Abstract
Recent evidence has shown that demyelination occurs along with axonal degeneration in spinal cord injury (SCI) during the secondary injury phase. Oligodendrocyte precursor cells (OPC) are present in the lesions but fail to differentiate into mature oligodendrocytes and form new myelin. Given the limited recovery of neuronal functions after SCI in adults without effective treatment available so far, it remains unknown whether enhancing OPC differentiation and myelination could benefit the recovery of SCI. To show the significance of myelin regeneration after SCI, the injury was treated with clemastine in the rat model. Clemastine is an FDA-approved drug that is potent in promoting oligodendrocyte differentiation and myelination in vivo, for four weeks following SCI. Motor function was assessed using sloping boards and grid walking tests and scored according to the Basso, Beattie, and Bresnahan protocol. The myelin integrity and protein expression were evaluated using transmission electron microscopy and immunofluorescence, respectively. The results indicated that clemastine treatment preserves myelin integrity, decreases loss of axons and improves functional recovery in the rat SCI model. The presented data suggest that myelination-enhancing strategies may serve as a potential therapeutic approach for the functional recovery in SCI.
Highlights
Spinal cord injury (SCI) is a violent trauma with high occurrence rate in events such as car accidents and falls that typically leads to sustained motor, autonomic and sensory dysfunction
The results suggest that demyelination can lead to axonal degeneration and prolongation of functional impairment, and that a cleamstine treatment strategy is a promising method for functional recovery, following SCI
Evidence suggests that the cessation of Oligodendrocyte precursor cells (OPC) differentiation in neurodegenerative diseases and neurological trauma is a key factor in the failure of myelin production, leading to progressive nervous system damage
Summary
Spinal cord injury (SCI) is a violent trauma with high occurrence rate in events such as car accidents and falls that typically leads to sustained motor, autonomic and sensory dysfunction. SCI is divided into primary injury and secondary injury. Primary injury is the initial mechanical injury caused by local. Myelin sheaths generated by oligodendrocytes in the central nervous system (CNS) insulate axons and provide metabolic support. Demyelinated axons are more vulnerable to detrimental microenvironments, promoting remyelination can protect axons against degeneration [5]. Recent evidence has shown a potential reason for demyelination in SCI [6] is due to oligodendrocyte (OL) apoptosis [7–10]. Given that myelin integrity is important for axon survival and function [11], this paper proposes that remyelination is beneficial for the recovery of neurofunctions following SCI [12–14]. Complete remyelination is possible as oligodendrocyte precursor cells (OPCs) exist abundantly in the CNS and maintain their abilities to differentiate and form new myelin
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