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Reprint of: revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease-resemblance to the effect of amphetamine drugs of abuse.
Free Radic Biol Med. 2013 Sep; 62:186-201.FR

Abstract

Parkinson disease (PD) is a chronic and progressive neurological disease associated with a loss of dopaminergic neurons. In most cases the disease is sporadic but genetically inherited cases also exist. One of the major pathological features of PD is the presence of aggregates that localize in neuronal cytoplasm as Lewy bodies, mainly composed of α-synuclein (α-syn) and ubiquitin. The selective degeneration of dopaminergic neurons suggests that dopamine itself may contribute to the neurodegenerative process in PD. Furthermore, mitochondrial dysfunction and oxidative stress constitute key pathogenic events of this disorder. Thus, in this review we give an actual perspective to classical pathways involving these two mechanisms of neurodegeneration, including the role of dopamine in sporadic and familial PD, as well as in the case of abuse of amphetamine-type drugs. Mutations in genes related to familial PD causing autosomal dominant or recessive forms may also have crucial effects on mitochondrial morphology, function, and oxidative stress. Environmental factors, such as MPTP and rotenone, have been reported to induce selective degeneration of the nigrostriatal pathways leading to α-syn-positive inclusions, possibly by inhibiting mitochondrial complex I of the respiratory chain and subsequently increasing oxidative stress. Recently, increased risk for PD was found in amphetamine users. Amphetamine drugs have effects similar to those of other environmental factors for PD, because long-term exposure to these drugs leads to dopamine depletion. Moreover, amphetamine neurotoxicity involves α-syn aggregation, mitochondrial dysfunction, and oxidative stress. Therefore, dopamine and related oxidative stress, as well as mitochondrial dysfunction, seem to be common links between PD and amphetamine neurotoxicity.

Authors+Show Affiliations

CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal.CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal.CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal; Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal. Electronic address: acrego@cnc.uc.pt.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

23743292

Citation

Perfeito, Rita, et al. "Reprint Of: Revisiting Oxidative Stress and Mitochondrial Dysfunction in the Pathogenesis of Parkinson Disease-resemblance to the Effect of Amphetamine Drugs of Abuse." Free Radical Biology & Medicine, vol. 62, 2013, pp. 186-201.
Perfeito R, Cunha-Oliveira T, Rego AC. Reprint of: revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease-resemblance to the effect of amphetamine drugs of abuse. Free Radic Biol Med. 2013;62:186-201.
Perfeito, R., Cunha-Oliveira, T., & Rego, A. C. (2013). Reprint of: revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease-resemblance to the effect of amphetamine drugs of abuse. Free Radical Biology & Medicine, 62, 186-201. https://doi.org/10.1016/j.freeradbiomed.2013.05.042
Perfeito R, Cunha-Oliveira T, Rego AC. Reprint Of: Revisiting Oxidative Stress and Mitochondrial Dysfunction in the Pathogenesis of Parkinson Disease-resemblance to the Effect of Amphetamine Drugs of Abuse. Free Radic Biol Med. 2013;62:186-201. PubMed PMID: 23743292.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reprint of: revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease-resemblance to the effect of amphetamine drugs of abuse. AU - Perfeito,Rita, AU - Cunha-Oliveira,Teresa, AU - Rego,Ana Cristina, Y1 - 2013/06/03/ PY - 2012/05/15/received PY - 2012/08/15/revised PY - 2012/08/16/accepted PY - 2013/6/8/entrez PY - 2013/6/8/pubmed PY - 2013/11/2/medline KW - 1-methyl-4-phenyl-1,2,3,6-tetrapyridine KW - 1-methyl-4-phenylpyridinium KW - 6-OHDA KW - 6-hydroxydopamine KW - ASK1 KW - Amphetamines KW - Apoptosis signaling-regulating kinase 1 KW - CMA KW - Chaperone-mediated autophagy KW - DAT KW - Dopamine KW - Dopamine transporter KW - ETC KW - Electron transport chain KW - Free radicals KW - Induced pluripotent stem KW - L-DOPA KW - LAMP-2A KW - LB KW - LN KW - LRR KW - LRRK2 KW - Leucine-rich repeat domain KW - Leucine-rich repeat kinase 2 KW - Lewy body KW - Lewy neurite KW - Lysosome-associated membrane protein 2A KW - MAO KW - MAP KW - MPP(+) KW - MPTP KW - Mitochondrial DNA KW - Mitochondrial dysfunction KW - Monoamine oxidase KW - N-methyl-d-aspartate KW - NAC KW - NMDA KW - Non-amyloid-β component KW - Oxidative stress KW - PD KW - PINK1 KW - PTEN-induced putative kinase 1 KW - Parkinson disease KW - ROS KW - Ras of complex protein KW - Reactive oxygen species KW - Roc KW - SN KW - SNCA KW - Short-interfering RNA KW - Substantia nigra pars compacta KW - TH KW - Thioredoxin 1 KW - Trx1 KW - Tyrosine hydroxylase KW - UCHL1 KW - UPS KW - Ub KW - Ubiquitin KW - Ubiquitin C-terminal hydrolase 1 KW - Ubiquitin proteasome system KW - VMAT2 KW - Vesicular monoamine transporter 2 KW - WT KW - Wild type KW - iPS KW - levo-3,4-dihydroxyphenylalanine KW - mitogen-activated protein KW - mtDNA KW - siRNA KW - α-syn KW - α-synuclein SP - 186 EP - 201 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 62 N2 - Parkinson disease (PD) is a chronic and progressive neurological disease associated with a loss of dopaminergic neurons. In most cases the disease is sporadic but genetically inherited cases also exist. One of the major pathological features of PD is the presence of aggregates that localize in neuronal cytoplasm as Lewy bodies, mainly composed of α-synuclein (α-syn) and ubiquitin. The selective degeneration of dopaminergic neurons suggests that dopamine itself may contribute to the neurodegenerative process in PD. Furthermore, mitochondrial dysfunction and oxidative stress constitute key pathogenic events of this disorder. Thus, in this review we give an actual perspective to classical pathways involving these two mechanisms of neurodegeneration, including the role of dopamine in sporadic and familial PD, as well as in the case of abuse of amphetamine-type drugs. Mutations in genes related to familial PD causing autosomal dominant or recessive forms may also have crucial effects on mitochondrial morphology, function, and oxidative stress. Environmental factors, such as MPTP and rotenone, have been reported to induce selective degeneration of the nigrostriatal pathways leading to α-syn-positive inclusions, possibly by inhibiting mitochondrial complex I of the respiratory chain and subsequently increasing oxidative stress. Recently, increased risk for PD was found in amphetamine users. Amphetamine drugs have effects similar to those of other environmental factors for PD, because long-term exposure to these drugs leads to dopamine depletion. Moreover, amphetamine neurotoxicity involves α-syn aggregation, mitochondrial dysfunction, and oxidative stress. Therefore, dopamine and related oxidative stress, as well as mitochondrial dysfunction, seem to be common links between PD and amphetamine neurotoxicity. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/23743292/Reprint_of:_revisiting_oxidative_stress_and_mitochondrial_dysfunction_in_the_pathogenesis_of_Parkinson_disease_resemblance_to_the_effect_of_amphetamine_drugs_of_abuse_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(13)00270-0 DB - PRIME DP - Unbound Medicine ER -