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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 2,501–2,525 of 3,529 studies · tagged Genetics (page 101 of 142) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

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.

Hallmarks of Alzheimer disease are evolving relentlessly in Metropolitan Mexico City infants, children and young adults. APOE4 carriers have higher suicide risk and higher odds of reaching NFT stage V at ≤ 40 years of age

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Environmental research 2018-03-26

Exposures to fine particulate matter (PM 2.5 ) and ozone (O 3 ) above USEPA standards are associated with Alzheimer's disease (AD) risk. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

APOE genotype influences the gut microbiome structure and function in humans and mice: relevance for Alzheimer's disease pathophysiology

✓ Peer-reviewed alzhub usefulness score 41 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2019-04-08

Apolipoprotein E ( APOE ) genotype is the strongest prevalent genetic risk factor for Alzheimer's disease (AD). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Amyloid beta protein precursor gene and hereditary cerebral hemorrhage with amyloidosis (Dutch)

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1990-06-01

Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those afflicted in their fifth or sixth decade. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The genetic defect in familial Alzheimer's disease is not tightly linked to the amyloid beta-protein gene

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1987-09-01

Amyloid beta-protein (AP) is a peptide of relative molecular mass (Mr) 42,000 found in the senile plaques, cerebrovascular amyloid deposits, and neurofibrillary tangles of patients with Alzheimer's disease and Down's syndrome (trisomy 21). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Beta amyloid gene duplication in Alzheimer's disease and karyotypically normal Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1987-03-01

With the recently cloned complementary DNA probe, lambda Am4 for the chromosome 21 gene encoding brain amyloid polypeptide (beta amyloid protein) of Alzheimer's disease, leukocyte DNA from three patients with sporadic Alzheimer's disease and two patients with karyotypically normal Down syndrome was found to contain three copies of this gene. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

CRISPR-Cas9 treatment partially restores amyloid-β 42/40 in human fibroblasts with the Alzheimer's disease PSEN 1 M146L mutation

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular therapy. Nucleic acids 2022-03-28

Presenilin 1 (PS1) is a central component of γ-secretase, an enzymatic complex involved in the generation of the amyloid-β (Aβ) peptide that deposits as plaques in the Alzheimer's disease (AD) brain. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E2 Stimulates Protein Synthesis and Promotes Melanoma Progression and Metastasis

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cancer research 2023-09-15

APOE germline variants impact melanoma progression through disparate mechanisms, such as the protein synthesis-promoting function of the APOE2 variant, indicating that germline genetic variants are causal contributors to metastatic outcomes. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E isoform-dependent effects on the processing of Alzheimer's amyloid-β

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Biochimica et biophysica acta. Molecular and cell biology of lipids 2021-05-24

Since the identification of the apolipoprotein E (apoE) *ε4 allele as a major genetic risk factor for late-onset Alzheimer's disease, significant efforts have been aimed at elucidating how apoE4 expression confers greater brain amyloid-β (Aβ) burden, earlier disease onset and worse clinical outcomes compared to apoE2 and apoE3. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases

✓ Peer-reviewed alzhub usefulness score 41 out of 100. International journal of molecular sciences 2022-08-31

A preponderance of evidence obtained from genetically modified mice and human population studies reveals the association of apolipoprotein E (apoE) deficiency and polymorphisms with pathogenesis of numerous chronic diseases, including atherosclerosis, obesity/diabetes, and Alzheimer's disease. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Human apolipoprotein E isoforms are differentially sialylated and the sialic acid moiety in ApoE2 attenuates ApoE2-Aβ interaction and Aβ fibrillation

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2022-01-15

The APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E4 has extensive conformational heterogeneity in lipid-free and lipid-bound forms

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2023-02-07

The ε4-allele variant of apolipoprotein E (ApoE4) is the strongest genetic risk factor for Alzheimer's disease, although it only differs from its neutral counterpart ApoE3 by a single amino acid substitution. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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