Regrowth of nerve fibers axons is essential to repair and functional recovery of the spinal cord. Tissue destruction with cysts and gliosis at the site of injury forms a barrier to regeneration.
Ongoing research is using tissue engineering with biodegradable polymer scaffolds PLGA, PCLF, OPF loaded with different growth-promoting cells Schwann cells, neural progenitor cells, mesenchymal stem cells and different growth factors GDNF, NT3, BDNF to bridge the gap, and to promote axonal regeneration and functional restoration in the spinal cords of rats and mice, eventually for future use in patients.
Further, Mayo Clinic researchers are investigating the effects of exercise training and local delivery of steroids on axon regeneration and functional recovery. Peripheral nerve regeneration and repair. The Center for Regenerative Medicine is developing strategies to expand the time window of opportunity and improve the functional recovery following peripheral nerve injury and repair.
One strategy is to apply polymer microspheres to deliver vascular endothelial growth factor VEGF to the nerve repair site in a controlled sustainable release manner. VEGF promotes angiogenesis and neurogenesis, and thus leads to a better functional outcome and larger window of opportunity for the nerve to be permissive to prolonged regeneration.
The other strategy is to counteract the lack of healthy Schwann cells at the nerve repair site by supplementing functioning Schwann cells derived from nerves prepared in an in vitro system or Schwann cells induced from stem cells of the adipose tissue.
Novel animal models are being developed to delineate the nature and time course of denervation muscle changes; identify the key indicators of muscle receptivity, including electromyographic changes, muscle fiber type changes and changes of myogenic genes; and evaluate the impact of these changes on nerve regeneration and the potential success of a nerve repair. Stroke neuroregeneration. After stroke , neurons near the penumbra are vulnerable to delayed but progressive damage as a result of ischemia.
There is no effective treatment to rescue such dying neurons. Researchers in the Center for Regenerative Medicine hypothesized that mesenchymal stem cells MSC can rescue damaged neurons after exposure to oxygen-glucose deprivation OGD stress. Studies have demonstrated that the MSC can differentiate into bone, cartilage and fat tissues. Experiments in animal models of hemorrhagic stroke showed MSC therapy improves limb function. Taken together, this data will form the basis for using MSC to treat patients with recent hemorrhagic stroke.
Neuro-oncology and neuroregenerative research. Research currently focuses on invasive brain tumors gliomas for which patients receive a very poor prognosis. However, there are other brain tumors — oligodendroglioma and astrocytoma — that have a much better prognosis. Mayo Clinic researchers are interested in the mutations that are involved in the development of each of these different tumor types and why the tumors behave differently.
A target locus in a gene-poor region initially discovered by genome scanning has been identified. Research efforts are focused on studying the function of this alteration. Using mouse models, murine and human neural stem cells, and human induced pluripotent stem cells, Mayo researchers are investigating how the alteration modifies glial cell development.
Neuroregeneration and inflammation. The limited capacity for repair in the nervous system is a significant medical challenge. The Center for Regenerative Medicine is developing new tools to effectively control the process of neural injury and degeneration and to create a microenvironment that enhances the capacity for innate repair and the efficacy of other regeneration strategies, including neural cell replacement and neurorehabilitation.
Research efforts focus on how highly druggable proteases kallikreins can be targeted to prevent the complex cascade of tissue injury and aberrant reorganization that is a well-recognized component of CNS trauma — and which is increasingly recognized as an integral factor underlying the progression of many neurological disorders, including those classified as neurodegenerative or neuroinflammatory as well as those having an oncogenic basis.
Efforts are directed at understanding the physiological and pathophysiological consequences of a family of G protein-coupled receptors protease-activated receptors, or PARs , and determining whether PARs or the proteases that activate them can be targeted therapeutically to prevent pathogenesis and to promote CNS plasticity and repair to improve patient functional outcomes.
Deep brain stimulation for Alzheimer's disease. Anecdotal and initial trial reports concerning deep brain stimulation DBS to the fornix and hypothalamus have been associated with improvement in memory function and reductions in expected cognitive decline in patients with early Alzheimer's disease. The fornix constitutes the major inflow and output pathway from the hippocampus and medial temporal lobe. Mayo researchers have started an innovative pilot study of dual-hemispheric stimulation of the subthalamic nucleus and fornix and hypothalamus to determine if this approach may have positive effects in attenuating cognitive decline.
If this study provides positive data, then the potential of using DBS of the fornix as a treatment for Alzheimer's disease will be considered. Pediatric anesthesia, apoptosis and safety. Researchers in the Center for Regenerative Medicine are working on a large project involving the detailed testing of 1, children to try to better define what injury if any may be associated with anesthetic exposure. While the body has a mechanism to help peripheral nerves reestablish connections after injury, this process is slow; damaged nerves regrow at an average rate of just one millimeter per day.
My lab seeks methods to accelerate this healing process. Limk1 controls the rate of nerve growth by regulating the activity of a protein called cofilin. This increased rate of nerve regrowth resulted in faster recovery of both motor and sensory functions as measured by how fast the injured mice regained the ability to walk and the sensation in their paws. This is significant because sensory function can take longer than motor function to recover after a traumatic injury, yet sensory function is critical to quality of life.
As a next step, Butler and her lab are using human stem cell-derived motor neurons to screen for drug candidates that could modify this molecular process and speed nerve regeneration in humans. They are also expanding the scope of their study by examining if adding more cofilin — rather than inhibiting Limk1 — could be even more effective in speeding up recovery from peripheral nerve injuries. Nerve damage can occur after any injury, with the results often being related to the severity of the injury.
Minor injuries may cause some nerve damage, but your body tries to heal itself whenever possible. However, more serious injuries can cause severe nerve damage which often requires nerve repairs. Nerves are made up of fibers, which are also called axons.
These fibers are covered with tissues that act as a type of insulation. Sometimes, after an injury, only the fibers are damaged. In the more serious scenarios, both the fibers and tissues are damaged. In some cases, the nerve is completely cut. Without properly functioning nerves, you are likely to experience uncomfortable or even painful sensations.
These occur because the nerves are not able to carry the correct signals from the brain to the spinal cord. The signs of nerve damage include the following:.
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