Revisiting the Mitochondrial Function and Communication in Neurodegenerative Diseases
- Authors: Wankhede N.1, Kale M.2, Umare M.1, Lokhande S.2, Upaganlawar A.3, Wal P.4, Taksande B.2, Umekar M.2, Khandige P.5, Singh B.6, Sadananda V.5, Ramniwas S.7, Behl T.8
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Affiliations:
- , Smt. Kishoritai Bhoyar College of Pharmacy
- , Smt Kishoritai Bhoyar College of Pharmacy
- , SNJBs Shriman Sureshdada Jain College of Pharmacy
- Department of Pharmacy, Pranveer Singh Institute of Technology
- Department of Conservative, Dentistry and Endodontics, AB Shetty Memorial Institute of Dental Sciences, NITTE (Deemed to be University)
- School of Pharmacy, Graphic Era Hill University
- University Centre for Research and Development, University of Biotechnolog, Chandigarh University
- Amity School of Pharmaceutical Sciences,, Amity University
- Issue: Vol 30, No 12 (2024)
- Pages: 902-911
- Section: Immunology, Inflammation & Allergy
- URL: https://snv63.ru/1381-6128/article/view/645516
- DOI: https://doi.org/10.2174/0113816128286655240304070740
- ID: 645516
Cite item
Full Text
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 Alzheimers disease (AD), Parkinsons disease (PD), and Huntingtons disease (HD).
About the authors
Nitu Wankhede
, Smt. Kishoritai Bhoyar College of Pharmacy
Email: info@benthamscience.net
Mayur Kale
, Smt Kishoritai Bhoyar College of Pharmacy
Author for correspondence.
Email: info@benthamscience.net
Mohit Umare
, Smt. Kishoritai Bhoyar College of Pharmacy
Email: info@benthamscience.net
Sanket Lokhande
, Smt Kishoritai Bhoyar College of Pharmacy
Email: info@benthamscience.net
Aman Upaganlawar
, SNJBs Shriman Sureshdada Jain College of Pharmacy
Email: info@benthamscience.net
Pranay Wal
Department of Pharmacy, Pranveer Singh Institute of Technology
Email: info@benthamscience.net
Brijesh Taksande
, Smt Kishoritai Bhoyar College of Pharmacy
Email: info@benthamscience.net
Milind Umekar
, Smt Kishoritai Bhoyar College of Pharmacy
Email: info@benthamscience.net
Prasanna Khandige
Department of Conservative, Dentistry and Endodontics, AB Shetty Memorial Institute of Dental Sciences, NITTE (Deemed to be University)
Email: info@benthamscience.net
Bhupendra Singh
School of Pharmacy, Graphic Era Hill University
Email: info@benthamscience.net
Vandana Sadananda
Department of Conservative, Dentistry and Endodontics, AB Shetty Memorial Institute of Dental Sciences, NITTE (Deemed to be University)
Email: info@benthamscience.net
Seema Ramniwas
University Centre for Research and Development, University of Biotechnolog, Chandigarh University
Email: info@benthamscience.net
Tapan Behl
Amity School of Pharmaceutical Sciences,, Amity University
Author for correspondence.
Email: info@benthamscience.net
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Supplementary files
