alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 351–375 of 1,002 studies in Risk genes beyond APOE marked Peer-reviewed (page 15 of 41) · 30,180 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; 15,654 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.

Amyloid Precursor Protein (APP) Metabolites APP Intracellular Fragment (AICD), Aβ42, and Tau in Nuclear Roles

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2015-08-21

Amyloid precursor protein (APP) metabolites (amyloid-β (Aβ) peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheimer disease. 3 key findings →

Evidence: low

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

γ-Secretase modulation inhibits amyloid plaque formation and growth and stimulates plaque regression in amyloid precursor protein/presenilin-1 mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of Pharmacology and Experimental Therapeutics 2025-02-12

γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease. 3 key findings →

Evidence: low

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

Systematic analysis of cellular cross-talk reveals a role for SEMA6D-TREM2 regulating microglial function in Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Science Translational Medicine 2025-07-30

Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →

Evidence: low

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

Soluble SorLA in CSF, a novel biomarker to explore disrupted trafficking of SorLA protein in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer s Research & Therapy 2025-05-07

The SorLA protein, encoded by the Sortilin-related receptor 1 ( SORL1 ) gene, is a major player in Alzheimer’s disease (AD) pathophysiology. 4 key findings →

Participants: 30 Evidence: low

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

Incomplete penetrance in familial Alzheimer's disease with PSEN1 Ala260Gly mutation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 2020-04-23

Presenilin1 (PSEN1) gene is the most common known genetic cause of early-onset familial Alzheimer's disease. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Identification of PSEN2 mutation p.N141I in Argentine pedigrees with early-onset familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurobiology of aging 2015-06-15

Presenilin 2 gene (PSEN2) mutations account for <5% of all early-onset familial Alzheimer's disease (EOFAD) cases and only 13 have strong evidence for pathogenicity. 1 key finding →

Participants: 19 Evidence: low

Full summary, score breakdown and related studies → Original source

Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2021-07-28

Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Evidence for seeding of beta -amyloid by intracerebral infusion of Alzheimer brain extracts in beta -amyloid precursor protein-transgenic mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2000-05-01

Many neurodegenerative diseases are associated with the abnormal sequestration of disease-specific proteins in the brain, but the events that initiate this process remain unclear. 4 key findings →

Evidence: low

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

The presenilin 1 protein is a component of a high molecular weight intracellular complex that contains beta-catenin

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 1998-06-01

The presenilin (PS) genes associated with Alzheimer disease encode polytopic transmembrane proteins which undergo physiologic endoproteolytic cleavage to generate stable NH2- and COOH-terminal fragments (NTF or CTF) which co-localize in intracellular membranes, but are tightly regulated in their stoichiometry and abundance. 4 key findings →

Evidence: low

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

S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular and cellular neurosciences 2005-01-01

Few diseases are characterized by high homocysteine (HCY) and low folate and vitamin B12 blood levels. 4 key findings →

Evidence: low

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

Age-related learning deficits in transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-06-01

The beta-amyloid precursor protein (beta-APP), from which the beta-A4 peptide is derived, is considered to be central to the pathogenesis of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2007-07-06

The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques. 4 key findings →

Evidence: low

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

The Alzheimer amyloid precursor protein. Identification of a stable intermediate in the biosynthetic/degradative pathway

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 1990-03-01

The amyloid forming beta-peptide of Alzheimer's disease is synthesized as part of a larger integral membrane precursor protein (beta APP) of which three alternatively spliced versions of 695, 751, and 770 amino acids have been described. 4 key findings →

Evidence: low

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

Localization of Alzheimer beta A4 amyloid precursor protein at central and peripheral synaptic sites

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Brain research 1991-11-01

We have recently shown that the amyloid beta A4 precursor protein (APP) is synthesized in neurons and undergoes fast axonal transport to synaptic sites [Koo et al., Proc. 3 key findings →

Evidence: low

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

[alpha]-Secretase ADAM10 as well as [alpha]APPs is reduced in platelets and CSF of Alzheimer disease patients

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular medicine (Cambridge, Mass.) 2002-02-01

The present study addresses the following major questions: 1) Are the levels of an alpha-secretase candidate (i.e., ADAM10) reduced in accessible cells of Alzheimer Disease (AD) patients? 2) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? 4 key findings →

Evidence: low

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

↑ Change the filters

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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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