Protective Effect of Antioxidants on Neuronal Dysfunction and Plasticity in Huntington's Disease

Oxid Med Cell Longev. 2017:2017:3279061. doi: 10.1155/2017/3279061. Epub 2017 Jan 12.

Abstract

Huntington's disease (HD) is characterised by movement disorders, cognitive impairments, and psychiatric problems. The abnormal generation of reactive oxygen species and the resulting oxidative stress-induced mitochondrial damage in neurons upon CAG mutations in the HTT gene have been hypothesized as the contributing factors of neurodegeneration in HD. The potential use of antioxidants against free radical toxicity has been an emerging field in the management of ageing and many neurodegenerative disorders. Neural stem cells derived adult neurogenesis represents the regenerative capacity of the adult brain. The process of adult neurogenesis has been implicated in the cognitive functions of the brain and is highly modulated positively by different factors including antioxidants. The supportive role of antioxidants to reduce the severity of HD via promoting the functional neurogenesis and neuroprotection in the pathological adult brain has great promise. This review comprehends the recent studies describing the therapeutic roles of antioxidants in HD and other neurologic disorders and highlights the scope of using antioxidants to promote adult neurogenesis in HD. It also advocates a new line of research to delineate the mechanisms by which antioxidants promote adult neurogenesis in HD.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants
  • Humans
  • Huntington Disease / pathology
  • Huntington Disease / therapy*
  • Mice
  • Neurodegenerative Diseases / pathology
  • Neurodegenerative Diseases / therapy*
  • Oxidative Stress
  • Rats
  • Reactive Oxygen Species

Substances

  • Antioxidants
  • Reactive Oxygen Species