UAMS.EDU

Neuroscience Track Faculty

The primary department of each Neuroscience track faculty member is listed.

Syed Ali, PhD
Biochemistry and Molecular Biology
My laboratory is studying the effects of nanomaterials on the central nervous system.We have demonstrated that NPs are capable of generating oxidative stress and free radicals, which may in turn produce neurotoxicity.  Carbon nanotubes (CNTs) and graphenes are considered to have revolutionized the field of nanotechnology because of their light weight. However, this property can be potentially hazardous if it allows CNTs or graphenes to reach the lung and blood stream after environmental exposure.  Using in vitro and in vivo approaches,We plans to investigate the potential of CNTs to produce adverse effects on cellular systems due to their ability to cross the blood brain barrier (BBB). In addition, we are also investigating the effects of cell phone radiation on BBB integrity using both cell culture models and whole animal approach.     In addiction,my research focused also on the study of cellular and molecular mechanisms of oxidative stress and free radical-induced neurodegeneration and potential neuroprotective mechanisms of antioxidants. DWe have demonstrated that selective CNS-acting drugs, drugs of abuse, dietary supplements, environmental agents, pesticides, and organometals induce neurotoxicity by generating free radicals. Using different pharmacological and genetic approaches We have also demonstrated that peroxynitrite is responsible in methamphetamine (METH)-induced dopaminergic neurotoxicity and compromises BBB integrity.  We have s l utilizes the MPTP-mouse model of Parkinson’s disease (PD) and to examine the neuroprotective role of nitric oxide inhibitors, protease inhibitors and selective dopaminergic agonists and antagonists.

Steven Barger, PhD
Geriatrics
Web profile 
My lab is focused on Alzheimer’s disease. Current research is examining the role of diabetes-related disruptions in glucose metabolism and the impact this has on brain function. Evidence indicates that both Alzheimer’s and diabetes involve processes connected to inflammation, which has been another of my longstanding areas of research.

Sarah Blossom, PhD
Pediatrics
Web profile
Developmental exposure to environmental toxicants in a mouse model and understanding mechanisms of exposures on immune system, neurodevelopment, and behavior

John Bowyer, PhD
NCTR
Over the last 25 years, my research has focused on the neurotoxic effects of stimulants, particularly the amphetamines, as it relates to seizures and hyperthermia.  In the last 10 years my research interests have focused primarily on the molecular biology/toxicology aspects of neurotoxic insults as they relate to brain vasculature, specifically, the adverse effects of amphetamines on the meninges and the choroid plexus.  Most recently, our group within the FDA has been looking at mechanisms to open up the BBB to test the neurotoxicity of drugs that have minimal access to the CNS.

Jason Chang, PhD
Neurobiology and Developmental Sciences
Web profile 
Apoptosis; Mercury toxicity; Tai Chi exercise for osteoarthritis pain

John Chelonis, PhD
Pediatrics
Behavioral assessment across species (rats, monkeys, and humans)

David Davies, PhD
Neurobiology and Developmental Sciences
Web profile
Current research is a two-year multifaceted education-related project to assess the efficacy of a joint interdisciplinary effort to increase the content of pathology in the curriculum’s new Human Structure module (formerly gross anatomy). A very significant element of the project is to have each of 35 dissection teams obtain biopsies from the donor’s cadaveric remains, and to have the Department of Pathology’s clinical laboratory process the tissue and prepare microscopic slides for the teams to examine. Because the dissection teams chose (with some guidance from the faculty) what organs to biopsy, they have to determine their own learning objectives and critically assess and share the findings of their anatomical investigation. Preliminary findings concerning the active learning and self-directed discovery features of the project have been published as abstracts for two national societies.
Previous NIH-supported experimental work focused on the pathogenesis of developmental and neurodegenerative disorders resulting from substance abuse. Specifically, the laboratory engaged in studies designed to determine the extent to which acute and chronic alcohol use alters the repair of cerebral tissue in the aftermath of traumatic injury. Cerebral cell and organotypic cultures, in vivo models were used to assess the responses of astrocytes and microglia to cytokines and/or alcohol. These studies endeavor to provide basic information regarding the cascade of cell proliferative and reactive mechanisms elicited at the site of brain lesions resulting from traumatic injury. Since alcohol abuse is a predisposing factor for trauma, an understanding of the influence of alcohol on the metabolism and reactivity of glial cells will be beneficial for the design of appropriate clinical treatment protocols. Dr. Davies directs the Human Structure (medical gross anatomy) course, is co-chairs the Basic Science Education Subcommittee of the College of Medicine Curriculum Committee and helps teach the Cellular and Developmental Neuroscience graduate course.

