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Research

32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 51–75 of 86 studies with an author at Washington University in St. Louis (US) (page 3 of 4) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 86 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 86 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; 17,651 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 and expression analyses with single-nucleotide polymorphisms in TOMM40 in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2011-08-01

Although we did not replicate the earlier association between the APOE 3-TOMM40 haplotypes and age at onset, we observed that the polyT polymorphism is associated with risk of LOAD in APOE 33 homozygotes in a large case-control series but in the opposite direction as in the previous study. 5 key findings →

Design: case-control study Evidence: moderate

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

Selective reduction of astrocyte apoE3 and apoE4 strongly reduces Aβ accumulation and plaque-related pathology in a mouse model of amyloidosis

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular neurodegeneration 2022-02-02

This study reveals an important role of astrocytic apoE3 and apoE4 on the deposition and accumulation of Aβ plaques as well as on certain Aβ-associated downstream effects. 5 key findings →

Evidence: low

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

Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2012-12-07

Although amyloid-beta (Aβ) peptide deposition into insoluble plaques is a pathological hallmark of Alzheimer disease; soluble oligomeric Aβ has been hypothesized to more directly underlie impaired learning and memory in dementia of the Alzheimer type. 4 key findings →

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

Lack of hepatic apoE does not influence early Aβ deposition: observations from a new APOE knock-in model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Molecular neurodegeneration 2019-10-17

These new knock-in strains offer a novel and dynamic tool to study the role of APOE in AD pathogenesis in a spatially and temporally controlled manner. 2 key findings →

Evidence: low

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

Alzheimer disease and cognitive reserve: variation of education effect with carbon 11-labeled Pittsburgh Compound B uptake

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Archives of neurology 2008-11-01

Uptake of carbon 11-labeled Pittsburgh Compound B ([(11)C]PiB) was measured for participants assessed between August 15, 2003, and January 8, 2008, at the Washington University Alzheimer's Disease Research Center and diagnosed either as nondemented (n = 161) or with dementia of the Alzheimer type (n = 37). 1 key finding →

Participants: 161 Evidence: low

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

APOE genotype regulates pathology and disease progression in synucleinopathy

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science translational medicine 2020-02-01

Apolipoprotein E ( APOE ) ε4 genotype is associated with increased risk of dementia in Parkinson's disease (PD), but the mechanism is not clear, because patients often have a mixture of α-synuclein (αSyn), amyloid-β (Aβ), and tau pathologies. 5 key findings →

Evidence: low

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

Alzheimer's disease-linked risk alleles elevate microglial cGAS-associated senescence and neurodegeneration in a tauopathy model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neuron 2024-09-30

The strongest risk factors for late-onset sporadic Alzheimer's disease (AD) include the ε4 allele of apolipoprotein E (APOE), the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), and female sex. 4 key findings →

Evidence: low

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

Proteomic clusters underlie heterogeneity in preclinical Alzheimer's disease progression

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Brain : a journal of neurology 2023-07-01

Heterogeneity in progression to Alzheimer's disease (AD) poses challenges for both clinical prognosis and clinical trial implementation. 3 key findings →

Design: longitudinal study Evidence: moderate

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

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

Neuronal expression of myeloperoxidase is increased in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Journal of neurochemistry 2004-08-01

Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation. 4 key findings →

Evidence: low

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

Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of life

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Archives of neurology 2005-12-01

Cases of early-onset Alzheimer disease (AD) with an autosomal dominant inheritance pattern (familial AD [FAD]) are rare but have greatly advanced our understanding of the molecular pathogenesis of AD. 4 key findings →

Evidence: low

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

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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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.

1,045 records (3.2% of the library) are not peer-reviewed — 966 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

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