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Redox Signaling in Neurotransmission and Cognition During Aging

Published on May 31, 2017in Antioxidants & Redox Signaling5.828
· DOI :10.1089/ars.2017.7111
Ashok Kumar26
Estimated H-index: 26
,
Brittney Yegla1
Estimated H-index: 1
,
Thomas C. Foster36
Estimated H-index: 36
Abstract
Abstract Significance: Oxidative stress increases in the brain with aging and neurodegenerative diseases. Previous work emphasized irreversible oxidative damage in relation to cognitive impairment. This research has evolved to consider a continuum of alterations, from redox signaling to oxidative damage, which provides a basis for understanding the onset and progression of cognitive impairment. This review provides an update on research linking redox signaling to altered function of neural circuits involved in information processing and memory. Recent Advances: Starting in middle age, redox signaling triggers changes in nervous system physiology described as senescent physiology. Hippocampal senescent physiology involves decreased cell excitability, altered synaptic plasticity, and decreased synaptic transmission. Recent studies indicate N-methyl-d-aspartate and ryanodine receptors and Ca2+ signaling molecules as molecular substrates of redox-mediated senescent physiology. Critical Issues: We review redox...
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