Neuroscience Discovery

Neuroscience Discovery

ISSN 2052-6946
Review

Mitochondrial dynamics in degenerative disease and disease models

Eric M. Merzetti and Brian E. Staveley*

*Correspondence: Brian E. Staveley bestave@mun.ca

Author Affliations

Department of Biology, Memorial University of Newfoundland, 232 Elizabeth Avenue, St. John's, Newfoundland and Labrador, A1B 3X9, Canada.

Abstract

Degenerative diseases cause the breakdown or destruction of a cell or group of cells over a period of time, leading to an array of physical or cognitive symptoms including impaired motor skills, memory loss and dementia. Often, degenerative diseases have been characterized as afflictions of the elderly but earlier onset forms of these diseases have been linked to genetic dysfunction. Mutant forms of genes often lead to the breakdown of the cell via interference with internal pathways involved in the removal of impaired cellular components and energy production. Mitochondria are dynamic organelles involved in cellular energy production and in intra-cellular signalling leading to cell death. The proper function and upkeep of these organelles is essential to maintaining a healthy cellular environment and preventing accumulation of harmful oxidative free radicals. Breakdown and improper functioning of mitochondria has been linked to the onset of a number of diverse neurological diseases including Alzheimer Disease, Huntington Disease, Parkinson Disease, Multiple Sclerosis, retinal abnormalities and muscle neuron linked motor impairment. In this review, we examine the role of mitochondria in degenerative disease and highlight common mechanisms of disease progression as well as potential targets for future therapeutic approaches.

Keywords: Neurodegenerative, parkinson disease, alzheimer disease, sclerosis, huntington disease, myositis

ISSN 2052-6946
Volume 1
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