Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders.

Abstract

Reactive species play an important role in physiological functions. Overproduction of reactive species, notably reactive oxygen (ROS) and nitrogen (RNS) species along with the failure of balance by the body's antioxidant enzyme systems results in destruction of cellular structures, lipids, proteins, and genetic materials such as DNA and RNA. Moreover, the effects of reactive species on mitochondria and their metabolic processes eventually cause a rise in ROS/RNS levels, leading to oxidation of mitochondrial proteins, lipids, and DNA. Oxidative stress has been considered to be linked to the etiology of many diseases, including neurodegenerative diseases (NDDs) such as Alzheimer diseases, Amyotrophic lateral sclerosis, Friedreich's ataxia, Huntington's disease, Multiple sclerosis, and Parkinson's diseases. In addition, oxidative stress causing protein misfold may turn to other NDDs include Creutzfeldt-Jakob disease, Bovine Spongiform Encephalopathy, Kuru, Gerstmann-Straussler-Scheinker syndrome, and Fatal Familial Insomnia. An overview of the oxidative stress and mitochondrial dysfunction-linked NDDs has been summarized in this review.

• Authors: Md Torequl Islam
• Journal: Neurological research (Neurol Res) Vol. 39 Issue 1 Pg. 73-82 (Jan 2017) ISSN: 1743-1328 [Electronic] England
• PMID: 27809706 (Publication Type: Journal Article, Review)

Topics

• Animals
• Humans
• Mitochondrial Diseases (etiology)
• Neurodegenerative Diseases (complications)
• Oxidative Stress (physiology)