Role of Microglia in Neurological Disorders and Their Potentials as a Therapeutic Target.
Microglia are resident macrophage-like immune cells in the central nervous system (CNS) and play a vital role in both physiological and pathological conditions, including restoring the integrity of the CNS and promoting the progression of neurodegenerative disorders. Upon stimulation, microglia typically convert from a surveillant to an activated phenotype. The major function of microglia is to maintain homeostasis and normal function of the CNS, both during development and in response to CNS injury. Microglia regulate multiple aspects of inflammation, such as repair, cytotoxicity, regeneration, and immunosuppression due to their different kind of activation states or phenotypes. Although microglia are involved in almost all neurodegenerative disorders, the mechanisms for microglial activation and their potential contributions to neuronal degeneration remain a matter of intense debate. In inflammatory process of the CNS, polarized M1 microglia can produce proinflammatory cytokines, neurotoxic molecules, which contribute to dysfunction of neural network and promoting inflammation reaction, whereas polarized M2 microglia secrete antiinflammatory mediators and neurotrophic factors that are involved in restoring homeostasis. Modulation of microglial activation for therapeutic purposes might be realized via suppressing the deleterious effects of these cells, while simultaneously retaining their protective functions. Here, we summarize the functions of microglia and discuss dual role of microglia in neurodegenerative diseases as well as multiple sclerosis.
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China.
Li
L
Du
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China.
Ying
Y
Zhang
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China.
Yang
Y
Chen
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China.|Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden.
Jie
J
Zhu
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China. doctoryangyi@163.com.
Yi
Y
Yang
Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, Changchun, 130021, China. drzhl@hotmail.com.|Department of Life Sciences, the National Natural Science Foundation of China, Beijing, China. drzhl@hotmail.com.
Hong-Liang
0000-0002-2916-1014
HL
Zhang
D000818:Animals; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism*; D017628:Microglia / Q000187:drug effects / Q000502:physiology*; D009414:Nerve Growth Factors / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism; D009422:Nervous System Diseases / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000008:administration & dosage
D018836:Inflammation Mediators; D009414:Nerve Growth Factors; D018696:Neuroprotective Agents
Inflammation; M1/M2 polarization; Microglia; Microglial activation; Neurodegenerative disorders