Bimodal regulation of axonal transport by the GDNF-RET signalling axis in healthy and diseased motor neurons.

ABSTRACT: Deficits in axonal transport are one of the earliest pathological outcomes in several models of amyotrophic lateral sclerosis (ALS), including SOD1^G93A mice. Evidence suggests that rescuing these deficits prevents disease progression, stops denervation, and extends survival. Kinase inhibitors have been previously identified as transport enhancers, and are being investigated as potential therapies for ALS. For example, inhibitors of p38 mitogen-activated protein kinase and insulin growth factor receptor 1 have been shown to rescue axonal transport deficits in vivo in symptomatic SOD1^G93A mice. In this work, we investigated the impact of RET, the tyrosine kinase receptor for glial cell line-derived neurotrophic factor (GDNF), as a modifier of axonal transport. We identi

SUBMITTER: Rhymes ER 

PROVIDER: S-EPMC9263112 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature