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Alpha-Synuclein and Mitochondrial Dysfunction in Parkinson Disease

Dolgacheva, LP; Fedotova, EI; Abramov, AY; Berezhnov, AV; (2018) Alpha-Synuclein and Mitochondrial Dysfunction in Parkinson Disease. Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology , 34 (5) pp. 4-14. 10.1134/S1990747818010038. Green open access

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Abstract

Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. The development of pathology is associated with the loss of dopaminergic neurons, mainly in substantia nigra pars compacta. Dopamine deficiency causes a whole range of severe motor symptoms, including bradykinesia, postural instability, muscle rigidity, and tremor. Studies have shown the primary role of the alpha-synuclein protein in this neurodegenerative disease. A large amount of data indicates different mechanisms of the toxic effect of alpha-synuclein. The process of neurodegeneration in PD is the result of significant disturbances in mitochondrial functions and/or genetic mutations. The number of mutated genes in hereditary and sporadic forms of Parkinson’s disease includes genes encoding PINK1 and Parkin, which are the main participants in the mitochondrial “quality control” system. The earliest biochemical hallmarks of the disease are disturbances of the mitochondrial interaction with endoplasmic reticulum, mitochondrial dynamics, Ca2+ homeostasis, and an increase in the level of mitochondrial reactive oxygen species. All these factors exert damaging effects on dopaminergic neurons.

Type: Article
Title: Alpha-Synuclein and Mitochondrial Dysfunction in Parkinson Disease
Open access status: An open access version is available from UCL Discovery
DOI: 10.1134/S1990747818010038
Publisher version: http://dx.doi.org/10.1134/S1990747818010038
Language: Russian
Additional information: This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
Keywords: Cell Biology, neurodegeneration, Parkinson's disease, alpha-synuclein, mitochondria, GATED CALCIUM-CHANNELS, COMPLEX-I DEFICIENCY, PROTEIN IMPORT, DAMAGED MITOCHONDRIA, DOPAMINE NEURONS, CELL-DEATH, MEMBRANE ASSOCIATION, OXIDATIVE STRESS, ACTIVATE PARKIN, OUTER-MEMBRANE
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences
URI: http://discovery.ucl.ac.uk/id/eprint/10048677
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