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Nitric oxide-mediated oxidative damage and the progressive demise of motor neurons in ALS

Content Provider	PubMed Central
Author	Drechsel, Derek A. Estévez, Alvaro G. Barbeito, Luis Beckman, Joseph S.
Abstract	Oxidative damage is a common and early feature of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders. Dr. Mark Smith and his colleagues have built the case for oxidative stress being a primary progenitor rather than a secondary end-stage epiphenomenon of neurodegeneration. They proposed that reactive oxygen species contribute to the “age-related cascade of neurodegeneration” whereby accumulative oxidative damage with age promotes other characteristic pathological changes in afflicted brain regions, including protein aggregation, metabolic deficiencies, and inflammation. Nitric oxide (NO) likely plays a critical role in this age-related cascade. NO is a major signaling molecule produced in the central nervous system (CNS) to modulate neurological activity through stimulating cyclic GMP synthesis. However, the same physiological concentrations of NO relevant in cellular signaling may also initiate and amplify oxidative damage by diffusion-limited reactions with superoxide (O2 ·−) to produce peroxynitrite (ONOO−). This is perhaps best illustrated in ALS where physiological levels of NO promote survival of motor neurons, but the same concentrations can stimulate motor neuron apoptosis and glial cell activation under pathological conditions. While these changes represent a complex mechanism involving multiple cell types in the pathogenesis of ALS, they also reveal general processes underlying neurodegeneration.
Related Links	http://dx.doi.org/10.1007/s12640-012-9322-y
Ending Page	264
Page Count	14
Starting Page	251
File Format	PDF
ISSN	10298428
e-ISSN	14763524
Journal	Neurotoxicity research
Issue Number	4
Volume Number	22
Language	English
Publisher Date	2012-11-01
Access Restriction	Open
Subject Keyword	Toxicology Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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