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Research

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

Find studies

Showing 201–225 of 242 studies with an author at Washington University in St. Louis (US) · tagged Genetics (page 9 of 10) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 242 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; 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.

Acute Trem2 reduction triggers increased microglial phagocytosis, slowing amyloid deposition in mice

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2021-07-01

Heterozygous genetic variants within the TREM2 gene show a strong association with increased Alzheimer's disease (AD) risk. 4 key findings →

Evidence: low

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

Cognitively normal APOE ε4 carriers have specific elevation of CSF SNAP-25

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurobiology of aging 2021-02-11

Cerebrospinal fluid (CSF) synaptosomal-associated protein 25 (SNAP-25) and neurogranin (Ng) are recently described biomarkers for pre- and postsynaptic integrity known to be elevated in symptomatic Alzheimer disease (AD). 2 key findings →

Participants: 274 Evidence: low

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

Early striatal amyloid deposition distinguishes Down syndrome and autosomal dominant Alzheimer's disease from late-onset amyloid deposition

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2018-03-01

Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment. 2 key findings →

Evidence: low

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

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

TREM2-Dependent Effects on Microglia in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in aging neuroscience 2018-07-09

Alzheimer's disease (AD) is a late-onset dementia characterized by the deposition of amyloid plaques and formation of neurofibrillary tangles (NFTs) which lead to neuronal loss and cognitive deficits. 4 key findings →

Evidence: low

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

Lecanemab in symptomatic PSEN1 p.Met233Val early-onset Alzheimer's disease: Neuroimaging safety, regional amyloid-PET dynamics, and longitudinal plasma biomarkers

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2026-07-01

No amyloid-related imaging abnormalities occurred. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Diffusion Tensor MRI Structural Connectivity and PET Amyloid Burden in Preclinical Autosomal Dominant Alzheimer Disease: The DIAN Cohort

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Radiology 2021-10-12

White matter structural connectivity was lower in autosomal dominant Alzheimer disease mutation carriers compared with noncarriers and correlated with estimated years to symptom onset. 5 key findings →

Design: cross-sectional Evidence: low

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

Whole exome sequencing study identifies novel rare and common Alzheimer's-Associated variants involved in immune response and transcriptional regulation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2018-08-14

The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Apolipoprotein E and low density lipoprotein receptor-related protein facilitate intraneuronal Abeta42 accumulation in amyloid model mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2006-09-29

The low density lipoprotein receptor-related protein (LRP) is highly expressed in the brain and has been shown to alter the metabolism of amyloid precursor protein and amyloid-beta peptide (Abeta) in vitro. 3 key findings →

Evidence: low

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

Genetic heterogeneity in Alzheimer disease and implications for treatment strategies

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Current neurology and neuroscience reports 2014-11-01

Since the original publication describing the illness in 1907, the genetic understanding of Alzheimer's disease (AD) has advanced such that it is now clear that it is a genetically heterogeneous condition, the subtypes of which may not uniformly respond to a given intervention. 5 key findings →

Evidence: low

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

Distribution and signaling of TREM2/DAP12, the receptor system mutated in human polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy dementia

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The European journal of neuroscience 2004-11-01

Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells. 4 key findings →

Evidence: low

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

TREM2 Function in Alzheimer's Disease and Neurodegeneration

✓ Peer-reviewed alzhub usefulness score 45 out of 100. ACS chemical neuroscience 2016-02-19

Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a complex neurodegenerative disease marked by the appearance of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. 4 key findings →

Evidence: low

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

Functional insights from biophysical study of TREM2 interactions with apoE and Aβ1-42

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2020-10-08

Triggering receptor expressed on myeloid cells-2 (TREM2) is an immune receptor expressed on microglia that also can become soluble (sTREM2). 4 key findings →

Evidence: low

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

γ-Secretase modulation inhibits amyloid plaque formation and growth and stimulates plaque regression in amyloid precursor protein/presenilin-1 mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of Pharmacology and Experimental Therapeutics 2025-02-12

γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease. 3 key findings →

Evidence: low

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

Systematic analysis of cellular cross-talk reveals a role for SEMA6D-TREM2 regulating microglial function in Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Science Translational Medicine 2025-07-30

Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →

Evidence: low

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

ApoE-calypse tau: ApoE–tau synergy in Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of Experimental Medicine 2025-08-05

Alzheimer's disease (AD), the most common cause of dementia, is characterized by the accumulation of amyloid-β (Aβ) in senile plaques and abnormally hyperphosphorylated tau proteins in neurofibrillary tangles. 2 key findings →

Evidence: low

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

CSF Tau phosphorylation at Thr205 is associated with loss of white matter integrity in autosomal dominant Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of disease 2022-03-28

However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s). 4 key findings →

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 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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