Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders

Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders

Sonia Sharma (Khalsa College, India), Paramjeet Kaur (Khalsa College, India), Shallina Gupta (Khalsa College, India) and Sushant Sharma (University of KwaZulu-Natal, South Africa)
DOI: 10.4018/978-1-5225-5282-6.ch005

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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Background

Various NDs have been recognized for centuries and research into their causes and effects has been taking place for decades. NDs are characterized by progressive loss of anatomically related neuronal systems. As life expectancy continues in developed countries, the occurrence of these disorders also increases. In the literature, much knowledge is being available concerning the mechanisms of disease, but the causing factors of these problems are still not well known. To date, many mechanisms have been recommended for explanation of protein aggregation metabolism, and misfolding, protein neuronal function, and cell signaling, but still it is difficult to understand the mechanism clearly at the cellular and molecular level (Tan et al, 2014). To understand these diseases, we need to understand how these cells function, their response to local environment and effect of dysfunctional organelles on these diseases. In this book chapter, authors focused on the role of mitochondria and GA on the dysfunction of neurons that result in various NDs. Mitochondrial play an important role in Ca2+ homeostasis, ATP generation, ROS formation, and even apoptosis etc. and any dysfunction in these processes results in the dysfunction of neurons in a large number of NDs (Baloyannis, 2006). Functional or structural alterations of the Golgi pathology also recognized as a constant pathological characteristic of various NDs including PD, AD, HD, ALS, and prion diseases (Canet-Avilés et al, 2004). The neuropathological changes observed in these diseases can vary with the type of mutation in mtDNA, and level of Golgi dysfunction. GA marked as fragmentation into disconnected cisternae, stacks, vesicles and tubules, and as atrophy (Canet-Avilés et al, 2004). These morphological changes in GA alternate the retrograde and anterograde transport in the secretary pathway in all the NDs. Mutations in the PD-associated genes such as α-synuclein (SNCA), Pink1, Parkin, LRRK2, DJ1 etc. have been shown to affect both functioning of mitochondria and Golgi structure (Lee et al, 2004).

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