Oxidative stress and <b>α</b>-synuclein conspire in vulnerable neurons to promote Parkinson’s disease progression

Kelvin C. Luk

doi:10.1172/JCI130351

Oxidative stress and α-synuclein conspire in vulnerable neurons to promote Parkinson’s disease progression

Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Address correspondence to: Kelvin C. Luk, 1/F Maloney Building, 3600 Spruce Street, Philadelphia, Pennsylvania 19104, USA. Phone: 215.615.3202; Email: kelvincl@pennmedicine.upenn.edu.

Find articles by Luk, K. in: JCI | PubMed | Google Scholar |

First published August 5, 2019 - More info

Published in Volume 129, Issue 9 on September 3, 2019
J Clin Invest. 2019;129(9):3530–3531. https://doi.org/10.1172/JCI130351.
© 2019 American Society for Clinical Investigation

First published August 5, 2019 - Version history

Patients with Parkinson’s disease (PD) show selective degeneration of dopaminergic neurons in the substantia nigra and cholinergic neurons in the dorsal motor nucleus (DMnX), but the drivers of this specific susceptibility are unknown. In this issue of the JCI, Musgrove et al. report on their use of an impressive array of in vivo and ex vivo tools for interrogating DMnX neurons and demonstrate that this population exhibits enhanced sensitivity to oxidative stress. Remarkably, this sensitivity was amplified by the overexpression of α-Synuclein (α-Syn), a pathological protein in PD. They further show that oxidative stress augments cell-cell transfer of α-Syn, which may be an important mechanism underlying the development and progression of PD.

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