Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 28, Issue 12, Pages 879-892Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2017.10.004
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Funding
- NIH [P01 HD29587, DP1 DA041722, R01 NS086890, R01 AG056259, RF1 AG057409]
- NINDS [P30 NS076411]
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The prevalence of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), is currently a major public health concern due to the lack of efficient disease-modifying therapeutic options. Recent evidence suggests that mitochondrial dysfunction and nitrosative/oxidative stress are key common mediators of pathogenesis. In this review, we highlight molecular mechanisms linking NO-dependent post-translational modifications, such as cysteine S-nitrosylation and tyrosine nitration, to abnormal mitochondrial metabolism. We further discuss the hypothesis that pathological levels of NO compromise brain energy metabolism via aberrant S-nitrosylation of key enzymes in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation, contributing to neurodegenerative conditions. A better understanding of these pathophysiological events may provide a potential pathway for designing novel therapeutics to ameliorate neurodegenerative disorders.
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