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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 85 studies with an author at University of Miami (US) · tagged Genetics (page 2 of 4) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 85 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.

Subjects

Authors

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

Other institutions

From OpenAlex; 16,851 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.

Exceptionally low likelihood of Alzheimer's dementia in APOE2 homozygotes from a 5,000-person neuropathological study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature communications 2020-02-03

Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. 2 key findings →

Evidence: low

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

The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Nature genetics 2007-01-14

The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. 4 key findings →

Evidence: low

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

Novel early-onset Alzheimer-associated genes influence risk through dysregulation of glutamate, immune activation, and intracellular signaling pathways

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Alzheimer's & Dementia 2025-06

EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification. 2 key findings →

Design: case-control Participants: 25,236 Evidence: moderate

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

Admixture mapping identifies novel Alzheimer's disease risk regions in African Americans

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Alzheimer's & Dementia 2022-12-20

Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus. 5 key findings →

Design: case-control Participants: 10,271 Evidence: moderate

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

Integrated Systems Approach Identifies Genetic Nodes and Networks in Late-Onset Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Cell 2013-04-01

The study constructed gene-regulatory networks in postmortem brain tissues from late-onset Alzheimer's disease patients and nondemented subjects to characterize associated molecular systems. 3 key findings →

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

TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2017-08-01

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features. 2 key findings →

Evidence: low

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

Increased APOE ε4 expression is associated with the difference in Alzheimer's disease risk from diverse ancestral backgrounds

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-02-01

AD patients with ELA expressed significantly greater levels of APOE than ALA APOE ε4 carriers. 3 key findings →

Participants: 60,908 Evidence: low

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

Genetic control of human brain transcript expression in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. American journal of human genetics 2009-04-01

We recently surveyed the relationship between the human brain transcriptome and genome in a series of neuropathologically normal postmortem samples. 4 key findings →

Participants: 188 Evidence: moderate

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

Novel sex‐specific candidate loci associated with Alzheimer disease identified through sex‐aware multi‐ancestry genome‐wide meta‐analysis

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer s & Dementia 2025-12-01

Cross-ancestry sex-stratified analyses identified several loci with evidence of interaction (p 0.05). 5 key findings →

Design: meta-analysis Participants: 25,284 Evidence: high

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

A multiancestry polygenic risk score for Alzheimer's disease is associated with cognitive decline and neuropathological hallmarks in diverse populations

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature genetics 2026-08-27

Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →

Design: cohort Evidence: high

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

Dementia revealed: novel chromosome 6 locus for late-onset Alzheimer disease provides genetic evidence for folate-pathway abnormalities

✓ Peer-reviewed alzhub usefulness score 56 out of 100. PLoS genetics 2010-09-23

Genome-wide association studies (GWAS) of late-onset Alzheimer disease (LOAD) have consistently observed strong evidence of association with polymorphisms in APOE. 5 key findings →

Design: case-control study Evidence: moderate

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

Controversies and priorities in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2013-03-01

Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were linked to mutations in the superoxide dismutase-1 (SOD1) gene, a substantial proportion of the remainder of cases of familial ALS have now been traced to an expansion of the intronic hexanucleotide repeat sequence in C9orf72. 1 key finding →

Evidence: low

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

Early-Onset Alzheimer Disease and Candidate Risk Genes Involved in Endolysosomal Transport

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2017-09-01

Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained. 4 key findings →

Design: case-control study Evidence: moderate

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

Defining mild cognitive impairment: impact of varying decision criteria on neuropsychological diagnostic frequencies and correlates

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2010-08-01

MCI diagnosis frequencies are substantively affected by the stringency of the criteria, but the relative rankings of MCI subtype diagnoses are fairly consistent regardless of the stringency of the criteria. 5 key findings →

Design: longitudinal study Participants: 373 Evidence: moderate

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

The effect of alcohol and tobacco consumption, and apolipoprotein E genotype, on the age of onset in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. International journal of geriatric psychiatry 2010-05-01

The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion. 2 key findings →

Design: cross-sectional Participants: 397 Evidence: moderate

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

Association of Rare Coding Mutations With Alzheimer Disease and Other Dementias Among Adults of European Ancestry

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA network open 2019-03-01

Some of the unexplained heritability of Alzheimer disease (AD) may be due to rare variants whose effects are not captured in genome-wide association studies because very large samples are needed to observe statistically significant associations. 4 key findings →

Participants: 5,617 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events