dementia 2026-02-16

The Dominantly Inherited Alzheimer Network Observational Study (DIAN Obs) is a longitudinal, global cohort study investigating brain aging and autosomal dominant Alzheimer’s disease (ADAD), a rare monogenic form of Alzheimer’s disease (AD). 5 key findings →

Design: cohort study Evidence: moderate

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

Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neuron 1995-11-01

Transgenic FVB/N mice overexpressing human (Hu) or mouse (Mo) Alzheimer amyloid precursor protein (APP695) die early and develop a CNS disorder that includes neophobia and impaired spatial alternation, with diminished glucose utilization and astrogliosis mainly in the cerebrum. 4 key findings →

Evidence: low

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

Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS medicine 2005-11-15

The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease. 4 key findings →

Evidence: low

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

Statins reduce amyloid-beta production through inhibition of protein isoprenylation

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2007-07-23

Epidemiological evidence suggests that long term treatment with hydroxymethylglutaryl-CoA reductase inhibitors, or statins, decreases the risk for developing Alzheimer disease (AD). 4 key findings →

Evidence: low

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

DAP12 Stabilizes the C-terminal Fragment of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) and Protects against LPS-induced Pro-inflammatory Response

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2015-05-08

Triggering receptor expressed on myeloid cells 2 (TREM2) is a DAP12-associated receptor expressed in microglia, macrophages, and other myeloid-derived cells. 4 key findings →

Evidence: low

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

Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Autophagy 2025-11-23

The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →

Evidence: low

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

The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2005-06-27

Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, vascular amyloid, neurofibrillary tangles, and progressive neurodegeneration. 4 key findings →

Evidence: low

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

Rodent A beta modulates the solubility and distribution of amyloid deposits in transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2007-06-07

The amino acid sequence of amyloid precursor protein (APP) is highly conserved, and age-related A beta aggregates have been described in a variety of vertebrate animals, with the notable exception of mice and rats. 4 key findings →

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

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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% 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