Journal
INFLAMMATION AND REGENERATION
Volume 40, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s41232-020-00137-4
Keywords
Neuroinflammation; Alzheimer’ s disease; Parkinson’ s disease; Amyotrophic lateral sclerosis
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Funding
- PRIME from AMED [JP18gm5910023]
- Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT) [19H04765]
- JSPS KAKENHI [17H05096]
- Toray Science and Technology Grant
- Mitsubishi Foundation
- Naito Foundation
- MSD Life Science Foundation
- Senri Life Science Foundation
- Ono Medical Research Foundation
- Grants-in-Aid for Scientific Research [19H04765, 17H05096] Funding Source: KAKEN
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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.
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