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Consider the impact of spinal cord injury and the potential scope of lifetime disability and sequelae...

  • Consider the impact of spinal cord injury and the potential scope of lifetime disability and sequelae associated with spinal cord injury. The greatest challenge facing the neuroscience community involves developing therapy that will allow damaged nerve tissue to be regrown and regenerated. Reflect on this article and discuss the importance of Schwann cells and their impact on damaged axons.
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Until World War II, a serious spinal cord injury (SCI) usually meant certain death. Anyone who survived such injury relied on a wheelchair for mobility in a world with few accommodations and faced an ongoing struggle to survive secondary complications such as breathing problems, blood clots, kidney failure, and pressure sores. Even today SCI is not fully reparable and here are an estimated 12,000 spinal cord injuries every year in the United States alone and more than a quarter of a million Americans are currently living with spinal cord injury. The greatest challenge facing the neuroscience community involves developing a therapy that will allow damaged nerve tissue to be regrown and regenerated.

The axons carry signals up and down the spinal cord and to the rest of the body. Thousands of axons are bundled into pairs of spinal nerves that link the spinal cord to the muscles and the rest of the body. The function of these nerves reflects their location along the spinal cord. Schwann cells are known for their roles in supporting nerve regeneration. Nerve injury triggers the conversion of myelin and non‐myelin (Remak) Schwann cells to a cell phenotype specialized to promote repair. Distal to damage, these repair Schwann cells provide the necessary signals and spatial cues for the survival of injured neurons, axonal regeneration, and target reinnervation. The conversion to repair Schwann cells involves de‐differentiation together with alternative differentiation, or activation, a combination that is typical of cell type conversions often referred to as (direct or lineage) reprogramming. Thus, injury‐induced Schwann cell reprogramming involves down‐regulation of myelin genes combined with activation of a set of repair‐supportive features, including up‐regulation of trophic factors, elevation of cytokines as part of the innate immune response, myelin clearance by activation of myelin autophagy in Schwann cells and macrophage recruitment, and the formation of regeneration tracks, and ,Bungner's bands, for directing axons to their targets. This repair program is controlled transcriptionally by mechanisms involving the transcription factor c‐Jun, which is rapidly upregulated in Schwann cells after injury. The rate of regeneration decreases with time. Successful axons can, therefore, reconnect with the muscles or organs they previously controlled with the help of Schwann cells, but specificity is not maintained and errors are frequent, especially when long distances are involved

.Because of their ability to impact regeneration of axons, Schwann cells have been connected to preferential motor reinnervation. If Schwann cells are prevented from associating with axons, the axons die. Regenerating axons will not reach any target unless Schwann cells are there to support them and guide them. They have been shown to be in advance of the growth cones. Schwann cells are essential for the maintenance of healthy axons. They produce a variety of factors, including neurotrophins, and also transfer essential molecules across to axons.

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