Basic Science Investigators
Circuits & Synapses
- Timothy Cope, Ph.D.
- Robert E.W. Fyffe, Ph.D.
- David R. Ladle., Ph.D.
- Mark Rich, M.D., Ph.D.
- Francisco J. Alvarez, Ph.D. (Institute Collaborator)
Cognitive & Behavioral Neuroscience
Learning and Memory
Computational Neuroscience & Bioinformatics
Molecular & Cellular Neuroscience
- Francisco Javier Alvarez-Leefmans, M.D., Ph.D.
- Kathrin Engisch, Ph.D.
- Mel Goldfinger, Ph.D.
- Ashot Kozak, Ph.D.
Cardiovascular Disease, Stroke
Control of Breathing and Chemosensing
Circuits & Synapses
Research in my laboratory focuses on motor control and sensorimotor integration in the mammalian spinal cord. Using predominantly electrophysiological methods, we study synaptic communication between spinal motoneurons and proprioceptive sensory neurons. We are actively examining how these neurons, synapses, and spinal circuits respond to peripheral nerve injury and regeneration, and our studies are yielding insight into the adaptive and maladaptive changes of the mature spinal cord. In addition we are studying activity patterns among populations of motoneurons recruited during movement in order to infer strategies and mechanisms used by the central nervous system to control movement. Ongoing collaborative efforts involve studies in peripheral neuropathy, regulation of motoneuron excitability and activity dependence of synaptic function.
The Fyffe laboratory has long been interested in synaptic mechanisms and integrative properties of neurons in spinal cord circuits involved in motor control and sensorimotor integration. The laboratory makes use of the extensive confocal and electron microscopy facilities in the Institute, as well as electrophysiological and computational approaches. Our current studies are focused on determining the patterns of expression, and the subcellular localization, of pre- and post-synaptic membrane ion channels and neurotransmitter receptors in spinal neurons. This work is focused on understanding the responses of motoneurons and other neurons in spinal circuits to nerve injury and repair, in order to develop more effective strategies for enhancing functional recovery.
My lab is interested in the development of neural circuits. The establishment of appropriate connections between specific neurons generates an organism's perception of the outside world and controls behavioral responses. We use the relatively simple circuits in the spinal cord that control reflex movements as a model system to understand the molecular and physiological mechanisms by which circuits develop. These studies employ a wide variety of techniques including mouse genetics, electrophysiology, immunohistochemistry, confocal microscopy and other advanced imaging techniques.
My research focuses on two areas. We study the cause of paralysis in patients with Critical Illness Myopathy. We have found that paralysis in this syndrome is due to abnormal behavior of skeletal muscle sodium channels. Our goal is to determine the cause of altered sodium channel behavior. We study the mechanisms underlying activity-induced changes in synaptic strength. We use the neuromuscular junction as a model synapse in which it is possible to determine both the signals triggering changes in synaptic strength as well as the types of changes underlying alterations in synaptic strength.
Institute Collaborator: Francisco J. Alvarez, Ph.D.
Adjunct Professor of Neuroscience, Cell Biology & Physiology, Wright State University
Associate Professor of Physiology, Emory University School of Medicine
Our lab is interested in the development of synaptic circuits in the spinal cord. Newborns express immature spinal circuits reflected in abnormal reflexes and limited capacity to make effective postural adjustments or fine movements. The neurobiological principles that drive the postnatal maturation of spinal cord motor circuits, in particular the development of inhibitory synapses and interneurons that modulate motoneuron activity, are largely unknown. Our laboratory uses electron microscopy, confocal microscopy and electrophysiological methods to study the postnatal maturation of structure, molecular composition and synaptic function of key inhibitory circuits in the spinal cord. Our latest work analyzes the postnatal specification of adult inhibitory interneurons from embryonic spinal neuronal groups. Using transgenic mice that carry linage markers for the subpopulation of embryonic neurons derived from the V1 group, we have shown that several different types of segmental ventral inhibitory adult interneurons derive from this group and therefore share a similar genetic background.
Cognitive & Behavioral Neuroscience
Paulette Gillig, M.D., Ph.D.
