Cerebral sterile inflammation in neurodegenerative diseases
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(2020) 40:28
Inflammation and Regeneration
REVIEW
Open Access
Cerebral sterile inflammation in neurodegenerative diseases Kento Otani1,2 and Takashi Shichita1,3*
Abstract Therapeutic strategies for regulating neuroinflammation are expected in the development of novel therapeutic agents to prevent the progression of central nervous system (CNS) pathologies. An understanding of the detailed molecular and cellular mechanisms of neuroinflammation in each CNS disease is necessary for the development of therapeutics. Since the brain is a sterile organ, neuroinflammation in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) is triggered by cerebral cellular damage or the abnormal accumulation of inflammatogenic molecules in CNS tissue through the activation of innate and acquired immunity. Inflammation and CNS pathologies worsen each other through various cellular and molecular mechanisms, such as oxidative stress or the accumulation of inflammatogenic molecules induced in the damaged CNS tissue. In this review, we summarize the recent evidence regarding sterile immune responses in neurodegenerative diseases. Keywords: Neuroinflammation, Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis
Background Inflammation is an important biological process in the pathologies of CNS. The cell death induced by various brain pathologies such as neurodegenerative diseases, ischemia, hemorrhage, trauma, and so on triggers inflammation. Conversely, inflammation in the peripheral organs or central nervous system can induce brain cell death. Some reports have demonstrated the relationships between the intestinal microbiome and cerebral inflammation. For example, gut microbiome dysbiosis is related to the dysregulation of the gut-brain axis and supports the neuroinflammatory responses in the brain, leading to the enhanced pathophysiology of AD [1]. Inflammation and brain pathologies thus worsen each other through various cellular and molecular mechanisms, leading to a poor prognosis in terms of quality of life. The brain consists of various cells, including neurons, astrocytes, microglia, oligodendrocytes, and endothelial * Correspondence: [email protected] 1 Stroke Renaissance Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan 3 Precursory Research for Innovative Medical Care (PRIME), Japan Agency for Medical Research and Development (AMED), Tokyo 100-0004, Japan Full list of author information is available at the end of the article
cells. If cerebral pathologies exist, all of these kinds of cells are implicated in cerebral inflammation. Neurons, astrocytes, and oligodendrocytes are activated by pathological insults and can become inflammatogenic factors. For example, oxidative stress within brain cells causes neurodegeneration in AD, PD, and ALS [2]. Brain trauma or ischemia induces oxidative stress in brain cells [3]. These oxidative stresses induce the production of reactive oxygen species (ROS) from
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