Cerebral sterile inflammation in neurodegenerative diseases

被引：33

作者：

Otani, Kento ^{[1
,2
,3
]}

Shichita, Takashi ^{[1
,4
]}

机构：

[1] Tokyo Metropolitan Inst Med Sci, Stroke Renaissance Project, Setagaya Ku, 2-1-6 Kamikitazawa, Tokyo 1568506, Japan

[2] Keio Univ, Fac Pharm, Div Biochem, Tokyo 1058512, Japan

[3] Keio Univ, Grad Sch Pharmaceut Sci, Tokyo 1058512, Japan

[4] Japan Agcy Med Res & Dev AMED, Precursory Res Innovat Med Care PRIME, Tokyo 1000004, Japan

来源：

INFLAMMATION AND REGENERATION | 2020年 / 40卷 / 01期

关键词：

Neuroinflammation; Alzheimer’ s disease; Parkinson’ Amyotrophic lateral sclerosis; AMYOTROPHIC-LATERAL-SCLEROSIS; FRONTOTEMPORAL LOBAR DEGENERATION; SYNUCLEIN ACTIVATES MICROGLIA; BLOOD-BRAIN-BARRIER; ALPHA-SYNUCLEIN; PARKINSONS-DISEASE; MOUSE MODEL; SIGNALING PATHWAY; OXIDATIVE STRESS; TIGHT JUNCTIONS;

D O I：

10.1186/s41232-020-00137-4

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页数：8

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