Aged Microglia in Neurodegenerative Diseases: Microglia Lifespan and Culture Methods

Microglia have been recognized as macrophages of the central nervous system (CNS) that are regarded as a culprit of neuroinflammation in neurodegenerative diseases. Thus, microglia have been considered as a cell that should be suppressed for maintaining a homeostatic CNS environment. However, microg...

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Published inFrontiers in aging neuroscience Vol. 13; p. 766267
Main Authors Yoo, Hyun-Jung, Kwon, Min-Soo
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 05.01.2022
Frontiers Media S.A
Subjects
Aging
Alzheimer's disease
Cell culture
Central nervous system
Cytokines
Growth factors
Homeostasis
Inflammation
Kinases
Life span
Macrophages
Microglia
microglia culture
microglia lifespan
Morphology
Neurodegenerative diseases
Neurodevelopmental disorders
Neuroscience
Ontogeny
neurodegenerative diseases
microglia culture
aging
microglia
microglia lifespan
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Summary:Microglia have been recognized as macrophages of the central nervous system (CNS) that are regarded as a culprit of neuroinflammation in neurodegenerative diseases. Thus, microglia have been considered as a cell that should be suppressed for maintaining a homeostatic CNS environment. However, microglia ontogeny, fate, heterogeneity, and their function in health and disease have been defined better with advances in single-cell and imaging technologies, and how to maintain homeostatic microglial function has become an emerging issue for targeting neurodegenerative diseases. Microglia are long-lived cells of yolk sac origin and have limited repopulating capacity. So, microglial perturbation in their lifespan is associated with not only neurodevelopmental disorders but also neurodegenerative diseases with aging. Considering that microglia are long-lived cells and may lose their functional capacity as they age, we can expect that aged microglia contribute to various neurodegenerative diseases. Thus, understanding microglial development and aging may represent an opportunity for clarifying CNS disease mechanisms and developing novel therapies.
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Edited by: Ferit Tuzer, Drexel University, United States
This article was submitted to Cellular and Molecular Mechanisms of Brain-aging, a section of the journal Frontiers in Aging Neuroscience
Reviewed by: Kathryn G. Todd, University of Alberta, Canada; Jenna Ziebell, University of Tasmania, Australia
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2021.766267