Noradrenergic regulation of inflammatory gene expression in brain

It is now well accepted that inflammatory events contribute to the pathogenesis of numerous neurological disorders, including multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease, and AID’s dementia. Whereas inflammation in the periphery is subject to rapid down regulation by incre...

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Bibliographic Details
Published in:Neurochemistry international 2002-11, Vol.41 (5), p.357-365
Main Authors: Feinstein, Douglas L, Heneka, Michael T, Gavrilyuk, Vitaliy, Russo, Cinzia Dello, Weinberg, Guy, Galea, Elena
Format: Article
Language:English
Subjects:
Alzheimer’s disease
Animals
Astrocyte
Brain Chemistry - genetics
Brain Chemistry - physiology
Denervation
Humans
Immunosuppression
Inflammation - genetics
Inflammation - pathology
Interleukin
Microglia
Multiple sclerosis
Nitric oxide
Noradrenaline
Norepinephrine - physiology
Plaque, Amyloid - pathology
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Summary:It is now well accepted that inflammatory events contribute to the pathogenesis of numerous neurological disorders, including multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease, and AID’s dementia. Whereas inflammation in the periphery is subject to rapid down regulation by increases in anti-inflammatory molecules and the presence of scavenging soluble cytokine receptors, the presence of an intact blood–brain barrier may limit a similar autoregulation from occurring in brain. Mechanisms intrinsic to the brain may provide additional immunomodulatory functions, and whose dysregulation could contribute to increased inflammation in disease. The findings that noradrenaline (NA) reduces cytokine expression in microglial, astroglial, and brain endothelial cells in vitro, and that modification of the noradrenergic signaling system occurs in some brain diseases having an inflammatory component, suggests that NA could act as an endogenous immunomodulator in brain. Furthermore, accumulating studies indicate that modification of the noradrenergic signaling system occurs in some neurodiseases. In this article, we will briefly review the evidence that NA can modulate inflammatory gene expression in vitro, summarize data supporting a similar immunomodulatory role in brain, and present recent data implicating a role for NA in attenuating the cortical inflammatory response to beta amyloid protein.
ISSN:0197-0186
1872-9754
DOI:10.1016/S0197-0186(02)00049-9