Relationship Between Mitochondria and α-Synuclein: A Study of Single Substantia Nigra Neurons | Dementia and Cognitive Impairment | JAMA Neurology | JAMA Network
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Original Contribution
Mar 2012

Relationship Between Mitochondria and α-Synuclein: A Study of Single Substantia Nigra Neurons

Author Affiliations

Author Affiliations: Centre for Brain Ageing and Vitality, Institute for Ageing and Health (Drs Reeve, Krishnan, McKeith, and Turnbull), Mitochondrial Research Group, Institute for Ageing and Health (Ms Park and Drs Campbell, Lax, Krishnan, Elson, and Turnbull), and Medical Toxicology Centre, Wolfson Unit (Dr Morris), Newcastle University; UK National Institute for Health Research Biomedical Research Centre for Ageing and Age-related Disease, Newcastle upon Tyne Hospitals National Health Service Foundation Trust (Drs Jaros and McKeith and Ms Hepplewhite); and Neuropathology/Cellular Pathology, Royal Victoria Infirmary (Dr Jaros), Newcastle upon Tyne, England.

Arch Neurol. 2012;69(3):385-393. doi:10.1001/archneurol.2011.2675

Objective To explore the relationship between α-synuclein pathology and mitochondrial respiratory chain protein levels within single substantia nigra neurons.

Design We examined α-synuclein and mitochondrial protein expression in substantia nigra neurons of 8 patients with dementia with Lewy bodies, 5 patients with Parkinson disease, and 8 control subjects. Protein expression was determined using immunocytochemistry followed by densometric analysis.

Patients We examined single substantia nigra neurons from 5 patients with idiopathic Parkinson disease (mean age, 81.2 years), 8 patients with dementia with Lewy bodies (mean age, 75 years), and 8 neurologically and pathologically normal control subjects (mean age, 74.5 years). The control cases showed minimal Lewy body pathology and cell loss. Patients with dementia with Lewy bodies and idiopathic Parkinson disease fulfilled the clinical and neuropathologic criteria for these diseases.

Results Our results showed that mitochondrial density is the same in nigral neurons with and without α-synuclein pathology. However, there are significantly higher levels of the respiratory chain subunits in neurons containing α-synuclein pathology.

Conclusions The finding of increased levels of respiratory chain complex subunits within neurons containing α-synuclein does not support a direct association between mitochondrial respiratory chain dysfunction and the formation of α-synuclein pathology.