Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
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(2020) 9:42
REVIEW
Open Access
Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes Hyuk Sung Kwon1 and Seong-Ho Koh1,2*
Abstract Neuroinflammation is associated with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Microglia and astrocytes are key regulators of inflammatory responses in the central nervous system. The activation of microglia and astrocytes is heterogeneous and traditionally categorized as neurotoxic (M1-phenotype microglia and A1-phenotype astrocytes) or neuroprotective (M2-phenotype microglia and A2phenotype astrocytes). However, this dichotomized classification may not reflect the various phenotypes of microglia and astrocytes. The relationship between these activated glial cells is also very complicated, and the phenotypic distribution can change, based on the progression of neurodegenerative diseases. A better understanding of the roles of microglia and astrocytes in neurodegenerative diseases is essential for developing effective therapies. In this review, we discuss the roles of inflammatory response in neurodegenerative diseases, focusing on the contributions of microglia and astrocytes and their relationship. In addition, we discuss biomarkers to measure neuroinflammation and studies on therapeutic drugs that can modulate neuroinflammation. Keywords: Neuroinflammation, Neurodegenerative diseases, Microglia, Astrocytes
Background With the increase in life expectancy, the global socioeconomic impact of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), is increasing considerably [1]. However, the pathological mechanisms underlying neurodegenerative diseases are not fully understood. Several factors including genetic, environmental, and endogenous factors are involved. Abnormal protein dynamics, oxidative stress with reactive oxygen species, mitochondrial dysfunction, DNA damage, dysfunction of neurotrophins, and neuroinflammatory processes are considered to be common pathophysiological * Correspondence: [email protected] 1 Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea 2 Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Republic of Korea
mechanisms [2]. Neuroinflammation is a defense mechanism that initially protects the brain by removing or inhibiting diverse pathogens [3]. This inflammatory response can have beneficial effects by promoting tissue repair and removing cellular debris. Sustained inflammatory responses, however, are detrimental, and they inhibit regeneration [4, 5]. Inflammatory stimulation can persist due to endogenous (e.g., genetic mutation and protein aggregation) or environmental (e.g., infection, trauma, and drugs) factors [6, 7]. The persistent inflammatory responses involve microglia and astrocytes and can lead to neurodegenerative diseases [4]. Two categories of cells populat
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