PINK1/Parkin in Neurodegenerative Disorders: Crosstalk Between Mitochondrial Stress and Neurodegeneration

PINK1/Parkin in Neurodegenerative Disorders: Crosstalk Between Mitochondrial Stress and Neurodegeneration

Mukesh Pandey (Department of Pharmaceutics, Delhi Institute of Pharmaceutical Sciences and Research, India), Shakir Saleem (Department of Public Health, College of Health Science, Saudi Electronic University, Riyadh, Saudi Arabia), Himani Nautiyal (Department of Pharmacology, Siddhartha Institute of Pharmacy, India), Faheem Hyder Pottoo (Department of Pharmacology, College of Clinical Pharmacy, Imam Abdulrahman Bin Faisal University, Saudi Arabia) and Md. Noushad Javed (School of Pharmaceutical Sciences, Apeejay Stya University, India)
Copyright: © 2020 |Pages: 20
DOI: 10.4018/978-1-7998-1317-0.ch011

Abstract

PTEN-induced kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase encoded by the PINK1 gene, is thought to protect cells from stress-induced mitochondrial dysfunction. The activity of PINK1 facilitates the binding of Parkin protein with depolarized mitochondria to induce autophagy. Mutations of PINK1causes a type of autosomal recessive early-onset Parkinson's disease. Cell depends on the surveillance systems or mechanisms like protein quality control to handle the alterations in the proteins that are induced because of these mutations. These mutant proteins are found to be pathogenic and are reported to be related to various neurodegenerative disorders. This chapter focuses on the role of PINK1/Parkin in mitochondria quality control and its subsequent effect in neurodegeneration.
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Protein Quality Control By Autophagy

Inside the cellular environment processes essential for the survival of the cells as well as the organism as a whole goes on continuously. These processes include energy generation mechanism, biological macromolecules utilization, synthesis of proteins, intercellular or intracellular transportation of essential molecules and new cells as well as new cell organelles generation. Sometimes these processes undergo alterations or deviations from the defined procedures or mechanism leading to the formation of defective end products of the process. It is necessary to remove such products for maintaining the hemostatic condition within the cell. The cell organelles also undergo wear and tear resulting in damage and these damaged ones are again needed to remove on an urgent basis to be replaced by the new or healthy ones. The process which ensures removal of such useless biological material or molecules is called autophagy.

Autophagy mechanism is accountable for removing dysfunctional proteins, unutilized biological macromolecules, damages or disfigured cell organelles, foreign biological material, and pathogens that invaded the cells. Different pathological proteins involved in neurodegeneration as shown in Table 1.

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