APOE4 drives neuroinflammation and lipid dysbiosis in Alzheimer's disease by modulating lipid compositions and cell adhesion molecules in brain‐derived extracellular vesicles
Our comprehensive analysis suggested that AD APOE4/4 BDEV may enhance transmissibility of tau pathology and neuroinflammation via enriched pro-inflammatory PUFA and cell adhesion molecules. Targeting these pathways presents a promising therapeutic strategy to mitigate disease progression, particularly in APOE4 individuals.
Authors
- Tadafumi C. Ikezu (ORCID: https://orcid.org/0000-0002-3511-6009)
- Tsuneya Ikezu (ORCID: https://orcid.org/0000-0002-3979-8596)
- Dennis W. Dickson (ORCID: https://orcid.org/0000-0001-7189-7917)
- Michael DeTure (ORCID: https://orcid.org/0000-0002-4363-1262)
- Ziteng Zhang
- Takahisa Kanekiyo (ORCID: https://orcid.org/0000-0001-6751-9374)
- Yang You (ORCID: https://orcid.org/0000-0002-5282-375X)
- Hanmei Bao (ORCID: https://orcid.org/0000-0003-0524-0719)
- Clara Scholes
- Seiko Ikezu (ORCID: https://orcid.org/0000-0001-9879-730X)
- Junmin Peng
- J. W Ellison
- Xianlin Han
- Bridgette Melvin
- Arun Reddy Ravula
- Kaiwen Yu
Institutions
- St. Jude Children's Research Hospital (US)
- The University of Texas at San Antonio Health Science Center (US)
- Jacksonville College (US)
- WinnMed (US)
- Mayo Clinic in Florida (US)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1002/alz70855_105076
- Primary Topic
- Extracellular vesicles in disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00