Ontology highlight
ABSTRACT: Introduction
Involvement of the peripheral nervous system (PNS) is relatively common in Parkinson's disease (PD) patients. PNS alterations appear early in the course of the disease and are responsible for some of the non-motor symptoms observed in PD patients. In previous studies, we have shown that environmental toxins can trigger the disease by acting on the enteric nervous system.Material and methods
Here, we analyzed the effect of mitochondrial Complex I inhibition on sympathetic neuritis in vivo and sympathetic neurons in vitro. Combining in vivo imaging and protein expression profiling.Results
we found that rotenone, a widely used mitochondrial Complex I inhibitor decreases the density of sympathetic neurites innervating the gut in vivo, while in vitro, it induces the redistribution of intracellular alpha-synuclein and neurite degeneration. Interestingly, sympathetic neurons are much more resistant to rotenone exposure than mesencephalic dopaminergic neurons.Conclusion
Altogether, these results suggest that enteric sympathetic denervation could be an initial pre-motor alteration in PD progression that could be used as an early biomarker of the disease.
SUBMITTER: Arnhold M
PROVIDER: S-EPMC4877429 | biostudies-literature | 2016 Jun
REPOSITORIES: biostudies-literature
Arnhold Mike M Dening Yanina Y Chopin Michaël M Arévalo Esteban E Schwarz Mathias M Reichmann Heinz H Gille Gabriele G Funk Richard H W RH Pan-Montojo Francisco F
Clinical autonomic research : official journal of the Clinical Autonomic Research Society 20160513 3
<h4>Introduction</h4>Involvement of the peripheral nervous system (PNS) is relatively common in Parkinson's disease (PD) patients. PNS alterations appear early in the course of the disease and are responsible for some of the non-motor symptoms observed in PD patients. In previous studies, we have shown that environmental toxins can trigger the disease by acting on the enteric nervous system.<h4>Material and methods</h4>Here, we analyzed the effect of mitochondrial Complex I inhibition on sympath ...[more]