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

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

Find studies

Showing 501–525 of 1,301 studies in Genetics · tagged Genetics (page 21 of 53) · 28,180 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; 13,658 studies have no institution on record and are not counted here.

What “Genetics” covers

Genetics — Inherited risk: APOE and the other risk genes, and what they do and don't tell you.

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.

Increased neuronal endocytosis and protease delivery to early endosomes in sporadic Alzheimer's disease: neuropathologic evidence for a mechanism of increased beta-amyloidogenesis

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1997-08-01

The early endosome is the first vacuolar compartment along the endocytic pathway. 5 key findings →

Evidence: low

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

Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-12-01

Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. 3 key findings →

Participants: 40 Evidence: low

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

Benefits of fatty fish on dementia risk are stronger for those without APOE epsilon4

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology 2005-11-01

In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele. 2 key findings →

Evidence: low

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

The number of trait loci in late-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. American journal of human genetics 2000-01-01

Although it is clear that apoE plays an important role in the genetics of late-onset Alzheimer disease (AD), evidence exists that additional genes may play a role in AD, and estimates of the total contribution of apoE to the variance in onset of AD vary widely. 2 key findings →

Participants: 742 Evidence: low

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

Multifaceted roles of APOE in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature reviews. Neurology 2024-06-21

For the past three decades, apolipoprotein E (APOE) has been known as the single greatest genetic modulator of sporadic Alzheimer disease (AD) risk, influencing both the average age of onset and the lifetime risk of developing AD. 1 key finding →

Evidence: low

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

Contribution to Alzheimer's disease risk of rare variants in TREM2, SORL1, and ABCA7 in 1779 cases and 1273 controls

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of aging 2017-07-14

We performed whole-exome and whole-genome sequencing in 927 late-onset Alzheimer disease (LOAD) cases, 852 early-onset AD (EOAD) cases, and 1273 controls from France. 4 key findings →

Evidence: low

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

Lack of hepatic apoE does not influence early Aβ deposition: observations from a new APOE knock-in model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Molecular neurodegeneration 2019-10-17

These new knock-in strains offer a novel and dynamic tool to study the role of APOE in AD pathogenesis in a spatially and temporally controlled manner. 2 key findings →

Evidence: low

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

Cognitive domain decline in healthy apolipoprotein E epsilon4 homozygotes before the diagnosis of mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Archives of neurology 2007-09-01

Of 214 participants, 48 showed no decline on any test, 126 showed decline on only 1 test in 1 or more domains, and 40 showed decline on 2 or more tests in 1 or more domains. 2 key findings →

Participants: 214 Evidence: low

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

Association of Early-Onset Alzheimer Disease With Elevated Low-Density Lipoprotein Cholesterol Levels and Rare Genetic Coding Variants of APOB

✓ Peer-reviewed alzhub usefulness score 51 out of 100. JAMA neurology 2019-07-01

Elevated LDL-C levels were associated with higher probability of having EOAD, and EOAD cases were enriched for rare coding variants in APOB, which codes for the major protein of LDL-C. 3 key findings →

Evidence: low

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

Apolipoprotein E Mimetic Peptide CN-105 and Postoperative Delirium in Older Patients

✓ Peer-reviewed alzhub usefulness score 51 out of 100. JAMA Network Open 2026-04-03

Among 203 enrolled patients, 186 (mean [SD] age, 68.7 [5.2] years; 119 males [64.0%]) were randomized (137 to the CN-105 group, 49 to the placebo group) and underwent surgery. 5 key findings →

Design: clinical trial Evidence: high

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

Multi-ancestry transcriptome-wide association study reveals shared and population-specific genetic effects in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. American Journal of Human Genetics 2026-04-30

Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →

Design: cross-sectional Participants: 751 Evidence: early

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

APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature genetics 2026-09-14

Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →

Design: case-control Evidence: high

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

Reelin and ApoE receptors cooperate to enhance hippocampal synaptic plasticity and learning

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2002-08-07

Two apolipoprotein E (apoE) receptors, the very low density lipoprotein (VLDL) receptor and apoE receptor 2 (apoER2), are also receptors for Reelin, a signaling protein that regulates neuronal migration during brain development. 3 key findings →

Evidence: low

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

Central Nervous System Lipoproteins: ApoE and Regulation of Cholesterol Metabolism

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Arteriosclerosis, thrombosis, and vascular biology 2016-05-12

ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS). 1 key finding →

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 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