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Enteric neurons from Parkinson’s disease patients display ex vivo aberrations in mitochondrial structure

Scientific Reports2016Vol. 6(1), pp. 33117–33117

Citations Over TimeTop 19% of 2016 papers

Aidos Baumuratov, Paul Antony, Marek Ostaszewski, Feng He, Luis Salamanca, L Antunes, Joseph Weber, Laura Longhino, Pascal Derkinderen, Werner J.H. Koopman, Nico J. Diederich

Abstract

Based on autopsy material mitochondrial dysfunction has been proposed being part of the pathophysiological cascade of Parkinson's disease (PD). However, in living patients, evidence for such dysfunction is scarce. As the disease presumably starts at the enteric level, we studied ganglionic and mitochondrial morphometrics of enteric neurons. We compared 65 ganglia from 11 PD patients without intestinal symptoms and 41 ganglia from 4 age-matched control subjects. We found that colon ganglia from PD patients had smaller volume, contained significantly more mitochondria per ganglion volume, and displayed a higher total mitochondrial mass relative to controls. This suggests involvement of mitochondrial dysfunction in PD at the enteric level. Moreover, in PD patients the mean mitochondrial volume declined in parallel with motor performance. Ganglionic shrinking was evident in the right but not in the left colon. In contrast, mitochondrial changes prevailed in the left colon suggesting that a compensatory increase in mitochondrial mass might counterbalance mitochondrial dysfunction in the left colon but not in the right colon. Reduction in ganglia volume and combined mitochondrial morphometrics had both predictive power to discriminate between PD patients and control subjects, suggesting that both parameters could be used for early discrimination between PD patients and healthy individuals.

Citations Over TimeTop 19% of 2016 papers

Abstract

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