Mitochondrial Dysfunction in Parkinson's Disease

Parkinson’s disease (PD) is the most common neurodegenerative movement disorder characterized by numerous motor symptoms, including bradykinesia, hypokinesia, rigidity, resting tremor, and postural instability and non-motor symptoms, such as autonomic dysfunction, sleep abnormalities, depression, and dementia [1-3]. The motor clinical manifestations are the preferential loss of dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc), resulting in dopamine deletion and derangements of neuronal circuits in the basal ganglia target regions of these neurons [1]. Another pathological hallmark of PD is round eosinophilic intracytoplasmic proteinaceous inclusion bodies that are mainly composed of fibrillar α-synuclein termed Lewy bodies (LBs) and dystrophic neurites (Lewy neurites) present in surviving neurons [4]. The manifestations of non-motor symptoms can contribute considerably to disability, and they usually are not responsive to dopamine replacement therapy [1]. Dementia is a major cause of disability, and currently there is no effective symptomatic treatment and 47% of PD patients show evidence of Mitochondrial Dysfunction in Parkinson’s Disease