Evidence map›Paper›PMID 42583767›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Inhibition of Moesin and CD44 in stem cell-derived neurons affects the pathological genetic signature associated with Alzheimer's disease.

Eiden H Brewer, Charles A Williams, Gregory A Cary, Ranjita Betarbet, Inez K A Pranoto, Elizabeth L Zoeller, Haian Fu, Allan I Levey, Jesse C Wiley, Gregory W Carter and 2 more

Abstract read
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In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Eiden H BrewerDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA.
Charles A WilliamsDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA.
Gregory A CaryThe Jackson Laboratory, Bar Harbor, Maine, USA.
Ranjita BetarbetDepartment of Neurology, Emory University School of Medicine, Atlanta, Georgia, USA.
Inez K A PranotoDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA.
Elizabeth L ZoellerDepartment of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, Georgia, USA.
Haian FuDepartment of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, Georgia, USA.
Allan I LeveyDepartment of Neurology, Emory University School of Medicine, Atlanta, Georgia, USA.
Jesse C WileyDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas, USA.
Gregory W CarterThe Jackson Laboratory, Bar Harbor, Maine, USA.
Jessica E YoungDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA.ORCID https://orcid.org/0000-0003-2106-0339
TREAT‐AD Consortium

Funding

TREAT AD Structural Biology CoreU54AG065187 · NIA · EMORY UNIVERSITY · PI Gregory W Carter, ALLAN I LEVEY · 2019 to 2026
$69.7M
University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI Amanda D. Boyd · 2020 to 2026
$29.0M
NIA NIH HHS P30 AG066509NIA NIH HHS U54 AG065187NIA NIH HHS U54AG065187
6 · The paper itself

Abstract

introductionPost mortem proteomic analysis of Alzheimer's disease (AD) brain tissue has identified novel target genes and proteins for potential therapeutic development. Moesin (MSN) and CD44 were identified as candidate targets. Using human induced pluripotent stem cells (hiPSCs)-derived neurons, we assayed how reducing gene expression of MSN and CD44 affected amyloid beta secretion, tau phosphorylation, and transcriptional state.

methodsKnockdown of MSN and CD44 in hiPSC-derived neurons was performed using short hairpin RNA (shRNA). Amyloid precursor protein processing and intracellular tau phosphorylation was measured using chemiluminescent ELISA assays. Global gene expression was analyzed by bulk RNA sequencing (RNA-seq).

resultsKnockdown of CD44 and MSN increased secretion of amyloid beta and soluble APP beta and differentially altered tau generation and phosphorylation. RNA-seq revealed diverse effects of CD44 and MSN knockdown and the reversal of some expression shifts found in late-onset AD. DISCUSSION: These findings connect reduced CD44 and MSN expression to AD-related signatures in neurons and inform their role in the disease.

Indexed as

Alzheimer DiseaseHyaluronan ReceptorsInduced Pluripotent Stem CellsNeuronsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorGene Knockdown TechniquesHumansMicrofilament ProteinsPhosphorylationtau ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCD44 protein, humanHyaluronan ReceptorsMicrofilament Proteinsmoesintau ProteinsAlzheimer's diseaseamyloid betaphosphorylated tautarget validationtranscriptome

Identifiers

PMID42583767
PMCPMC13463313

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.