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A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury
Published on: September 13, 2018
Neuroprotection and its molecular mechanism following spinal cord injury
1Spinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Department of Neurological Surgery & Goodman Campbell Brain and Spine, Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Abstract:
Acute spinal cord injury initiates a complex cascade of molecular events termed 'secondary injury', which leads to progressive degeneration ranging from early neuronal apoptosis at the lesion site to delayed degeneration of intact white matter tracts, and, ultimately, expansion of the initial injury. These secondary injury processes include, but are not limited to, inflammation, free radical-induced cell death, glutamate excitotoxicity, phospholipase A2 activation, and induction of extrinsic and intrinsic apoptotic pathways, which are important targets in developing neuroprotective strategies for treatment of spinal cord injury. Recently, a number of studies have shown promising results on neuroprotection and recovery of function in rodent models of spinal cord injury using treatments that target secondary injury processes including inflammation, phospholipase A2 activation, and manipulation of the PTEN-Akt/mTOR signaling pathway. The present review outlines our ongoing research on the molecular mechanisms of neuroprotection in experimental spinal cord injury and briefly summarizes our earlier findings on the therapeutic potential of pharmacological treatments in spinal cord injury.
Insights
This review explores neuroprotection strategies for acute spinal cord injury. Research focuses on targeting secondary injury mechanisms like inflammation and apoptosis for improved functional recovery.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Acute spinal cord injury triggers secondary injury, a cascade of molecular events causing progressive degeneration.
- Secondary injury involves inflammation, excitotoxicity, and apoptosis, presenting therapeutic targets for neuroprotection.
- Existing research shows promise in targeting these pathways for functional recovery in spinal cord injury models.
Purpose of the Study:
- To review ongoing research on molecular mechanisms of neuroprotection in experimental spinal cord injury.
- To summarize findings on the therapeutic potential of pharmacological treatments targeting secondary injury pathways.
Main Methods:
- Review of experimental studies on spinal cord injury models.
- Analysis of molecular mechanisms underlying neuroprotection.
- Evaluation of pharmacological interventions targeting secondary injury processes.
Main Results:
- Identifying key molecular targets within secondary injury pathways.
- Demonstrating the neuroprotective and functional recovery potential of targeting inflammation, phospholipase A2, and the PTEN-Akt/mTOR pathway.
- Summarizing earlier findings on pharmacological treatments for spinal cord injury.
Conclusions:
- Targeting secondary injury mechanisms offers a promising neuroprotective strategy for acute spinal cord injury.
- Pharmacological interventions modulating specific molecular pathways can promote functional recovery.
- Further research into these molecular mechanisms is crucial for developing effective spinal cord injury treatments.
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