February 26, 2015

Review by Fischer and Maier accepted in Oxidative Stress and Cellular Longevity

Interrelation of oxidative stress and inflammation in neurodegenerative disease: role of TNF

Review accepted in Oxidative Stress and Cellular Longevity:

Interrelation of oxidative stress and inflammation in neurodegenerative disease: role of TNF

Roman Fischer and Olaf Maier

Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany

 

Abstract

Neuroinflammation and mitochondrial dysfunction are common features of chronic neurodegenerative diseases of the central nervous system. Both conditions can lead to increased oxidative stress by excessive release of harmful reactive oxygen and nitrogen species (ROS and RNS), which further promote neuronal damage and subsequent inflammation resulting in a feed forward loop of neurodegeneration. The cytokine tumor necrosis factor (TNF), a master regulator of the immune system, plays an important role in the propagation of inflammation due to the activation and recruitment of immune cells via its receptor TNF receptor 1 (TNFR1). Moreover, TNFR1 can directly induce oxidative stress by the activation of ROS and RNS producing enzymes. Both, TNF induced oxidative stress and inflammation interact and cooperate to promote neurodegeneration. However, TNF plays a dual role in neurodegenerative disease, since stimulation via its second receptor, TNFR2, is neuroprotective and promotes tissue regeneration. Here we review the interrelation of oxidative stress and inflammation in the two major chronic neurodegenerative diseases, Alzheimer’s and Parkinson’s disease, and discuss the dual role of TNF in promoting neurodegeneration and tissue regeneration via its two receptors.

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