Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Impaired Mitochondrial Mobility in Charcot-Marie-Tooth Disease

Version 1 : Received: 5 November 2020 / Approved: 6 November 2020 / Online: 6 November 2020 (08:55:15 CET)

How to cite: Schiavon, C.; Manor, U. Impaired Mitochondrial Mobility in Charcot-Marie-Tooth Disease. Preprints 2020, 2020110227 (doi: 10.20944/preprints202011.0227.v1). Schiavon, C.; Manor, U. Impaired Mitochondrial Mobility in Charcot-Marie-Tooth Disease. Preprints 2020, 2020110227 (doi: 10.20944/preprints202011.0227.v1).

Abstract

Charcot-Marie-Tooth (CMT) disease is the most commonly inherited neurological disorder, defined by progressive deterioration of the peripheral nerves. Clinical manifestations of CMT mutations are typically limited to peripheral neurons, the longest cells in the body. Currently, mutations in at least 80 different genes are associated with CMT and new mutations are regularly being discovered. A large portion of the proteins mutated in axonal CMT have documented roles in mitochondrial mobility. This suggests that trafficking defects may be a common underlying mechanism in CMT. This review will focus on the potential role of altered mitochondrial mobility in the pathogenesis of axonal CMT, highlighting the challenges and opportunities to this “impaired mobility” model of the disease.

Subject Areas

Organelle transport; Charcot-Marie-Tooth; Axonal transport deficiency; Neurodegeneration; Cytoskeleton; Mitochondria

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