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

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 251–275 of 590 studies in Genetics · free to read (page 11 of 24) · 28,580 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; 14,058 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.

Glutathione S-transferase omega genes in Alzheimer and Parkinson disease risk, age-at-diagnosis and brain gene expression: an association study with mechanistic implications

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Molecular neurodegeneration 2012-04-11

These results suggest that GSTO locus variants may lower brain GSTO2 levels and consequently confer AD risk in older age. 5 key findings →

Evidence: low

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

Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2011-03-01

We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus. 5 key findings →

Design: longitudinal study Evidence: moderate

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

Significant association between SCN8A and Alzheimer disease in Puerto Ricans

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer s & Dementia 2025-12-01

) within the first intron of SCN8A on chromosome 12 (Figure 1), overlapping a significant region in the previous admixture mapping analysis. eHiCA revealed more and stronger interactions between rs4761988 and SLC4A8, SCN8A and FIGNL2 in EU compared to AF genome (Figure 2), consistent with the admixture mapping result. 4 key findings →

Design: meta-analysis Participants: 867 Evidence: high

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

Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Nature reviews. Neurology 2019-07-31

Polymorphism in the apolipoprotein E (APOE) gene is a major genetic risk determinant of late-onset Alzheimer disease (AD), with the APOE*ε4 allele conferring an increased risk and the APOE*ε2 allele conferring a decreased risk relative to the common APOE*ε3 allele. 2 key findings →

Evidence: low

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

Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-10-01

Amyloid beta-peptide (A beta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). 2 key findings →

Evidence: low

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

PGC-1alpha expression decreases in the Alzheimer disease brain as a function of dementia

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2009-03-01

Therapeutic preservation of neuronal PGC-1alpha expression promotes the nonamyloidogenic processing of amyloid precursor protein precluding the generation of amyloidogenic Abeta peptides. 4 key findings →

Design: case-control study Evidence: moderate

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

Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2008-10-01

This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. 3 key findings →

Participants: 97 Evidence: moderate

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

Apolipoprotein E: Structural Insights and Links to Alzheimer Disease Pathogenesis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2020-11-10

Apolipoprotein E (ApoE) is of great interest due to its role as a cholesterol/lipid transporter in the central nervous system (CNS) and as the most influential genetic risk factor for Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Enhanced risk for Alzheimer disease in persons with type 2 diabetes and APOE epsilon4: the Cardiovascular Health Study Cognition Study

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2008-01-01

These data suggest that having both diabetes and APOE epsilon4 increases the risk of dementia, especially for AD and mixed AD. 2 key findings →

Evidence: moderate

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

Age at onset in two common neurodegenerative diseases is genetically controlled

✓ Peer-reviewed alzhub usefulness score 53 out of 100. American journal of human genetics 2002-03-01

To identify genes influencing age at onset (AAO) in two common neurodegenerative diseases, a genomic screen was performed for AAO in families with Alzheimer disease (AD; n=449) and Parkinson disease (PD; n=174). 2 key findings →

Participants: 449 Evidence: low

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

Neuropsychiatric symptoms as risk factors for progression from CIND to dementia: the Cache County Study

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2013-02-06

These data confirm that NPS are risk factors for conversion from CIND to dementia. 1 key finding →

Participants: 230 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.

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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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