α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson's Disease Pathogenesis

被引：25

作者：

Butkovich, Laura M. ^{[1
]}

Houser, Madelyn C. ^{[1
]}

Tansey, Malu G. ^{[1
]}

机构：

[1] Emory Univ, Sch Med, Dept Physiol, Tansey Lab, Atlanta, GA 30322 USA

来源：

FRONTIERS IN NEUROSCIENCE | 2018年 / 12卷

关键词：

alpha-synuclein; locus coeruleus; Parkinson's disease; neuroinflammation; norepinephrine; immune cell; SLEEP BEHAVIOR DISORDER; DOPAMINE-BETA-HYDROXYLASE; NEUROGENIC ORTHOSTATIC HYPOTENSION; ADRENERGIC-RECEPTOR ACTIVATION; COLLAGEN-INDUCED ARTHRITIS; NECROSIS-FACTOR-ALPHA; REGULATORY T-CELLS; BRAIN-STEM NUCLEI; LOCUS-COERULEUS; SUBSTANTIA-NIGRA;

D O I：

10.3389/fnins.2018.00626

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

alpha-synuclein (alpha-syn) pathology and loss of noradrenergic neurons in the locus coeruleus (LC) are among the most ubiquitous features of Parkinson's disease (PD). While noradrenergic dysfunction is associated with non-motor symptoms of PD, preclinical research suggests that the loss of LC norepinephrine (NE), and subsequently its immune modulatory and neuroprotective actions, may exacerbate or even accelerate disease progression. In this review, we discuss the mechanisms by which alpha-syn pathology and loss of central NE may directly impact brain health by interrupting neurotrophic factor signaling, exacerbating neuroinflammation, and altering regulation of innate and adaptive immune cells.

引用

页数：13

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