Neural Regeneration Research ›› 2021, Vol. 16 ›› Issue (6): 1212-1213.doi: 10.4103/1673-5374.300442

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ULK1 as a novel therapeutic target in neurodegeneration

Björn Friedhelm Vahsen, Paul Lingor*   

  1. Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford, UK (Vahsen BF)
    Department of Neurology, University Medical Center Göttingen, Göttingen, Germany (Vahsen BF, Lingor P)
    Center for Biostructural Imaging of Neurodegeneration (BIN), DFG Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), University Medical Center Göttingen, Göttingen; Department of Neurology, Rechts der Isar Hospital of the Technical University Munich, Munich, Germany (Lingor P)
  • Online:2021-06-15 Published:2020-12-31
  • Contact: Paul Lingor, MD, paul.lingor@tum.de.
  • Supported by:
    BFV was supported by a scholarship from the Department of Neurology, University Medical Center Göttingen. PL received funding from the Cluster of Excellence and DFG Research Center Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), Göttingen. 

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Abstract: Axonal degeneration is an early and key pathophysiological feature of many traumatic and neurodegenerative disorders of the central nervous system (CNS), such as spinal cord injury (SCI), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). As the regenerative capacity of injured axons is severely restricted in the CNS, axonal degeneration frequently results in the irreversible loss of neuronal connections causing progressive neurological deficits and clinical disability. A better understanding of the mechanisms of axon degeneration is therefore hoped to unravel new therapeutic avenues to combat neurodegeneration (Lingor et al., 2012).