Professor of Psychiatry
Dr. Gillig's research interest is the interface of the clinical neurosciences of psychiatry, neurology and psychology. She currently is the editor of the series "Psychiatry and Neurology" for the journal Innovations in Clinical Neurosciences, where she has coauthored articles on components of nervous system function relevant to clinical psychiatry (including cerebellar and brainstem function, gait, the extrapyramidal system and the visual system and other cranial nerves). In collaboration with Julie Gentile, M.D., associate professor of psychiatry and director of the Division of Intellectual Disability, Dr. Gillig's current area of research interest is the effect of cerebellar function on executive functions, language production, emotional regulation and the modulation of cognitive decision making processes and behavior.
My research focuses on the connections between prenatal neural insults and developmental disabilities, such as cerebral palsy or autism, as well as later onset dysfunction of prenatal origins, such as Parkinson's disease. In order to study these intriguing connections, also known as the Fetal Basis of Adult Disease (FeBAD), my laboratory uses several mouse models of Parkinson's disease. Recently we have developed a guinea pig model designed for studying lifespan trajectories of biobehavioral development. Prior to birth, we observe behavioral development in the guinea pig fetus using high-resolution ultrasound with real-time 3D/4D. After birth, we track altered pathways (trajectories) of development across the lifespan with a series of behavioral assessments. Changes in neural development and functioning are examined using NMR quantification of metabolites, in collaboration with Dr. Nick Reo at the Cox Institute, and immunohistochemical methods. The goal of this research is to identify biobehavioral profiles that typify developmental pathways in FeBAD. As an applied goal, my laboratory is currently developing prenatal assessments for state, movement, and movement coordination in the fetus that hold promise as prenatal diagnostics for developmental disabilities of the central nervous system.
Cognitive & Behavioral Neuroscience: Dementia
Established in July of 2006, the Department of Geriatrics works with faculty members across the School of Medicine to incorporate the principles of geriatric medicine into the Biennium I and Biennium II curricula. Members of the department also participate in the education of family medicine and internal medicine residents. An accredited fellowship in geriatric medicine was established in July 2008 and trains two fellows each year. Current research activities include interdisciplinary work on falls, delirium, dementia, long term care of frail older adults and caregiver advocacy. A major research goal for the department is the study of interventions and models of care that will allow older adults in the Miami Valley to remain safely in their homes for as long as possible.
Cognitive & Behavioral Neuroscience: Development of Learning & Memory
My research focuses on the development of learning and memory. A variety of behavioral procedures, with a special emphasis on classical eyeblink conditioning, enable us to study both the neural and behavioral processes that support different forms of associative learning across different stages of infant development. We are especially interested in characterizing the parallels between learning in human infants and in young rats pups that can be explained by similarities in central nervous system development. These studies focus on relating developmental changes in the cerebellum, hippocampus, amygdala, and prefrontal cortex to changes in associative learning skills during infancy. Recently, we have been exploring, in rats, the detrimental effects of elevated plasma corticosterone levels on learning during critical periods of postnatal development, looking into potential interventions to reduce the impairment, and using immunohistochemical methods and confocal fluorescence microscopy to examine changes brain development. The ultimate goal of this type of research is to enhance our understanding of developmental learning disorders and how memory processing changes over the course of the developmental life span.
Cognitive & Behavioral Neuroscience: Stress Response
Patricia Schiml, Ph.D.
Lecturer in Psychology
Basic research in our lab focuses on how psychosocial stressors influence neural, endocrine, and inflammatory processes underlying development. For highly social species such as guinea pigs, the removal of critical social partners (attachment figures) can rapidly induce physiological stress responses, whereas the presence of these partners can mitigate (i.e., buffer) responses to stressors. Exposure to psychosocial stressors early in life can have either adaptive or pathological influences on biobehavioral development. To better understand these processes, we examine the conditions under which attachment-figure separation induces hypothalamic-pituitary-adrenal (HPA) stress responses during the life span, as well as the neural mechanisms underlying attachment-figure separation and social buffering effects on HPA responses.
