Craniofacial muscles are essential muscles for normal daily life. They are involved in facial expressions (facial muscles), blinking and eye movement (eye muscles), as well as speaking and eating (tongue and pharyngeal muscles).
Interestingly, craniofacial muscles have differential susceptibility to several muscular dystrophies. For example, craniofacial muscles are the most affected muscles in oculopharyngeal muscular dystrophy but the least affected muscles in Duchenne muscular dystrophy. Among craniofacial muscles, dysfunction of tongue and pharyngeal muscles could cause an eating disability, called dysphagia, afflicts almost 15 million Americans including elderly, neuronal (Parkinson’s disease and bulbar-onset amyotrophic lateral sclerosis) and muscular disease (oculopharyngeal muscular dystrophy) patients. However, no cure or therapeutic treatment exists for dysphagia caused by muscular dystrophy. Elucidation of the mechanism(s) behind these differing susceptibilities of craniofacial muscles could lead to development of potential therapeutics targeted to specific skeletal muscles involved in particular types of muscular dystrophy.
The mechanisms of skeletal muscles are of interest here because skeletal muscle cells are multinucleated cells. Typically, skeletal muscle cells contain hundreds of nuclei in a single cell since they are generated by fusion of muscle precursor cells during development or by fusion of muscle specific stem cells, called satellite cells, in adult skeletal muscles. However, it is unclear how skeletal muscle cells regulate the quantity and quality of these multi-nuclei. Since craniofacial skeletal muscles, such as extraocular and pharyngeal muscles, have active satellite cell fusion in comparison to limb muscles, they are therefore suitable models to study myonuclear addition and homeostasis.
Cardiovascular diseases are the leading causes of death and disability worldwide. We are dedicated to developing new therapies to help cardiac patients by identifying, testing, and moving new therapies towards clinical use. We study stem cell therapies to prevent heart damage and promote repair. We use biomaterials to increase cell retention, increase efficacy, and target activity.
Dr. Coulter is a Board Certified Pediatric Clinical Specialist through the APTA practicing in the field of pediatrics for 38 years. For the past 28 years, Dr. Coulter has worked alongside orthotists and prosthetists in the Orthotics and Prosthetics Department at Children’s Healthcare of Atlanta. She is the team leader for the Limb Deficiency Program and has taught and lectured on topics relating to development and limb deficiencies in children. Dr. Coulter also serves as the physical therapist in the Cranial Remolding and Scoliosis Programs at Children’s Healthcare of Atlanta The focus of one of her studies is the effect of torticollis on the skull, posture and movement. For the past 8 years, she has joined the Children’s team teaching the MSP&O students at GA Tech and is involved in the clinical rotations of the GA Tech MSO&P students and physical therapy students on clinical affiliations at Children’s. She is an adjunct assistant professor at Emory University Department of Physical Therapy.
Neuromodulation using multielecrode arrays, closed loop control theory, and optogenetics for epilepsy and movement disorders. Computational modeling of epilepsy networks for model-based and non-model based feedback control of optogenetic and electrical neuromodulation. Neurorestoration using gene and cell-therapy based approaches for degenerative and injury conditions.
The Translational Neuroengineering Research Lab uses neuromodulation for epilepsy using a combination of the following advanced techniques: 1) Multimicroelectrode electrical stimulation using novel parameters informed by optimization of input/output relationships (both model- and non-model based MIMO) using closed-loop control theory including adaptive learning and machine learning approaches; 2) Optogenetic activation and inhibition using all forms of available channels including step-function opsins. These approaches identify novel brain regions that have more widespread control and targets specific cell types for activation and inhibiton. Closed loop control using multielecrode arrays informs and controls neuromodulation. 3) Hardware independent ‘luminopsins’: novel gene therapy approaches combining bioluminescent proteins with optogenetic channels for hardware independent, widespread and activity-regulatable neuromodulation. We use a combination of in vitro models, animal models (mouse, rat, non-human primate) and human patients undergoing epilepsy and deep brain stimulation surgery as our experimental models.
In addition, the laboratory has developed novel gene therapy vectors for neurorestoration targeting key pivotal proteins regulating axon outgrowth in regenerative situations, including for Parkinson’s disease, spinal cord injury and retinal degeneration.