USU Neuroscience

janders@usuhs.mil
 

Lab Focus:

Dr. Anders current research activities include:
 
1.The use of photobiomodulation (light therapy [LT]) to promote regeneration of acutely injured spinal cord. We have shown that 810 nm light is an effective therapy in both dorsal hemisection and contusion rodent models of spinal cord injury (SCI). The non-invasive transcutaneous application of 810 nm light at the injury site caused a significant increase in the number of regenerating corticospinal tract axons and the length of axonal re-growth. Functional recovery was achieved with ladder crossing time and angle of hind paw rotation returning to baseline levels 9 weeks post-injury. LT significantly decreased the invasion of cells involved in secondary damage to the spinal cord, including macrophages/activated microglia and T lymphocytes from 48 hours to 5 weeks post-injury, and astrogliosis was reduced at early time points. Treatment also resulted in a significant suppression of pro-inflammatory cytokine and chemokine expression, including reduced IL6, monocyte chemoattractant protein-1 and iNOS. Using microarray and PCR analysis, we also found that genes involved in the immune response, cellular proliferation and growth factor receptors were significantly altered by LT after SCI. Optimization of the laser parameters for translation to treatment of patients with SCI are a current focus of the laboratory.
 
2 Repair of severely damaged peripheral nerves. In a rabbit sciatic nerve injury model, laser therapy and surgical methods currently used clinically to repair transected and severely damaged peripheral nerves will be assessed for the repair of severely injured peripheral nerves. Based on our previous research on injury to the central and peripheral nervous systems, laser therapy will be used to enhance nerve regeneration and suppress the immune response and scarring associated with post-traumatic injury of peripheral nerves.
 
3. Traumatic brain injury and stress. Traumatic brain injuries (TBIs) are associated with an increased risk of psychiatric illness with depression as a common complication. Currently, it is not known why some survivors of TBI develop depression and others do not. It has been reported that the state of stress of the individual at the time of TBI may be a factor in developing post-TBI depression and impaired cognition. A hypothesis linking depression and declining neurogenesis has been developing. Current therapy for depression after TBI emphasizes pharmaco-therapeutics. Recent studies have documented that laser generated infrared light applied to the scalp can pass transcranially and penetrate the brain. In this project changes in BDNF expression, neuronal protection, and cell migration and differentiation will be examined in the hippocampi of rats. Changes in these parameters will be assessed in non-stressed and chronically mildly stressed rats that are either sham TBI injured or TBI injured. Efficacy of Transcranial infrared light therapy will be compared against treatment with a currently used antidepressant.
 
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