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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 66 studies with an author at Rush University Medical Center (US) · tagged Genetics (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 66 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.

Apolipoprotein E ε4-dependent associations between carotenoids and cognitive decline: Findings from the MIND (Mediterranean-DASH Intervention for Neurodegenerative delay) randomized controlled trial

✓ Peer-reviewed alzhub usefulness score 62 out of 100. The American journal of clinical nutrition 2025-08-27

Higher plasma carotenoid concentrations were associated with slower cognitive decline in APOE ε4 carriers, potentially mitigating genetic risk. 3 key findings →

Design: randomized controlled trial Participants: 442 Evidence: high

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

TOMM40'523 variant and cognitive decline in older persons with APOE ε3/3 genotype

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2017-01-20

Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory. 1 key finding →

Design: cohort study Evidence: moderate

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

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

Utility of the apolipoprotein E genotype in the diagnosis of Alzheimer's disease. Alzheimer's Disease Centers Consortium on Apolipoprotein E and Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The New England journal of medicine 1998-02-01

APOE genotyping does not provide sufficient sensitivity or specificity to be used alone as a diagnostic test for Alzheimer's disease, but when used in combination with clinical criteria, it improves the specificity of the diagnosis. 5 key findings →

Participants: 2,188 Evidence: low

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

Plasma phosphorylated tau 217 concentrations, APOE genotype, and timing of cognitive impairment in individuals across diverse racial and ethnic groups: a pooled analysis of prospective cohort studies

✓ Peer-reviewed alzhub usefulness score 59 out of 100. The Lancet. Neurology 2026-09-09

Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →

Design: cohort Participants: 8,582 Evidence: high

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

Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Acta neuropathologica 2007-06-20

Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. 3 key findings →

Evidence: low

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

TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions

✓ Peer-reviewed alzhub usefulness score 59 out of 100. The American journal of pathology 2007-07-01

TAR DNA-binding protein 43 (TDP-43) is a major pathological protein of sporadic and familial frontotemporal lobar degeneration with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). 1 key finding →

Participants: 36 Evidence: low

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

The apolipoprotein E epsilon 4 allele and decline in different cognitive systems during a 6-year period

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Archives of neurology 2002-07-01

The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →

Design: cohort study Participants: 624 Evidence: moderate

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

Genetic susceptibility for Alzheimer disease neuritic plaque pathology

✓ Peer-reviewed alzhub usefulness score 57 out of 100. JAMA neurology 2013-09-01

These findings enhance understanding of AD risk factors by relating validated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic variation at the APP locus in the earliest, presymptomatic stages of AD. 4 key findings →

Participants: 114 Evidence: moderate

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

GBA Variants are associated with a distinct pattern of cognitive deficits in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Movement disorders : official journal of the Movement Disorder Society 2015-08-21

Loss-of-function mutations in the GBA gene are associated with more severe cognitive impairment in PD, but the nature of these deficits is not well understood and whether common GBA polymorphisms influence cognitive performance in PD is not yet known. 4 key findings →

Participants: 60 Evidence: low

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

Multiple gene variants linked to Alzheimer's-type clinical dementia via GWAS are also associated with non-Alzheimer's neuropathologic entities

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurobiology of disease 2022-09-30

The classic pathologic hallmarks of Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles (AD neuropathologic changes, or ADNC). 4 key findings →

Participants: 273 Evidence: moderate

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

The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Stroke 2005-03-17

Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). 1 key finding →

Design: longitudinal study Participants: 96 Evidence: moderate

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

Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Neurology 2007-05-01

These results strongly support the concept that synapse loss is a structural correlate involved very early in cognitive decline in mild Alzheimer disease (mAD) and supports mild cognitive impairment as a transitional stage between mAD and no cognitive impairment. 2 key findings →

Evidence: low

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

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

Neuropathologic intermediate phenotypes enhance association to Alzheimer susceptibility alleles

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neurology 2009-04-01

Discovery efforts for susceptibility loci for Alzheimer disease could benefit from the use of neuropathologic intermediate phenotypes as a complement to other approaches. 2 key findings →

Participants: 625 Evidence: low

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

Integrative brain transcriptome analysis links complement component 4 and HSPA2 to the APOE ε2 protective effect in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular psychiatry 2021-09-03

Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. 4 key findings →

Participants: 982 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
  • Randomized / 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
  • Multicenter 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