We are especially interested in the relation between social separation and depression. In human children, disruption of the attachment relationship with parents not only can produce a depressive reaction during the disturbance, but it can also increase the odds of developing major depressive disorder in later life. In work with our guinea pig model, we are testing our hypothesis that stress-induced inflammatory processes are important mediators of both the immediate and long-term effects of attachment disruption on depressive behavior.
In addition to basic studies, we conduct applied work in the community assessing means by which human interaction can reduce stress, and improve the welfare, of dogs confined in animal shelters.
Computational Neuroscience & Bioinformatics
Dr. Doom applies computational and statistical techniques to identify, retrieve, classify, simulate, characterize, and analyze data. As codirector of WSU BiRG lab, much of his research involves the analysis of biological data, including raw instrumentation data, as well as processed DNA sequence, protein sequence, metabolite, or population data. Current research includes techniques for forensic DNA analysis (cited by the Supreme Court), improved quantification techniques and Kernal-based binning methods for NMR spectroscopic data, isolation and visualization of translational efficiency biases, characterization and synthesis of 1H NMR spectroscopic data, and knowledge discovery in large biological data sets.
My research is on mathematical cognitive modeling as a framework for both understanding human cognition and for measuring performance. My applied research includes using cognitively based metrics to assess three-dimensional visual displays and various approaches to information fusion. I also apply cognitive modeling to study individual differences in human performance, both in the general population and in clinical groups. I am working with a group that includes researchers at the University of Utah and the University of Newcastle in Australia to identify individuals with extraordinary multitasking abilities and understand how they differ from ordinary people in terms of cognitive processing. I am working with clinical researchers at Indiana University to use mathematical modeling to understand the nature of working memory deficits associated with externalizing disorders, such as alcohol dependence. In another project with Indiana University researchers, I am using mathematical models to characterize differences in the word perception between individuals with dyslexia and normal reading adults.
My research focuses on high-level cognitive processes such as strategic thinking and executive control of cognition and affect. My approach stems from the ACT-R* theory and cognitive architecture; I use computational cognitive modeling to interpret behavioral and brain data from a variety of experimental paradigms such as task switching, multitasking, and dynamic decision-making. For example, my collaborators and I are developing cognitive models of inhibitory control in task switching, learning acceleration following brain stimulation, hemodynamic changes related to learning, and transfer of learning in strategic interaction.
*ACT-R stands for Adaptive Control of Thought – Rational (Anderson, 2007).
Research in my laboratory involves the development of analytical and simulation algorithms to investigate a wide range of problems in biochemistry and molecular biology. Our computational research interests include pattern analysis in high-dimensionality data sets, evolutionary computation and optimization, empirical simulation and multivariate statistics. We apply these techniques to a variety of problems in biochemistry and molecular biology. We currently have projects underway in neuroscience, toxicology, molecular evolution, protein structure modeling and remote homolog search.
Molecular & Cellular Neuroscience
Research in my laboratory focuses on the molecular and cellular physiology of carrier protein molecules that actively transport chloride ions (Cl-) across the plasma membrane of neurons and epithelial cells. Specifically, we study some members of the cation-coupled-chloride contransporter gene/protein family SLC12A: the Na+,K+,2 Cl- cotransporters (NKCC1 and NKCC2) and the K+-Cl- cotransporters (KCC1, 2, 3 and 4). These carrier proteins play key roles in: intracellular Cl- homeostasis in neurons, GABA- and glycine-mediated synaptic signaling, neuronal development, sensory transduction including nociception, transepithelial salt transport, cell water volume control, and extracellular K+ scavenging. Not surprisingly, altered function of these proteins underlies several pathologies and hence they have become significant targets for therapeutic interventions and translational research. To study the function of these proteins we use state-of-the-art live-cell imaging microscopy and fluorescent probes for measuring and manipulating intracellular ions and water in dissociated neurons and choroid plexus epithelial cells. Some of these optical methods have been developed in the lab. We also use molecular methods, knockout models, and several microanatomical techniques. Our current research involves two projects:
- Mechanisms regulating intracellular chloride in primary afferent neurons and their impact on GABA-mediated presynaptic inhibition. This project aims at understanding the molecular mechanisms that determine intracellular Cl- concentration in primary afferent neurons, their regulation, and the role they play in presynaptic inhibition, acute somatic pain, neurogenic inflammation and proprioception.
