Evidence map›Paper›PMID 37157042›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2023

Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation.

Ana C Valencia-Olvera, Deebika Balu, Naomi Faulk, Aspasia Amiridis, Yueting Wang, Christine Pham, Eva Avila-Munoz, Jason M York, Gregory R J Thatcher, Mary Jo LaDu

Open access · hybridAbstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
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

19 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  4. Article
  5. Science advances · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
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  15. Article
  16. Article
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  18. Article
  19. Frontiers in aging neuroscience · 2023
    Article
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

10 authors at 4 institutions in 1 country.

Ana C Valencia-OlveraDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Deebika BaluDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Naomi FaulkDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Aspasia AmiridisUniversity of Wisconsin - Madison, Madison, WI, 53706, USA.
Yueting WangDepartment of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Christine PhamDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Eva Avila-MunozSyneos Health, Av. Gustavo Baz 309, La Loma, Tlalnepantla de Baz, 54060, Mexico.
Jason M YorkDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Gregory R J ThatcherDepartment of Pharmacology & Toxicology, University of Arizona, 1703 E Mabel St., Tucson, AZ, 85721, USA. grjthatcher@arizona.edu.
Mary Jo LaDuDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, 60612, USA.ORCID 0000-0003-2141-1450
University of Illinois Chicago · USAbbVie (United States) · USUniversity of Arizona · USUniversity of Wisconsin–Madison · US

Funding

R01 Estrogen therapy and APOE4 risk in Alzheimer's tested in female EFAD miceR01AG057008 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LADU, MARY JO, THATCHER, GREGORY R. J · 2017 to 2020
$2.5M
NIA NIH HHS R01 AG057008
6 · The paper itself

Abstract

APOE4, encoding apolipoprotein E4 (apoE4), is the greatest genetic risk factor for Alzheimer's disease (AD), compared to the common APOE3. While the mechanism(s) underlying APOE4-induced AD risk remains unclear, increasing the lipidation of apoE4 is an important therapeutic target as apoE4-lipoproteins are poorly lipidated compared to apoE3-lipoproteins. ACAT (acyl-CoA: cholesterol-acyltransferase) catalyzes the formation of intracellular cholesteryl-ester droplets, reducing the intracellular free cholesterol (FC) pool. Thus, inhibiting ACAT increases the FC pool and facilitates lipid secretion to extracellular apoE-containing lipoproteins. Previous studies using commercial ACAT inhibitors, including avasimibe (AVAS), as well as ACAT-knock out (KO) mice, exhibit reduced AD-like pathology and amyloid precursor protein (APP) processing in familial AD (FAD)-transgenic (Tg) mice. However, the effects of AVAS with human apoE4 remain unknown. In vitro, AVAS induced apoE efflux at concentrations of AVAS measured in the brains of treated mice. AVAS treatment of male E4FAD-Tg mice (5xFAD

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoprotein E3Apolipoprotein E4Apolipoproteins ECholesterolHumansMaleMiceMice, KnockoutMice, TransgenicAmyloid beta-PeptidesApolipoprotein E3Apolipoprotein E4Apolipoproteins ECholesterolACAT-1Alzheimer’s diseaseAPOE4APP processingNeuroinflammationOligomeric Aβ

Identifiers

PMID37157042
PMCPMC10457278
OpenAlexW4375955184

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.