Open Access Mini Review Article

The Role of Mitochondrial Dysfunction in the Mechanism of Neurodegenerative Diseases

Esra Çelen1,2* and Hasibe Cingilli Vural2

1Faculty of Agriculture and Natural Sciences, Konya Food and Agriculture University, Turkey

2Department of Medical Biology, Meram Faculty of Medicine, Necmettin Erbakan University, Turkey

Corresponding Author

Received Date: October 15, 2018;  Published Date: November 09, 2018


The increase in the incidence of neurodegenerative diseases negatively affects the life quality of the individuals and is also a great burden to health sector. Neurodegenerative diseases, which are the most common forms of dementia, are Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis and Multiple Sclerosis. They are progressive diseases showing premature death of neurons and can be triggered by genetic and environmental factors. The nature of age-dependence of these diseases supports the view that the mechanisms of these diseases are linked to mitochondrial mutations. As the proportion of mutant mitochondria in the tissue increases, ATP production becomes inefficient and dysfunction is observed. Some mitochondrial functions are affected in neurodegenerative diseases. Some of them include decreased glucose metabolism, mitochondrial enzymatic damage and increased production of ROS. Changes in mitochondrial dynamics are mitochondrial fission and fusion disruption, reduction of mitochondria transport on axons, decrease in intracellular mitochondria rate, and deformation in shape. There is still no effective treatment option for neurodegenerative diseases. In this review, the known mechanisms of neurodegenerative diseases and mitochondrial bases will be discussed, and the roles of mitochondrial dysfunction in these diseases will be reviewed.

Keywords: Dementia; Mitochondria; Neurodegenerative disease; ROS; Aging

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