Maxim Dobretsov, PhD
Anesthesiology
Web profile
Studies of mechanisms of physiological and neuropathic pain and pharmacological treatment of pain  Studies of the role of isoforms of Na,K-ATPase in neuronal function and disease  Studies of the effects of physiological effects of microgravity and low-grade irradiation in rat models

Paul Drew, PhD
Neurobiology and Developmental Sciences
Web profile
Neuroimmunology

William Fantegrossi, PhD
Pharmacology and Toxicology
Web profile
Research in my laboratory is currently focused on several categories of emerging drugs of abuse, including synthetic cannabinoids (constituents of K2/”Spice” smoking blends), analogues of cathinone (present in “bath salts” preparations), and novel arylcyclohexylamines (related to PCP and ketamine.) In an effort to better understand the biological actions of these emerging drugs of abuse, we use behavioral pharmacology techniques in rodents to compare these compounds with more the well-known drugs of abuse which these emerging drugs are designed to mimic (such as the phytocannabinoid delta9-THC, psychostimulants like MDMA and methamphetamine, and PCP).

Sherry Ferguson, PhD
National Center for Toxicological Research
Neurobehavioral toxicology

Edgar Garcia-Rill, PhD
Neurobiology and Developmental Sciences
Web profile
Neuroscience

Paul Gottschall, PhD
Pharmacology and Toxicology
Web profile
Synaptic plasticity is a neuronal mechanism essential for memory formation and recall, and alterations in plasticity occur in various types of dementia including Alzheimer’s disease.  Data from my laboratory has supported the concept that extracellular matrix is a key modulator of synaptic plasticity and changes in matrix deposition with age and in Alzheimer’s disease contribute to the decline in plasticity that occurs, pre-clinically, in disease progression.  Thus, particular matrix molecules that interact with the synapse provide a novel target for testing pharmacological compounds that affect matrix synthesis, deposition and signaling which would improve synaptic plasticity and delay or inhibit the progression of Alzheimer’s disease.

John Greenfield, MD, PhD
Neurology
Web profile 
My laboratory investigates the electrophysiological basis of epilepsy and mechanisms of action of antiepileptic drugs, with particular focus on inhibitory neurotransmission and the GABA-A receptor..  I also conduct clinical research related to epilepsy and comorbid conditions, as well as  novel anticonvulsants.

Abdallah Hayar, PhD
Neurobiology and Developmental Sciences
Web profile
Electrophysiology of olfactory bulb and cerebellar neurons – Alcohol research – Rhythmic motor movements such as licking and running – Effects of radiation on neuronal function – Imaging neuronal network – Synchronous bursting of neurons.

Andrew James, PhD
Psychiatry
Web profile
Improving functional neuroimaging methodology to understand normative variance in neural encoding of cognition, in order to better translate fMRI research into clinical practice.

Cynthia Kane, PhD
Neurobiology and Developmental Sciences
Web profile
We are team investigating the impact of alcohol consumption on brain function. We study the impact of alcohol across the lifespan, from the impact on a fetus when a mother drinks alcohol, through the impact of adolescent and adult binge and chronic drinking, to the impact on the aging brain.

Mahmoud Kiaei, PhD
Neurobiology and Developmental Sciences
Web profile
Investigating the mechanism(s) of motor neuron degeneration in ALS, development of efficacious therapeutic strategy for ALS and other neurodegenerative diseases. Development of transgenic mouse model for ALS carrying profilin1 mutation. Investigation of mutant profilin1 toxicity.

Linda Larson-Prior, PhD
Psychiatry
Web profile
The focus of my laboratory (http://eon.wustl.edu) is on the dynamic neural network re-configurations that occur as the brain changes its state under both normal conditions such as sleep, and in abnormal conditions such as induced shifts in conscious awareness (anesthesia) or pathological shifts in cognitive awareness (fluctuating consciousness, sleep parasomnias and neurodegenerative disease states).  We have developed the use of simultaneous acquisition of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) to help us better understand these shifts in network connectivity and function as the brain shifts state over the course of 24 hours.  We have extended our neuroimaging (fMRI) data to examine changes in large-scale functional brain network connectivity with neural state using graph theoretical techniques.  As part of the Human Connectome Project, my laboratory worked with a large international team to define the time-varying connection patterns in over 1200 normal adult human subjects (http://www.humanconnectome.org).  The laboratory maintains extensive collaborations with other research teams interested in the use of functional network methods in EEG, MEG, fMRI and EEG/fMRI to examine brain dynamics in both health and disease.

