Abstract
Parkinson's disease (PD) is a neurodegenerative movement disorder of unknown etiology. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, depletion of dopamine in the striatum, abnormal mitochondrial and proteasomal functions, and accumulation of α-synuclein that may be closely associated with pathological and clinical abnormalities. Increasing evidence indicates that both oxidative stress and inflammation may play a fundamental role in the pathogenesis of PD. Oxidative stress is characterized by increase in reactive oxygen species (ROS) and depletion of glutathione. Lipid mediators for oxidative stress include 4-hydroxynonenal, isoprostanes, isofurans, isoketals, neuroprostanes, and neurofurans. Neuroinflammation is characterized by activated microglial cells that generate proinflammatory cytokines, such as TNF-α and IL-1β. Proinflammatory lipid mediators include prostaglandins and platelet activating factor, together with cytokines may play a prominent role in mediating the progressive neurodegeneration in PD.
Highlights
IntroductionParkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, which project to the striatum, the output of which governs locomotor behavior [1, 2]
Parkinson’s disease (PD) is a neurodegenerative disorder of unknown etiology
The molecular mechanism of vulnerability of dopaminergic neurons in the substantia nigra pars compacta is not known, it is suggested that monoamine oxidase-mediated abnormal dopamine metabolism, hydrogen peroxide generation, abnormal mitochondrial and proteasomal dysfunctions along with microglial cell activation may be closely associated with neurodegenerative process [5]
Summary
PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, which project to the striatum, the output of which governs locomotor behavior [1, 2]. The molecular mechanism of vulnerability of dopaminergic neurons in the substantia nigra pars compacta is not known, it is suggested that monoamine oxidase-mediated abnormal dopamine metabolism, hydrogen peroxide generation, abnormal mitochondrial and proteasomal dysfunctions along with microglial cell activation may be closely associated with neurodegenerative process [5]. The loss of dopaminergic neurons in the substantia nigra pars compacta may be related to resting tremor, rigidity, bradykinesia, postural instability, and gait disturbance in PD patients. Mutation and deposition of α-synuclein, Iron induction of Lewy bodies and Excitotoxicity deposition of neuromelanin
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