Format

Send to

Choose Destination
Biology (Basel). 2019 May 11;8(2). pii: E38. doi: 10.3390/biology8020038.

Mitochondrial Dysfunction in Parkinson's Disease-Cause or Consequence?

Author information

1
Wellcome Centre for Mitochondrial Research, Institute for Neuroscience, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. c.chen20@ncl.ac.uk.
2
Newcastle University LLHW Centre for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. c.chen20@ncl.ac.uk.
3
Wellcome Centre for Mitochondrial Research, Institute for Neuroscience, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. doug.turnbull@newcastle.ac.uk.
4
Newcastle University LLHW Centre for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. doug.turnbull@newcastle.ac.uk.
5
Wellcome Centre for Mitochondrial Research, Institute for Neuroscience, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. amy.reeve@newcastle.ac.uk.
6
Newcastle University LLHW Centre for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. amy.reeve@newcastle.ac.uk.

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.

KEYWORDS:

Parkinson’s disease; ageing; mitochondria; neurodegenerative disease

PMID:
31083583
DOI:
10.3390/biology8020038
Free full text

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI)
Loading ...
Support Center