Kim Light, PhD
Pharmaceutical Sciences
Web profile
Mechanisms of damage to Purkinje neurons and cerebellar circuits resulting from third-trimester alcohol exposure.  These studies are exploring the nature and extent of damage that can result from a single binge use of ethanol at specific times in the early third trimester. We have found that Purkinje neurons die within 12 hours from apoptosis proportionate to the peak BEC achieved. In addition we have identified damage to the developing Climbing Fiber innervation and alterations of cerebellar circuits that suggest possible avenues for pharmacological assistance to children with this type of alcohol-induced damage.

Melanie MacNicol, PhD
Neurobiology and Developmental Sciences
Web profile 
I am working on identification of the cellular mechanisms that control cell growth and development.  I am particularly interested in the role and regulation of stem cells in neural development and in cancer.

Angus MacNicol, PhD
Neurobiology and Developmental Sciences
Web profile
Cell cycle control, stem cells, cancer stem cells, drug discovery, mRNA translation, vertebrate development

Merle Paule, PhD
Pharmacology and Toxicology
Behavioral Pharmacology and Toxicology; Using behavioral tasks of cognitive function to assess the effects of drugs and other chemical on brain function, from animal models–including rodents and nonhuman primates–to humans with a focus on pediatric aspects.   The developmental neurotoxicity associated with pediatric general anesthesia.

Kevin D. Phelan, PhD
Neurobiology and Developmental Sciences
Web profile
Ethanol regulation of neuroimmune mechanisms in the brain. Role of TRPC channels in seizure generation, epilepsy and stroke.

Robert Reis, PhD
Geriatrics
Web profile 
My research focuses on the molecular genetics of longevity and age-associated diseases. I was trained in genetics, and turned to C. elegans as a model system in which to develop gene mapping methods to characterize genes that govern longevity.  We developed new methods for this, and succeeded in mapping over 27 highly-significant loci for lifespan, resistance to stresses, and Darwinian fitness.  Using chromosomal mapping, my group was the first to identify the Pirin gene on the X chromosome as a determinant of post-menopausal bone loss in women, a discovery later confirmed in a Chinese population.  We also pioneered the role of homologous recombination in the development and progression of myeloma, prostate, and breast cancers. We were the first to note that cells from many different cancer types feature very high levels of homologous recombination, and high expression of the Rad51 recombinase complex that mediates it. We are now working chiefly on genetic factors that regulate lifespan, and that contribute to protein aggregation — key toxic intermediates in neurodegenerative diseases.

William Slikker, PhD
NCTR
Web profile
Developmental neurotoxicology

William Wessinger, PhD
Pharmacology and Toxicology
Web profile
My research employs in vivo pharmacology and behavioral analysis to study the effects of drugs of abuse. A variety of techniques and models are used including drug discrimination, drug self-administration, locomotor activity, receptor binding and pharmacokinetics, to gain a better understanding of the psychopharmacology of drug abuse, drug tolerance and drug dependence.

Patricia Wight, PhD
Physiology and Biophysics
Web profile
The focus of research in my laboratory is centered on CNS development, particularly with regard to the formation and maintenance of myelin. Myelin is the tightly compacted multilamellar sheath, which surrounds axons and promotes saltatory conduction of nerve impulses. The myelin proteolipid protein gene (PLP1) encodes the most abundant protein found in mature myelin from the CNS. Expression of the gene is regulated spatiotemporally, with maximal expression occurring in oligodendrocytes during the myelination period of CNS development. PLP1 expression is tightly controlled; misregulation of the gene in humans can result in the X-linked dysmyelinating disorder Pelizaeus-Merzbacher disease (PMD), and in transgenic mice carrying a null mutation or extra copies of the gene can result in a variety of conditions from late onset demyelination and axonopathy to severe early onset dysmyelination. With the use of transgenic and transfection paradigms, we have been able to show that the first intron of the PLP1 contains an enhancer region that is required for expression in oligodendrocytes as well as in other cell types that express PLP1. This region also overlaps a couple of recently discovered, alternatively spliced exons that are primarily restricted to the human species. Current efforts in the laboratory are focused on: identifying the transcription factors/architectural proteins that mediate enhancer function in PLP1 intron 1; test whether critical mutations in the enhancer could be the cause of PMD in patients with unaltered PLP1 coding sequence and gene dosage; understand the and spatiotemporal expression and function of intron 1-dervied splice isoforms in man. We are also using our PLP1-lacZ transgenic mice as a tool to screen for small molecules that stimulate myelination as a possible therapeutic for demyelinating diseases such as multiple sclerosis.

Fang Zheng, PhD
Pharmacology and Toxicology
Web profile
Molecular and celllular mechanisms of epilepsy, stroke and other neurological diseases and the discovery of novel therapeutics