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PO2-2-37

Abnormal expression patterns of nociceptors in Parkinson's disease-specific iPSC-derived sensory neurons

[Speaker] Chizuru Iwasawa:1
[Co-author] Naoko Kuzumaki:1, Reona Asano:1, Hideki Tamura:2, Nobutaka Hattori:3, Hideyuki Okano:2,4, Minoru Narita:1,2
1:Department of Pharmacology, Hoshi University, Japan, 2:L-StaR, Hoshi University, Japan, 3:Department of Neurology, Juntendo University School of Medicine, Japan, 4:Department of Physiology, Keio University School of Medicine, Japan

Parkinson's disease (PD) has motor symptoms and non-motor symptoms, such as sensory neuropathy, depression, dementia and sleep disorder. Sensory neuropathy has been observed in autosomal recessive juvenile parkinsonism (ARJP/PARK2) and a part of sporadic PD. However, little is known about the mechanism of sensory neuropathy in PD patient. In the present study, we investigated the mechanisms of sensory neuropathy along with motor dysfunction using sensory neurons derived from PARK2-specific induced pluripotent stem cells (iPSCs). We established sensory neurons using iPSCs derived from PARK2 patients. The iPSC-derived sensory neurons expressed dorsal root ganglion (DRG) neuron markers, BRN3A and ISL1, and nociceptive neuron markers, TRPV1 and NTRK1. In addition, we detected the action potential of iPSC-derived sensory neurons. Under these conditions, we analyzed the gene expression of nociceptors and voltage-gated ion channels. As a result, we observed a decrease in the expression of some ion channels according to neural maturation in PARK2-derived sensory neurons compared to healthy control. This observation indicates that alterations in PARK2-derived sensory neurons may reflect, at least in part, the pathophysiology of sensory neuropathy in PD. To further investigate the functional abnormalities of sensory neurons in PD, we are now analyzing the gene expression profile at each neurodevelopmental and recovered stages.
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