Neural Regeneration Research ›› 2021, Vol. 16 ›› Issue (11): 2201-2203.doi: 10.4103/1673-5374.310684

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Mitofusin activation enhances mitochondrial motility and promotes neuroregeneration in CMT2A

Gerald W. Dorn II   

  1. Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
  • Online:2021-11-15 Published:2021-04-13
  • Contact: Gerald W. Dorn II, MD, gdorn@wustl.edu.
  • Supported by:
    The present work was supported by NIH R35HL135736, R41NS113642, R41NS115184, and Research Grant 628906 from the Muscular Dystrophy Association (to GWD). GWD is the Philip and Sima K. Needleman-endowed Professor and a Scholar-Innovator awardee of the Harrington Discovery Institute. 

    GWD is an inventor on patent applications PCT/US18/028514 submitted by Washington University and PCT/US19/46356 submitted by Mitochondria Emotion, Inc. that cover the use of small molecule mitofusin agonists to treat chronic neurodegenerative diseases, and is a founder of Mitochondria in Motion, Inc., a Saint Louis based biotech R&D company focused on enhancing mitochondrial trafficking and fitness in neurodegenerative diseases.

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Abstract: Human brains represent only 2% of body mass, but their high relative metabolic activity accounts for ~20% of total body adenosine triphosphate (ATP) consumption. ATP generated by neuronal mitochondria fuels nerve signaling and homeostatic repair. In the peripheral nervous system, which has greater capacity for regeneration after physical, toxic or genetic injury than the central nervous system, ATP also powers actin polymerization/depolymerization for growth cone formation and axon extension. Mitochondrial ATP generation is therefore a central component of neuronal functioning in the central and peripheral nervous systems.