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• W2484321034 abstract "Within the brain, mitochondria serve as the primary producers of ATP to meet the high energy requirements of individual neurons. Through its electron transport chain (ETC), mitochondria generate most of this ATP in an oxygen-dependent manner, with toxic reactive oxidative stress (ROS) also released from the same process. Over time an accumulation of this ROS can severely damage the mitochondrial population within the neuron, ultimately causing apoptosis of the affected neurons. Mitochondrial dysfunction is often implicated in disorders of the brain, in particular Parkinson’s disease (PD), an incurable movement disorder caused by the progressive neurodegeneration of dopaminergic neurons (DA).Compared to other neurons, DA neurons are more vulnerable to ROS due to their intrinsic pacemaking ability. As a consequence, these neurons are under constant oxidative stress that can cause irreparable damage to mitochondria. To cope with this stress, surveillance mechanisms exist to eliminate dysfunctional mitochondria and prevent a domino effect of damage spreading to neighboring mitochondria. Central to this surveillance process are PINK1 and Parkin, two proteins encoded by genes associated with early onset PD. In this chapter, we describe the removal of damaged or dysfunctional mitochondria in detail, outlining the structures and function of both PINK1 and Parkin, and how this pathway may be implicated in mitochondrial quality control within neurons." @default.
• W2484321034 created "2016-08-23" @default.
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• W2484321034 date "2015-01-01" @default.
• W2484321034 modified "2023-09-24" @default.
• W2484321034 title "The Role of Parkin and PINK1 in Mitochondrial Quality Control" @default.
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• W2484321034 doi "https://doi.org/10.1016/b978-0-12-801032-7.00018-6" @default.
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