Main Article Content
Parkinson’s disease is one of the most common neurodegenerative diseases in the elderly. The motor symptoms occur predominantly due to substantial dopamine depletion, caused by degeneration of the dopaminergic neurons in substantia nigra pars compacta. Apoptosis has been implicated as the main mechanism of neuronal death in Parkinson’s disease. Apoptosis is mediated by a number of initiator and executioner caspases, and occurs via the intrinsic or extrinsic pathways. Activation of initiator caspase-9 mediates the intrinsic pathway—also called the mitochondria-mediated pathway. Alternatively, activation of initiator caspase-8 mediates the extrinsic apoptotic pathway—the cell death receptor–mediated pathway. Both initiator caspases converge onto a common pathway of executioner caspases, involving caspase-3 and caspase-6. Activation of the executioner caspases leads to the morphological features characteristic of apoptosis, such as DNA cleavage and its subsequent fragmentation. Proapoptotic factors, such as Bax, have been implicated in neuronal cell death in Parkinson’s disease, and there is evidence that both the intrinsic and extrinsic apoptotic pathways may play a role. This chapter provides an overview of apoptosis and its significance in Parkinson’s disease.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Copyright of individual chapters belongs to the respective authors. The authors grant unrestricted publishing and distribution rights to the publisher. The electronic versions of the chapters are published under Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Users are allowed to share and adapt the chapters for any non-commercial purposes as long as the authors and the publisher are explicitly identified and properly acknowledged as the original source. The books in their entirety are subject to copyright by the publisher. The reproduction, modification, republication and display of the books in their entirety, in any form, by anyone, for commercial purposes are strictly prohibited without the written consent of the publisher.