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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 58 studies in Risk genes beyond APOE with an author at Harvard University (US) (page 1 of 3) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of these 58 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; 13,259 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.

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

Cohort Profile Update: The ‘Seguimiento Universidad de Navarra’ (SUN) study after 24 years of follow-up

✓ Peer-reviewed alzhub usefulness score 59 out of 100. International Journal of Epidemiology 2025-08-01

In 2018, Carlos et al. [2] reviewed 21 studies from the SUN project that focused on the association between the MDP and several incident chronic diseases, concluding that high Mediterranean diet adherence was associated with a lower incidence of all-cause mortality, cardiovascular disease, type 2 diabetes, weight gain, metabolic syndrome, depression, cognitive decline, and nephrolithiasis, and with a lower heart rate and mitigation of the effects of obesity on cardiovascular disease (CVD) and type 2 diabetes, and our results suggested that the Mediterranean diet may improve fertility. 5 key findings →

Design: cohort study Participants: 79 Evidence: moderate

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

Associations between biomarkers and age in the presenilin 1 E280A autosomal dominant Alzheimer disease kindred: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2015-03-01

Age-associated changes in brain imaging and fluid biomarkers are characterized and compared in presenilin 1 (PSEN1)E280A mutation carriers and noncarriers from the world's largest known autosomal dominant Alzheimer disease (AD) kindred. 4 key findings →

Design: cross-sectional Evidence: low

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

Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 1992-10-01

Altered processing of the amyloid precursor protein (APP) is a central event in the formation of amyloid deposits in the brains of individuals with Alzheimer's disease. 3 key findings →

Evidence: low

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

The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature medicine 1996-10-01

Missense mutations in the presenilin 1 (PS1) gene cause the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated with increased levels of amyloid beta-peptides (A beta) ending at residue 42 (A beta 42) in plasma and skin fibroblast media of gene carriers. 4 key findings →

Evidence: low

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

Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2003-12-01

Converging evidence suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD) reflects an imbalance between the production and degradation of this self-aggregating peptide. 3 key findings →

Evidence: low

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

Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Science (New York, N.Y.) 1996-12-01

Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. 4 key findings →

Evidence: low

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

Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-03-01

The cellular mechanism underlying the generation of beta-amyloid in Alzheimer disease and its relationship to the normal metabolism of the amyloid precursor protein are unknown. 4 key findings →

Evidence: low

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

Amyloid beta-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2005-09-09

Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer disease (AD), and purified ACE has been reported to cleave synthetic amyloid beta-protein (Abeta) in vitro. 4 key findings →

Evidence: low

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

Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurobiology of aging 2005-06-13

Alzheimer disease (AD) is characterized neuropathologically by intracellular neurofibrillary tangles (NFT) and of extracellular senile plaques (SP), the central core of which is amyloid beta-peptide (Abeta) derived from amyloid precursor protein (APP), a transmembrane protein. 4 key findings →

Evidence: low

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

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

Beta-amyloid precursor protein of Alzheimer disease occurs as 110- to 135-kilodalton membrane-associated proteins in neural and nonneural tissues

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-10-01

Progressive cerebral deposition of extracellular filaments composed of the beta-amyloid protein (beta AP) is a constant feature of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5'-untranslated region sequences

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 1999-03-01

The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD. 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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