Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF

By Roman Fischer, O. Maier. Oxidative Medicine and Cellular Longevity, 2015

697 citations recorded by the source corpus.

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.

Subfields: Complementary and alternative medicine, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/4e9ef67dbbde3a0c6fd197d4a7b532e9595a059d

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Citations in the corpus

• Reactive Oxygen Species: Drivers of Physiological and Pathological Processes (2020, neutral): “106,107 Dysregulation of these processes elicits inflammatory diseases and cancer.”
• Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease (2019, background): “Endothelial dysfunction has been demonstrated in aging retinal vessels [42] and also implicated as a contributor in neurodegenerative disease [43, 44].”