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Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders

Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders
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Author(s): Sonia Sharma (Khalsa College, India), Paramjeet Kaur (Khalsa College, India), Shallina Gupta (Khalsa College, India)and Sushant Sharma (University of KwaZulu-Natal, South Africa)
Copyright: 2019
Pages: 27
Source title: Handbook of Research on Critical Examinations of Neurodegenerative Disorders
Source Author(s)/Editor(s): Md. Sahab Uddin (Southeast University, Bangladesh)and Md. Shah Amran (University of Dhaka, Bangladesh)
DOI: 10.4018/978-1-5225-5282-6.ch005

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Abstract

Neurodegenerative disorders (NDs) are characterized by dysfunction and loss of neurons associated with altered proteins that accumulate in the human brain and peripheral organs. Mitochondrial and Golgi apparatus (GA) dysfunctions are supposed to be responsible for various NDs. Damaged mitochondria do not produce sufficient adenosine triphosphate (ATP) and produce reactive oxygen species (ROS) and pro-apoptotic factors. Mitochondrial dysfunctions may be caused by various factors such as environmental causes, mutations in both nuclear or mitochondrial deoxyribonucleic acid (DNA), that code many mitochondrial components. Three factors that are mainly responsible for the morphological changes in GA are certain pathological conditions, drugs, and over expression of Golgi associated proteins. In this chapter, common aspects of mitochondrial and GA dysfunction concerned about NDs are summarized and described for Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD).

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