SLC38A9 Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease-Related Protein Deposition.
Overview
- Department of Geriatrics, Huadong Hospital Affiliated to Fudan University, Shanghai, China
- Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai, China
- Shanghai Institute of Geriatrics and Gerontology, Shanghai, China
- Department of General Practice, Huadong Hospital Affiliated to Fudan University, Shanghai, China
Abstract
Aims: Impaired autophagy‐mediated clearance of Alzheimer's disease (AD)‐related proteins is a critical event in AD pathogenesis. SLC38A9, a member of the Solute Carrier 38 family, acts as an arginine sensor and plays an important role in regulating autophagy. Although the activation of autophagy regulated by the SLC38A9 may have a mitigating effect on AD, this aspect still awaits further exploration.
Methods: APP/
Results: We show that decreasing SLC38A9 could promote the hippocampal neuronal autophagic clearance of AD‐related proteins, reduce neuronal apoptosis, and improve cognitive function.
Conclusion: Our results demonstrate SLC38A9 is involved in AD‐related pathology and its cognitive impairment, and may offer new therapeutic targets to AD.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
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Data
Datasets cited
- geo:GSE48350, at NCBI GEO; found in the text, “Increased Expression of SLC38A9 in Hippocampus…”
Data Availability Statement
The datasets used and/
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 30 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 5 authors, 4 keywords, 13 MeSH terms, 4 funders, 38 references.
Cite
This paper
Chen, Y., Ji, X., Zhao, J., Bao, Z., & Huang, Y. (2026). SLC38A9 Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease-Related Protein Deposition. CNS neuroscience & therapeutics, 32(3), e70823. https://
BibTeX
@article{chen2026slc38a9
author = {Chen, Yixin and Ji, Xueying and Zhao, Jiaxiu and Bao, Zhijun and Huang, Yiqin},
title = {{SLC38A9 Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease-Related Protein Deposition}},
journal = {CNS neuroscience \& therapeutics},
year = {2026},
month = mar,
volume = {32},
number = {3},
pages = {e70823},
publisher = {Wiley},
issn = {1755-5930},
doi = {10.1002/
url = {https://
pmid = {41811103},
pmcid = {PMC12977986}
}
RIS
TY - JOUR
AU - Chen, Yixin
AU - Ji, Xueying
AU - Zhao, Jiaxiu
AU - Bao, Zhijun
AU - Huang, Yiqin
TI - SLC38A9 Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease-Related Protein Deposition
T2 - CNS neuroscience & therapeutics
J2 - CNS Neurosci Ther
PY - 2026
DA - 2026/
VL - 32
IS - 3
SP - e70823
SN - 1755-5930
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
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