Microglia replacement therapy for neurological diseases: a mechanistic perspective focused on the Golgi apparatus.
10 affiliations
- 1Department of Health Management, The Third Xiangya Hospital, Central South University, Changsha, China.
- 2Postdoctoral Station of Clinical Medicine, The Third Xiangya Hospital, Central South University, Changsha, China.
- 3School of Computer Science and Engineering, Central South University, Changsha, 410083, China.
- 4Department of Neurology, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
- 5Department of Neurology, The Third Xiangya Hospital, Central South University, Changsha, 410013, China. [email protected].
- 6Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, China. [email protected].
- 7Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, 410008, China. [email protected].
- 8National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, China. [email protected].
- 9Hunan International Scientific and Technological Cooperation Base of Neurodegenerative and Neurogenetic Diseases, Changsha, 410008, China. [email protected].
- 10National International Collaborative Research Center for Medical Metabolomics, Central South University, Changsha, 410008, China. [email protected].
Abstract
Microglia-mediated neuroinflammation is a pathological hallmark of various neurological diseases. Altered microglial states promote disease progression and induce an inflammatory microenvironment. Therapies aimed at modulating microglial signaling demonstrate certain therapeutic effects, yet their efficacy is limited in terms of durability and may sometimes have a double-edged impact. This is presumably because disease-associated microglial dysfunction stems from its multi-layered and self-reinforcing mechanisms. Microglia replacement therapy has emerged as an approach that first depletes resident microglia and then either directly transplants microglia or induces the repopulation/engraftment of microglia in the niche. This strategy shows therapeutic effects in pre-clinical models, but the intracellular mechanisms supporting its therapeutic durability remain unclear. In this review, we present a Golgi-centered, evidence-stratified perspective, proposing that Golgi homeostasis may represent a candidate organelle-level checkpoint for post-replacement microglial state stability. As a structural and signaling hub that integrates receptor maturation, innate immune signaling, lipid handling, and secretory competence, the Golgi apparatus provides a testable framework for understanding how intracellular organization may contribute to durable microglial recalibration after replacement. Direct evidence linking microglial replacement to Golgi homeostasis remains limited, and whether Golgi recovery contributes to therapeutic durability requires future validation.
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BibTeX
@article{deng2026microglia,
title = {{Microglia replacement therapy for neurological diseases: a mechanistic perspective focused on the Golgi apparatus.}},
author = {Shuwen Deng and Rong Qiu and Jinze Wu and Hong Jiang},
journal = {Journal of neuroinflammation},
year = {2026},
month = aug,
doi = {10.1186/s12974-026-03996-9},
url = {https://europepmc.org/article/MED/42958291},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Microglia replacement therapy for neurological diseases: a mechanistic perspective focused on the Golgi apparatus.
AU - Shuwen Deng
AU - Rong Qiu
AU - Jinze Wu
AU - Hong Jiang
PY - 2026
DA - 2026/08/03
JO - Journal of neuroinflammation
DO - 10.1186/s12974-026-03996-9
UR - https://europepmc.org/article/MED/42958291
AB - Microglia-mediated neuroinflammation is a pathological hallmark of various neurological diseases. Altered microglial states promote disease progression and induce an inflammatory microenvironment. Therapies aimed at modulating microglial signaling demonstrate certain therapeutic effects, yet their efficacy is limited in terms of durability and may sometimes have a double-edged impact. This is presumably because disease-associated microglial dysfunction stems from its multi-layered and self-reinforcing mechanisms. Microglia replacement therapy has emerged as an approach that first depletes resident microglia and then either directly transplants microglia or induces the repopulation/engraftment of microglia in the niche. This strategy shows therapeutic effects in pre-clinical models, but the intracellular mechanisms supporting its therapeutic durability remain unclear. In this review, we present a Golgi-centered, evidence-stratified perspective, proposing that Golgi homeostasis may represent a candidate organelle-level checkpoint for post-replacement microglial state stability. As a structural and signaling hub that integrates receptor maturation, innate immune signaling, lipid handling, and secretory competence, the Golgi apparatus provides a testable framework for understanding how intracellular organization may contribute to durable microglial recalibration after replacement. Direct evidence linking microglial replacement to Golgi homeostasis remains limited, and whether Golgi recovery contributes to therapeutic durability requires future validation.
SN - 1742-2094
ER -