Mitochondrial dysfunction and oxidative stress in Parkinson’s disease

By S. Subramaniam, M. Chesselet. Progress in neurobiology, 2013

831 citations recorded by the source corpus.

Parkinson’s disease is a movement disorder that is characterized by the progressive degeneration of dopaminergic neurons in substantia nigra pars compacta resulting in dopamine deficiency in the striatum. Although majority of the PD cases are sporadic several genetic mutations have also been linked to the disease thus providing new opportunities to study the pathology of the illness. Studies in humans and various animal models of PD reveal that mitochondrial dysfunction might be a defect that occurs early in PD pathogenesis and appears to be a widespread feature in both sporadic and monogenic forms of PD. The general mitochondrial abnormalities linked with the disease include mitochondrial electron transport chain impairment, alterations in mitochondrial morphology and dynamics, mitochondrial DNA mutations and anomaly in calcium homeostasis. Mitochondria are vital organelles with multiple functions and their dysfunction can lead to a decline in energy production, generation of reactive oxygen species and induction of stress-induced apoptosis. In this review, we give an outline of mitochondrial functions that are affected in the pathogenesis of sporadic and familial PD, and hence provide insights that might be valuable for focused future research to exploit possible mitochondrial targets for neuroprotective interventions in PD.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/fe190966bb4584dfb701f3e260b6a117e54ac613

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Citations in the corpus

Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “363 In PD patients, mitochondrial dysfunction, including respiratory hypofunction, mtDNA mutation, and decreased mitophagy were found to be involved in the pathogenesis of PD. Earlier studies focusing on post-mortem brains from PD patients veri ﬁ ed the decline of OXPHOS, especially complex I…”
Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, positive): “Parkinson disease (PD) is a condition characterized by deposition of Lewy bodies within the brain and progressive loss of dopaminergic neurons in the substantia nigra, leading to movement-related issues such as tremor and rigidity of movements [465].”
The Role of the Reactive Oxygen Species and Oxidative Stress in the Pathomechanism of the Age-Related Ocular Diseases and Other Pathologies of the Anterior and Posterior Eye Segments in Adults (2016, background): “Cell’s death induced by the excessive ROS production and the oxidative stress is involved in pathomechanismofmany general neurodegenerative pathologies such as Alzheimer’s disease [8], Parkinson’s disease [9], prion disease [10], protein misfolding diseases [11], and ophthalmological diseases [12].”
Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? (2016, background): “In fact, experimental data show the simultaneous existence of low-grade chronic inflammation and oxidative stress in many chronic diseases like diabetic complications, cardiovascular and neurodegenerative diseases, alcoholic liver disease, and chronic kidney disease [1–8, 17–19].”