Reactive Oxygen Species Effects on Mitochondrial Dynamicity that may Lead to Parkinson's Disease: A Review

Abstract

Parkinson’s disease (PD), is the second common and deadliest neuronal and a multisystem disorder that contributes to significant morbidity and healthcare burden in the world. Its causes are poorly understood and there is no proven therapeutic line of attack to foil the disease progression. The neuropathological studies of Parkinson’s disease brains show irreversible relapse of dopaminergic neurons in substantia nigra and other brain regions, and a simultaneous loss of dopamine (DA) in the striatum may be one of the main reasons for this disease. But now a days it is known that mitochondria, has a great role to promote so many neurological disorders along with Parkinson’s disease. Defects in neuronal development and neuronal plasticity are related with the deregulation of the mitochondrial fusion or fission process. On the other hand result of mitochondrial dis-regulation is, generation of reactive oxygen species (ROS), which also activate some specific pathways that cause ultimately cell damage and finally neurological disorder like PD. In this review it is intended to gather current knowledge about the relation between mitochondria and ROS with PD. It is true that this is playing key role in PD so, targeting all the pathways related to this dysfunction and modification in this field can be helpful to create a new therapy.