Neuronal endoplasmic reticulum stress in axon injury and neurodegeneration

Authors

  • Shaohua Li MD, PhD,

    1. Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine, Philadelphia, PA
    2. Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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  • Liu Yang PhD,

    1. Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine, Philadelphia, PA
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  • Michael E. Selzer MD, PhD,

    1. Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine, Philadelphia, PA
    2. Department of Neurology, Temple University School of Medicine, Philadelphia, PA
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  • Yang Hu MD, PhD

    Corresponding author
    1. Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine, Philadelphia, PA
    • Address correspondence to Dr Hu, Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine, 3500 N Broad Street, Medical Education and Research Building, 6th Floor, Philadelphia, PA 19140. E-mail: yanghu@temple.edu

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Abstract

Injuries to central nervous system axons result not only in Wallerian degeneration of the axon distal to the injury, but also in death or atrophy of the axotomized neurons, depending on injury location and neuron type. No method of permanently avoiding these changes has been found, despite extensive knowledge concerning mechanisms of secondary neuronal injury. The autonomous endoplasmic reticulum (ER) stress pathway in neurons has recently been implicated in retrograde neuronal degeneration. In addition to the emerging role of ER morphology in axon maintenance, we propose that ER stress is a common neuronal response to disturbances in axon integrity and a general mechanism for neurodegeneration. Thus, manipulation of the ER stress pathway could have important therapeutic implications for neuroprotection. Ann Neurol 2013;74:768–777

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