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

Thirunavukkarasu Velusamy, Archana S. Panneerselvam, Meera Purushottam, Muthuswamy Anusuyadevi, Pramod Kumar Pal, Sanjeev Jain, Musthafa Mohamed Essa, Gilles J. Guillemin*, Mahesh Kandasamy

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

41 Citations (Scopus)

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.

Original languageEnglish
Article number3279061
JournalOxidative Medicine and Cellular Longevity
Volume2017
DOIs
Publication statusPublished - 2017

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Cell Biology

Fingerprint

Dive into the research topics of 'Protective Effect of Antioxidants on Neuronal Dysfunction and Plasticity in Huntington's Disease'. Together they form a unique fingerprint.

Cite this