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Molecular Chaperones in Neurodegeneration: Mechanisms of Regulation in Cellular Proteostasis

Molecular Chaperones in Neurodegeneration: Mechanisms of Regulation in Cellular Proteostasis

Mukesh Pandey, Jahangir Nabi, Nahida Tabassum, Faheem Hyder Pottoo, Renuka Khatik, Niyaz Ahmad
ISBN13: 9781799813170|ISBN10: 1799813177|EISBN13: 9781799813187
DOI: 10.4018/978-1-7998-1317-0.ch014
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MLA

Pandey, Mukesh, et al. "Molecular Chaperones in Neurodegeneration: Mechanisms of Regulation in Cellular Proteostasis." Quality Control of Cellular Protein in Neurodegenerative Disorders, edited by Md. Sahab Uddin and Ghulam Md. Ashraf, IGI Global, 2020, pp. 354-379. https://doi.org/10.4018/978-1-7998-1317-0.ch014

APA

Pandey, M., Nabi, J., Tabassum, N., Pottoo, F. H., Khatik, R., & Ahmad, N. (2020). Molecular Chaperones in Neurodegeneration: Mechanisms of Regulation in Cellular Proteostasis. In M. Uddin & G. Ashraf (Eds.), Quality Control of Cellular Protein in Neurodegenerative Disorders (pp. 354-379). IGI Global. https://doi.org/10.4018/978-1-7998-1317-0.ch014

Chicago

Pandey, Mukesh, et al. "Molecular Chaperones in Neurodegeneration: Mechanisms of Regulation in Cellular Proteostasis." In Quality Control of Cellular Protein in Neurodegenerative Disorders, edited by Md. Sahab Uddin and Ghulam Md. Ashraf, 354-379. Hershey, PA: IGI Global, 2020. https://doi.org/10.4018/978-1-7998-1317-0.ch014

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Abstract

Cellular chaperones are essential players to this protein quality control network that functions to prevent protein misfolding, refold misfolded proteins, or degrade them, thereby maintaining neuronal proteostasis. Moreover, overexpression of cellular chaperones is considered to inhibit protein aggregation and apoptosis in various experimental models of neurodegeneration. Alterations or downregulation of chaperone machinery by age-related decline, molecular crowding, or genetic mutations are regarded as key pathological hallmarks of neurodegenerative disorders like Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and Prion diseases. Therefore, chaperones may serve as potential therapeutic targets in these diseases. This chapter presents a generalized view of misfolding and aggregation of proteins in neurodegeneration and then critically analyses some of the known cellular chaperones and their role in several neurodegenerative disorders.

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