- Roles of cation-coupled-chloride contransporters of choroid plexus epithelial cells in the regulation of cerebrospinal fluid ion composition. The choroid plexus epithelial cells (CPEC) form the blood-cerebrospinal fluid (CSF) barrier. CPECs secrete CSF and regulate its electrolyte composition. Regulation of CSF ion levels is fundamental for maintaining normal electrical activity of the brain and cell water homeostasis of glial cells and neurons. The aim of this project is to understand how NKCC1 and K+-Cl- cotransporters control the ion composition of the cerebrospinal fluid, with special emphasis on the concentration of K+.
For more information, visit Dr. Alvarez-Leefmans' web page.
Synaptic plasticity, the ability of synaptic transmission to be modulated up or down, over short time scales (milliseconds and seconds) and long time scales (minutes, hours, days, forever) underlies every aspect of normal and abnormal brain function. However, our understanding of the underlying mechanisms of synaptic transmission and its modulation is far from complete.
In our laboratory we study the basic mechanisms of neurotransmitter release in three different preparations. At the mouse nerve-muscle synapse (the neuromuscular junction) we use two electrode voltage clamp to record acetylcholine-activated currents in individual muscle fibers. In a neuroendocrine cell from the adrenal gland, adrenal chromaffin cells, we use perforated patch clamp to record tiny increases in cell capacitance that occur when vesicle membrane adds to the plasma membrane surface area. We also use carbon fiber amperometry to detect released norepinephrine and epinephrine from individual adrenal chromaffin cells. More recently we have added cultures of cortical neurons to our repertoire. Here we can record spontaneously occurring synaptic currents that arise from release of glutamate-containing vesicles from presynaptic terminals. Our laboratory has used these three preparations to study the function of Rab3A, a small GTPase associated with the membrane of synaptic vesicles. We have found that Rab3a plays multiple roles in neurotransmitter release, including regulating release of vesicles during repetitive stimulation, and regulating the kinetics of the single release event itself.
Currently, our laboratory is very interested in one form of synaptic plasticity that we believe affects the way the nervous system responds to injury and loss of synaptic inputs. To mimic such an injury, we block the activity of neurons for prolonged periods of time. It is well known that neurons respond to such a dramatic loss in activity with changes that attempt to bring the activity of the neurons back to normal. We are studying one aspect of this response, the increase in the amplitude of the spontaneously occurring miniature synaptic event, which corresponds to the response of a neuron to the release of a single vesicle of neurotransmitter. We find that at the neuromuscular junction, the normal increase in the miniature current amplitude after activity blockade is abolished in mice expressing a mutant form of Rab3A. We are currently examining whether a similar loss of plasticity occurs in cortical neuron cultures prepared from mice lacking Rab3A or mice expressing the mutant form.
Research in this lab addresses impulse propagation in geometrically-inhomogenious axons. Exact cable equation boundary conditions are determined directly using analog computation (extensive compartmental RC circuits configured with branch points), recording voltages and currents directly from the circuitry. Voltage-dependencies and epiphenomena such as periaxonal K+ accumulations are added using numerical simulations. Recent studies incorporate Markovian kinetics to estimate the probability distributions of Na channel substates during action potential propagation.
Research in my laboratory focuses on the study of ion channel behavior and regulation. We are particularly interested in cation channels of the transient receptor potential (TRP) family and their involvement in the sensing of intracellular and extracellular signals. TRPM7 is a protein with dual ion channel and protein kinase functions that is highly expressed in T lymphocytes, macrophages and microglia. We are currently studying the biophysical mechanisms underlying regulation of TRPM7 by Mg2+ , H+ and phospholipids and its function in the immune response. A second area of interest in the lab is the modulation of ion channels by amyloid β peptides.
