The motor deficiency control commonly characterizes Parkinson’s disease (PD), resulting in impairment of neuromuscular command, because of basal ganglia nuclei degeneration and late formation of Lewy’s bodies in the remaining dopaminergic (DA) neurons. Motor signals are triggered in high cortical motor areas and go toward the midbrain regions, where the final tuning movement takes place. PD is characterized primarily by the death of dopaminergic neurons in the regions known as substantia nigra compacta (STNc). Mutations in a couple of genes, such as Parkin1 and DJ1, correspond to the usual familial form of the disease, due to its association with oxidative stress and depolarization of mitochondrial membrane. However, this form does not explain the selective pattern of apoptosis between the neuronal dopaminergic areas of midbrain regions. In this chapter, we are putting forward the hypothesis of oxidative stress and mitochondrial changes as the apparent most relevant cause in PD, as well as the neuroprotective role played by Kir6.2, a potassium-ATP channel and calcium voltage-gated v1.3.
Part of the book: Parkinson's Disease and Beyond