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

Autor: Werner J.H. Koopman, Luis Salamanca, Nico J. Diederich, P. Derkinderen, Laurent Antunes, Aidos Baumuratov, Laura Longhino, Marek Ostaszewski, Paul Antony, J Weber, Feng He
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Pathology
medicine.medical_specialty
Parkinson's disease
Colon
Neurology [D14] [Human health sciences]
Autopsy
Disease
Neurons/metabolism/pathology
Biology
Mitochondrion
Enteric Nervous System
Article
03 medical and health sciences
0302 clinical medicine
medicine
Humans
Colon/innervation/metabolism/pathology
Aged
Neurons
Multidisciplinary
Enteric Nervous System/pathology
Neurologie [D14] [Sciences de la santé humaine]
Mitochondria/metabolism/pathology
Parkinson Disease/metabolism/pathology
Parkinson Disease
Metabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]
Middle Aged
medicine.disease
Pathophysiology
Ganglion
Mitochondria
030104 developmental biology
Mitochondrial structure
medicine.anatomical_structure
Female
030217 neurology & neurosurgery
Ex vivo
Zdroj: Scientific Reports, 6
Scientific reports, 6, 33117. England (2016).
Scientific Reports
ISSN: 2045-2322
DOI: 10.1038/srep33117
Popis: Contains fulltext : 172471.pdf (Publisher’s version ) (Open Access) 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.
Databáze: OpenAIRE