Molecular & Cellular Neuroscience: Brain Edema
Through our basic science research projects, we hope to better understand (1) why edema develops in the brain following injury or ischemia, (2) how neurons and glial cells adapt to the changes in intracellular and extracellular volume which characterize brain edema, (3) what processes of osmolyte transport are activated during brain edema to maintain function, and (4) whether brain edema per se can lead to injury secondary to the primary pathological insult. We use electrophysiological techniques and radiolabel measurements to study membrane channels and transporters responsible for volume regulation of neurons and astroglial cells grown in tissue culture. With the understanding of the effectors of cellular volume regulation, we examine how extracellular purinergic and glutaminergic signaling pathways and intracellular kinase cascades regulate these membrane channels and transporters, both in tissue culture systems and with acutely prepared brain slices. We also use animal models of pathological conditions which precipitate brain edema to obtain basic information on which organic and inorganic osmolytes which are lost during the brain’s adaptation to the increased brain tissue fluid. With these animal models we also examine the regulation of the astroglial membrane channel responsible for controlling water transport across the blood-brain barrier. Finally, we investigate the role of reactive oxygen species both as a cause of brain edema and as signaling molecules which activate the adaptive response to cell swelling.
Our laboratory also is examining clinical consequences of brain edema and evaluating novel diagnostic modalities for assessing changes in brain water content which may be applied for patient care. In clinical studies, we explore whether the presence of brain edema is an independent prognostic indicator of poor outcome in patients who present with a traumatic brain injury. In a series of pilot investigations with a local technology company, we are exploring changes in brain tissue electrical properties which are modified by brain edema and which can be measured with a low-power microwave detector.
Molecular & Cellular Neuroscience: Cardiovascular Disease & Stroke
My laboratory is interested in cerebrovascular diseases including ischemic and hemorrhage stroke, and stem cell studies. Current studies are focused on investigating the roles and mechanisms of the two renin-angiotensin system (RAS) axes (ACE/Ang II/AT1 and ACE2/Ang 1-7/Mas axes), the stromal cell derived factor-1a (SDF-1a) and its receptor CXCR4 signaling pathway in cerebral ischemic/hemorrhage stroke, as well as exploring potential gene- and stem cell- based therapeutic avenues (angiogenesis and neurogenesis) for these cerebrovascular diseases. Gene modified mice models (transgenic or gene deletion), integrative methods, gene transfection and silencing, in conjunction with cellular and molecular approaches are used for the studies. Our primary collaborators include colleagues in the medical school (Dr. Mariana Morris, Dr. David Cool, Dr. James Olson, Dr. Lawrence Amesse, Dr. Glen Solomon). My current projects are supported by National Institutes of Health and American Diabetes Association.
My current research interests are in developing post-stroke pharmacological treatments for improved functional recovery. Currently, approximately 92 percent of ischemic stroke patients have no medical treatment other than giving aspirin in the week following stroke, because they arrive at the hospital too late for the clot-buster drug (three-hour window after stroke induction). I am currently focusing on a small ischemic stroke in the cortex, and my pharmacological treatments begin 24 hours after stroke induction with daily medication. I am focusing on a combination of drugs (already FDA approved for other uses) that works to enhance brain-derived neurotrophic factor, vascular epithelial growth factor and neurogenesis in the aged brain. In very preliminary work, I am seeing an increase in neurogenesis in the group taking this drug combination that appears to correlate with functional recovery from the stroke. Future work will evaluate the mechanisms behind the functional recovery, and will determine if the functional recovery remains once the medication is stopped.
Molecular & Cellular Neuroscience: Control of Breathing
My research interests include examining how animals adapt to environmental (temperature changes) and metabolic (exercise, feeding, etc.) perturbations to their acid-base status. Alterations in breathing are the primary, acute response to a metabolic acidosis or alkalosis. Current projects in my lab involve experiments designed to understand how central (brainstem) chemoreceptors sense changes in blood gases and pH. We use the combined techniques of fluorescence imaging microscopy and whole-cell electrophysiology to measure neuronal responses to changes in CO2, O2, and pH in brainstem neurons. We also use behavioral physiology to investigate the organismal response to altered O2 or CO2 environments. I am interested in understanding how these chemoreceptors are altered by changes in the animal's environment.
