The role of Toll-like receptors and neuroinflammation in Parkinson’s disease

神经炎症 黑质 小胶质细胞 神经退行性变 促炎细胞因子 帕金森病 神经科学 先天免疫系统 炎症 TLR2型 医学 免疫系统 免疫学 多巴胺能 生物 多巴胺 病理 疾病
作者
Arash Heidari,Niloufar Yazdanpanah,Nima Rezaei
出处
期刊:Journal of Neuroinflammation [Springer Nature]
卷期号:19 (1) 被引量:97
标识
DOI:10.1186/s12974-022-02496-w
摘要

Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder, characterized by motor and non-motor symptoms, significantly affecting patients' life. Pathologically, PD is associated with the extensive degeneration of dopaminergic neurons in various regions of the central nervous system (CNS), specifically the substantia nigra. This neuronal loss is accompanied by the aggregation of misfolded protein, named α-synuclein.Recent studies detected several clues of neuroinflammation in PD samples using postmortem human PD brains and various PD animal models. Some evidence of neuroinflammation in PD patients included higher levels of proinflammatory cytokines in serum and cerebrospinal fluid (CSF), presence of activated microglia in various brain regions such as substantia nigra, infiltration of peripheral inflammatory cells in affected brain regions, and altered function of cellular immunity like monocytes phagocytosis defects. On the other side, Toll-like receptors (TLRs) are innate immune receptors primarily located on microglia, as well as other immune and non-immune cells, expressing pivotal roles in recognizing exogenous and endogenous stimuli and triggering inflammatory responses. Most studies indicated an increased expression of TLRs in the brain and peripheral blood cells of PD samples. Besides, this upregulation was associated with excessive neuroinflammation followed by neurodegeneration in affected regions. Therefore, evidence proposed that TLR-mediated neuroinflammation might lead to a dopaminergic neural loss in PD patients. In this regard, TLR2, TLR4, and TLR9 have the most prominent roles.Although the presence of inflammation in acute phases of PD might have protective effects concerning the clearance of α-synuclein and delaying the disease advancement, the chronic activation of TLRs and neuroinflammation might lead to neurodegeneration, resulting in the disease progression. Therefore, this study aimed to review additional evidence of the contribution of TLRs and neuroinflammation to PD pathogenesis, with the hope that TLRs could serve as novel disease-modifying therapeutic targets in PD patients in the future.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
王紫绯发布了新的文献求助10
刚刚
汉堡包应助luha采纳,获得10
刚刚
顺利萧完成签到,获得积分10
刚刚
马俣辰发布了新的文献求助20
1秒前
1秒前
Jennifer完成签到,获得积分10
2秒前
2秒前
2秒前
hl_sci完成签到,获得积分10
2秒前
3秒前
李爱国应助yan采纳,获得10
4秒前
afeiwoo发布了新的文献求助10
5秒前
YY关闭了YY文献求助
6秒前
xh发布了新的文献求助10
6秒前
6秒前
善人发布了新的文献求助10
7秒前
英俊的铭应助Labman采纳,获得10
8秒前
8秒前
小蘑菇应助科研糊涂神采纳,获得10
8秒前
三侠发布了新的文献求助10
9秒前
淡然的怜容完成签到,获得积分10
10秒前
wanci应助Ella采纳,获得10
11秒前
馒头发布了新的文献求助10
11秒前
努力加油煤老八完成签到 ,获得积分10
12秒前
13秒前
13秒前
liangjiangbo完成签到,获得积分10
13秒前
小明发布了新的文献求助10
14秒前
Jasper应助xh采纳,获得10
15秒前
16秒前
屁颠屁颠_狼完成签到 ,获得积分0
16秒前
小艾完成签到,获得积分10
17秒前
18秒前
QF发布了新的文献求助10
18秒前
20秒前
珊珊发布了新的文献求助10
23秒前
24秒前
虚幻的溪灵完成签到,获得积分10
27秒前
新青年完成签到,获得积分0
27秒前
28秒前
高分求助中
The late Devonian Standard Conodont Zonation 2000
The Lali Section: An Excellent Reference Section for Upper - Devonian in South China 1500
Nickel superalloy market size, share, growth, trends, and forecast 2023-2030 1000
Smart but Scattered: The Revolutionary Executive Skills Approach to Helping Kids Reach Their Potential (第二版) 1000
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 800
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 800
A new species of Coccus (Homoptera: Coccoidea) from Malawi 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3245628
求助须知:如何正确求助?哪些是违规求助? 2889319
关于积分的说明 8257790
捐赠科研通 2557674
什么是DOI,文献DOI怎么找? 1386378
科研通“疑难数据库(出版商)”最低求助积分说明 650327
邀请新用户注册赠送积分活动 626633