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Review Article

Revisiting the Mitochondrial Function and Communication in Neurodegenerative Diseases

Author(s): Nitu L. Wankhede, Mayur B. Kale*, Mohit D. Umare, Sanket Lokhande, Aman B. Upaganlawar, Pranay Wal, Brijesh G. Taksande, Milind J. Umekar, Prasanna Shama Khandige, Bhupendra Singh, Vandana Sadananda, Seema Ramniwas and Tapan Behl*

Volume 30, Issue 12, 2024

Published on: 12 March, 2024

Page: [902 - 911] Pages: 10

DOI: 10.2174/0113816128286655240304070740

Price: $65

Abstract

Neurodegenerative disorders are distinguished by the progressive loss of anatomically or physiologically relevant neural systems. Atypical mitochondrial morphology and metabolic malfunction are found in many neurodegenerative disorders. Alteration in mitochondrial function can occur as a result of aberrant mitochondrial DNA, altered nuclear enzymes that interact with mitochondria actively or passively, or due to unexplained reasons. Mitochondria are intimately linked to the Endoplasmic reticulum (ER), and ER-mitochondrial communication governs several of the physiological functions and procedures that are disrupted in neurodegenerative disorders. Numerous researchers have associated these disorders with ER-mitochondrial interaction disturbance. In addition, aberrant mitochondrial DNA mutation and increased ROS production resulting in ionic imbalance and leading to functional and structural alterations in the brain as well as cellular damage may have an essential role in disease progression via mitochondrial malfunction. In this review, we explored the evidence highlighting the role of mitochondrial alterations in neurodegenerative pathways in most serious ailments, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD).

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