MITOCHONDRIA : AS A PROTAGONIST IN NEUROLOGICAL DISORDERS IN BRIEF OVERVIEW

Role of mitochondria in neurological disorders

Authors

  • Karthick Dharmalingam
  • Shailata Prisi Lady Hardinge Medical College
  • Sarita Choudhary

DOI:

https://doi.org/10.47743/jemb-2023-73

Keywords:

Antioxidants; Apoptosis; Mitochondrial DNA; Reactive Oxygen Species; Neuroinflammation; Neurological disorders.

Abstract

Neurological disorders pose a great burden in general health. It is not astounding that mitochondrial malfunction emerging as a leading factor in myriad of neurological disorders. Mitochondria are extremely active cell organelles performing various functions most importantly, providing ATP to sustain cellular processes. Mitochondrial dysfunction results in altered neuronal bioenergetics, redox equilibrium and dynamics of cell and acts as focal point of pathogenesis in many human diseases including neurological disorders. Mitochondrial dynamics regulates pathways involving oxidative stress and apoptosis. Often mitochondrial division imbalance and fusion leads to mitochondrial functional impairment. Extreme variations in mitochondrial fusion causes increased mutation rate which along with increased oxidative stress can facilitate development of various neurological disorders such as Parkinson’s disease, Alzheimer’s disease, Huntington’s diseases and so on. Mitochondria has a key role in regulation of apoptosis. Mitochondrial dysfunction and mutations can have deleterious effects on neuronal functioning as neurons have high energy demand with restricted regenerative potential. Certain neuroprotective agents restores the functions of mitochondria and acts therapeutic regimens of neurodegenerative diseases.

Published

2023-03-31 — Updated on 2023-09-18

How to Cite

Dharmalingam, K., Prisi, S., & Choudhary, S. (2023). MITOCHONDRIA : AS A PROTAGONIST IN NEUROLOGICAL DISORDERS IN BRIEF OVERVIEW: Role of mitochondria in neurological disorders. Journal of Experimental and Molecular Biology, 24(2), 115–130. https://doi.org/10.47743/jemb-2023-73