My laboratory studies the cellular neuroscience of respiratory control. We focus on the neurons from the brainstem of neonatal rats and their response to elevated levels of CO2. It is believed that these neurons play a major role in controlling breathing and our work is thus of relevance to disorders that involve altered respiratory drive, such as sudden infant death syndrome (SIDS) and sleep apnea. The main thrust of our work is the characterization of the cellular signaling pathways and the ion channel targets involved in the sensing of elevated CO2 by central chemosensitive neurons. This work involves pH- and calcium-sensitive fluorescent dyes to study changes of intracellular pH and intracellular calcium and their role in CO2-induced increased firing rate of these neurons. We also employ whole cell current clamp to study the change in electrophysiological properties of these neurons as well as immunohistochemical and whole cell voltage clamp techniques to characterize the ion channel targets of the chemosensitive signals. We are using these data to develop a mathematical model of excitability in central chemosensitive neurons to determine the channels, signals and properties that make a neuron chemosensitive.
Recently, we have begun to study CO2-sensitivity of neurons believed to be involved in the generation of panic disorders using a knock-out mouse model that lacks a key G-coupled receptor protein on T cells. This work involves electrophysiology and measurements of breathing using whole body plethysmography and is addressing the interesting possibility that the control of breathing and panic disorders may involve inflammatory responses within the brain.
Early detection of an oxygen deficit in the bloodstream is essential to initiate corrective changes in the breathing pattern of mammals. My research focuses on the critical role in this process of specialized oxygen-sensing organs called the carotid bodies. These tiny neurotransmitter rich organs are located at the bifurcation of the carotid arteries and respond to a fall in blood pO2 and pH with transmitter release. This mechanism evokes an increase in the firing frequency of the carotid sinus nerve which innervates the respiratory centers in the brain and ultimately corrects the pattern of breathing. The laboratory uses a combination of techniques including electrophysiology, cellular imaging, amperometry, immunocytochemistry and molecular biology to address the following questions: 1.) What are the precise physiological and molecular mechanisms that underpin the oxygen-sensitivity of the carotid body? and 2.) How do pathological disease states that impact upon respiration alter the physiology of the carotid body? This research specifically addresses the modulation of the carotid body by chronic and chronic intermittent hypoxia. My recent research has indicated that the energy-sensing enzyme AMP-activated protein kinase is critical in the transduction of hypoxic-signalling by the carotid body. Future research will determine the importance of this enzyme not only in acute hypoxic-signalling but also in the plasticity observed in the carotid body during such disease states as sleep apnea.
Molecular & Cellular Neuroscience: Genomics
The specific aims of my current project are to use comparative genomic hybridization to characterize genomic changes in melanoma samples, in order to design DNA-based diagnostic tools. An additional project recently described post-transcriptional regulation of MDM4, an important negative regulator of the p53 tumor suppressor, by a microRNA. We hope to expand on this project by examining MDM4 regulation in melanomas, where it has been described as a strong potential drug candidate. A variety of other projects are ongoing through my role in directing the Center for Genomics Research.
Molecular & Cellular Neuroscience: Endocrine System
My current research interests involve investigating neuroinflammation and neurodegeneration in mice exposed to organophosphates such as sarin or chlorpyrifos. For this we are analyzing dozens of cytokines from specific brain regions, i.e., amygdala, hippocampus, dentate gyrus. The goal is to determine if specific inhibitors of caspases can attenuate or protect the brain long term after exposure to these agents. In addition, we are also studying how the proteome and peptidome of the hypothalamic, pituitary, adrenal, pancreatic-axis (HPAP-Axis) are affected in diseases or under chemical challenge conditions. My research involves studying the expression, sorting, processing and secretion of HPAP peptide hormones such as vasopressin, oxytocin, insulin and ACTH. A third branch of my research is to study the effects of fractionated snake venom proteins on different tissues, e.g., muscle, skin, neuronal, and lung. My long term goals are to identify and investigate the effects that specific venom proteins have on cytokines, hormone signaling, surfactant production, actin structure and collagen production.
