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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 68 studies with an author at Mayo Clinic in Florida (US) (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 68 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 68 studies tagged precursor — clear

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.

Association between apolipoprotein E genotype and Alzheimer disease in African American subjects

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Archives of neurology 2002-04-01

Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →

Design: case-control study Participants: 338 Evidence: moderate

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

ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2022-03-16

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →

Evidence: low

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

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 1998-01-01

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. 4 key findings →

Evidence: low

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

Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of neurology 2007-03-01

The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD. 5 key findings →

Participants: 53 Evidence: moderate

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

Multi Layered Omics Approaches Reveal Glia Specific Alterations in Alzheimer's Disease: A Systematic Review and Future Prospects

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Glia 2024-12-09

Alzheimer's disease (AD) is the most common neurodegenerative dementia with multi-layered complexity in its molecular etiology. 1 key finding →

Design: systematic review Evidence: high

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

Autosomal dominant and sporadic late onset Alzheimer's disease share a common in vivo pathophysiology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2022-10-01

The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →

Participants: 559 Evidence: low

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

C9orf72 hexanucleotide repeat expansions in clinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2013-06-01

Hexanucleotide repeat expansions in the chromosome 9 open reading frame 72 (C9orf72) gene underlie a significant fraction of frontotemporal dementia and amyotrophic lateral sclerosis. 4 key findings →

Design: case-control study Evidence: moderate

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

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

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

APOE epsilon 4 lowers age at onset and is a high risk factor for Alzheimer's disease; a case control study from central Norway

✓ Peer-reviewed alzhub usefulness score 53 out of 100. BMC neurology 2008-04-16

The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway. 4 key findings →

Participants: 376 Evidence: low

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

Location of pathogenic variants in PSEN1 impacts progression of cognitive, clinical, and neurodegenerative measures in autosomal-dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Aging cell 2023-06-08

Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →

Design: cross-sectional Evidence: moderate

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

Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Cold Spring Harbor perspectives in medicine 2012-03-01

Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective. 5 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

APOE4-specific changes in Aβ accumulation in a new transgenic mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2012-10-11

APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation. 5 key findings →

Evidence: low

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

Levels of soluble apolipoprotein E/amyloid-β (Aβ) complex are reduced and oligomeric Aβ increased with APOE4 and Alzheimer disease in a transgenic mouse model and human samples

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2013-01-04

Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels. 5 key findings →

Evidence: moderate

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