Abstract
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.
Highlights
Microglia were recognized as a type of connective tissue or passive bystander of the central nervous system (CNS) physiology for a century since their discovery by Pio del Rio Hortega in 1919
Microglia are defined as multifunctional cells that communicate with the peripheral system as well as other CNS cells, such as neurons, astrocytes, and oligodendrocytes, in physiological states
Highly pure microglia (CD11bhighCD45int) isolated from the human parietal cortex with the elimination of meningeal macrophages by fluorescence-activated cell sorting (FACS) indicated that microglia of physiologically aged mice do not recapitulate the effect of aging on human microglia, FIGURE 2 | In vitro microglial culture
Summary
Microglia were recognized as a type of connective tissue or passive bystander of the central nervous system (CNS) physiology for a century since their discovery by Pio del Rio Hortega in 1919. Another microglia-specific marker, TMEM119, plays a key role in the validation of the microglial cell model as a signature gene that is expressed only in adult microglia (Bennett et al, 2016). One of the main causes is associated with previous microglial markers such as Iba-1 and CD11b that cannot discriminate resident microglia from infiltrated monocytes/macrophages because microglia signature genes, including P2RY12 and TMEM119, were established after 2014 as mentioned above.
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