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Mitochondrial Dysfunction in Parkinson’s Disease—Cause or Consequence?

1
Wellcome Centre for Mitochondrial Research, Institute for Neuroscience, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK
2
Newcastle University LLHW Centre for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK
*
Author to whom correspondence should be addressed.
Biology 2019, 8(2), 38; https://doi.org/10.3390/biology8020038
Received: 21 December 2018 / Revised: 25 January 2019 / Accepted: 5 February 2019 / Published: 11 May 2019
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases of Ageing)
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Abstract

James Parkinson first described the motor symptoms of the disease that took his name over 200 years ago. While our knowledge of many of the changes that occur in this condition has increased, it is still unknown what causes this neurodegeneration and why it only affects some individuals with advancing age. Here we review current literature to discuss whether the mitochondrial dysfunction we have detected in Parkinson’s disease is a pathogenic cause of neuronal loss or whether it is itself a consequence of dysfunction in other pathways. We examine research data from cases of idiopathic Parkinson’s with that from model systems and individuals with familial forms of the disease. Furthermore, we include data from healthy aged individuals to highlight that many of the changes described are also present with advancing age, though not normally in the presence of severe neurodegeneration. While a definitive answer to this question may still be just out of reach, it is clear that mitochondrial dysfunction sits prominently at the centre of the disease pathway that leads to catastrophic neuronal loss in those affected by this disease. View Full-Text
Keywords: Parkinson’s disease; mitochondria; ageing; neurodegenerative disease Parkinson’s disease; mitochondria; ageing; neurodegenerative disease
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Chen, C.; Turnbull, D.M.; Reeve, A.K. Mitochondrial Dysfunction in Parkinson’s Disease—Cause or Consequence? Biology 2019, 8, 38.

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