Sherif M. Elbasiouny, Ph.D., P.E., P.Eng.
Assistant Professor of Neuroscience, Cell Biology & Physiology and
Assistant Professor of Biomedical, Industrial & Human Factors Engineering
Director, Neuroengineering & Neurorehabilitation Laboratory
My research interest is in the fields of neuroengineering and rehabilitation neuroscience. My work relies on combining computer modeling and electrophysiological recording techniques for studying the role of spinal neurons in integrating the sensorimotor signals at the cellular and system levels for movement control during health and in neurological disorders (e.g., after spinal cord injury, SCI, and in the neurodegenerative disease amyotrophic lateral sclerosis, ALS). In particular, I investigate the cellular mechanisms regulating the neuronal excitability (e.g., cell morphology, membrane electrical properties, voltage-dependent ion channels, synaptic inputs) and their contribution to the motor system output in the healthy state, and study the changes in these mechanisms after neurological injury or disease. Computational methods are employed to develop realistic three-dimensional anatomically-based electrical models of healthy and diseased neurons. These models are composed of thousands of compartments represented through complex arrangements of resistor-capacitor (RC) networks that possess multimodal time-varying and voltage-dependent behaviors to reproduce the intricate electrical events seen during experimental recordings. These electrical models are also used to design electrical stimulation paradigms that modulate the aberrant neuronal excitability in neurological disorders. In-vitro experiments, on the other hand, are employed to test and validate the results of computer simulations. With this knowledge, my research work aims in the long term to develop electrical stimulation-based biodevices, called smart implantable neural prostheses (SIN prostheses), for alleviating motor disabilities and restoring motor function after SCI and ALS.
Nasser Kashou, Ph.D.
Assistant Professor of Biomedical, Industrial & Human Factors Engineering
Dr. Kashou has a background in medical imaging and image processing. In his previous position, he was the director of Experimental Research in the Department of Radiology at Nationwide Children’s Hospital. Within the last eight years, he has worked on neuroimaging analysis and support, specifically in the field of magnetic resonance imaging (MRI). Some of this analysis has included functional MRI (fMRI), diffusion tensor imaging (DTI) and volumetric analysis. His minor areas of specialization have been vision science and neuroscience, specifically oculomotor function. Most recently, he has been working on segmentation of brain regions, DTI and fMRI for mild traumatic brain injury, infantile nystagmus syndrome, convergence insufficiency and the effects of anesthesia on adolescents. Other research interests include neuroimaging using diffuse optical tomography (DOT).
Dr. Kashou currently runs the biomedical imaging lab (BMIL) at WSU. He is also the director of the fNIRS (functional Near Infrared Spectroscopy) lab under the BMIL core. This lab consists of a NIRS system along with a portable physiological monitoring unit. Both these labs and the resources available therein are available to potential research students.
Jason Parker is a board-certified diagnostic medical physicist specializing in advanced neuroimaging methods that include high-resolution MRI, functional MRI, MR spectroscopy, diffusion tensor imaging, and phase contrast MR. He is employed by the Wright State Research Institute where he is the technical lead for the Neuroscience and Medical Imaging Program. In this capacity, he leads neuroscience research collaborations with the 711th Human Performance Wing of the Air Force Research Laboratory that seek to leverage advanced neuroimaging tools to improve the assessment and performance of human operators. Parker is also actively involved in clinical medical physics testing and consulting at hospital and outpatient clinics throughout Ohio. Previously, he worked as the senior scientist and lead MR physicist at the Kettering Health Network. In this role, he managed the Imaging Science Research Department, an inter-disciplinary translational research initiative focused on developing and applying emerging imaging techniques to improve the treatment of disease. During this time he also had quality control and safety responsibilities at KHN-owned facilities, including 17 clinical magnets covering a 50-mile radius. Parker received his B.S. in Applied Physics at Rensselaer Polytechnic Institute and his Ph.D. in Medical Physics from the University of Florida.