Smeyne Research

Richard Jay Smeyne, PhD is Chair and Professor of Neuroscience at Thomas Jefferson University and Director of the Jefferson Comprehensive Parkinson's Center within the Vickie & Jack Farber Institute for Neuroscience. His scientific career has bridged academic research and pharmaceutical discovery, with a sustained focus on the cellular mechanisms that determine neuronal vulnerability and resilience in Parkinson's disease. He earned a B.S. in Biology from Saint Joseph's University, did Master’s work in Experimental Psychology at the University of Hrtford and earned a Ph.D. in Neuroanatomy from Thomas Jefferson University. He completed postdoctoral training at the Roche Institute of Molecular Biology with James Morgan and Tom Curran, where he contributed to early transgenic approaches, including the generation of the c-fos-lacZ transgenic mouse, which was the first transgenic animal that faithfully expressed an inducible transgene under direction of its ocgnate promoter. He subsequently held research leadership positions at Bristol Myers Squibb, where he worked with Dr. Mariano Barbacid to define the key neurological role of the Trk-family of neurotrophin receptors and Hoffmann-La Roche where he was their first Director of Neurogenetics. After leaving Pharma, he became a founding faculty member in the department of Developmental Neurobiology at St. Jude Children's Research Hospital. After 20 years at SJCRH, he was recruited to Thomas Jefferson University in 2016 as Full Professor and became Chair of the department in 2022.

Across more than three decades of independent investigation, Richard Smeyne has developed genetic, toxicant, inflammatory, and infectious models of parkinsonism. His laboratory provided one of the first studies showing that early adult environmental enrichment and sustained exercise can protect substantia nigra dopamine neurons from MPTP toxicity, then identified HIF-1alpha as a necessary component of this exercise-induced protection. This work helped establish a mechanistic preclinical foundation for the expanding use of structured exercise in Parkinson's care and research.

Richard Smeyne also helped advance a multi-hit framework for Parkinson's disease in which infection, systemic inflammation, genetic susceptibility, and toxic exposures interact over time. His studies have shown that both non-neurotropic respiratory viruses can alter brain immune states even when virus is not detected in the brain, and that prior infection can increase vulnerability to subsequent mitochondrial or environmental stress. More recent work has directly implicated mutant LRRK2 in peripheral lymphocytes and circulating IL-6 as drivers of neurodegeneration in inflammatory models.

Across his career, Richard Smeyne has also provided signifcant service to the scientific community. For 25 years, from 2000 to 2025, he served on the Parkinson's Foundation Scientific Advisory Board with the final 2 years serving as its Chair. He continues to work with the Parkinson’s Foundation on a number of review committees and also serves as a reviewer on many NIH and DoD panels as well as other Parkinson’s disease foundations around the world.

Michelle Smeyne is a neuroscientist whose research has focused on neuronal signaling, glial biology, and experimental models of Parkinson’s disease. She earned a B.A. in Psychology from West Chester University, completed advanced training in neuroscience at the University of Hartford, and received an M.S. in Anatomy and Neurobiology from the Medical College of Pennsylvania. 

Michelle Smeyne began her research career at Thomas Jefferson University and the Medical College of Pennsylvania before joining the Roche Institute of Molecular Biology as an Assistant Scientist. She subsequently served as a Senior Pharmacologist in the CNS Disorders program at Wyeth-Ayerst Research and later became an Associate Scientist in the Department of Developmental Neurobiology at St. Jude Children’s Research Hospital . 

Her early research helped define cellular mechanisms underlying synaptic plasticity in cerebellar Purkinje neurons. This work examined long-term depression of AMPA-receptor currents, protein kinase C signaling, sodium-dependent postsynaptic mechanisms, and metabotropic glutamate receptor-mediated calcium mobilization. These studies contributed to a broader understanding of how intracellular signaling regulates neuronal function and adaptive changes at synapses.

Michelle Smeyne later applied her expertise in cellular neuroscience to Parkinson’s disease research. Her studies demonstrated that glial cells contribute to strain-dependent differences in susceptibility to MPTP- and MPP⁺-induced parkinsonism. She also developed a method for culturing postnatal substantia nigra tissue as an in vitro model of experimental Parkinson’s disease and this work led to an underatnading of how interactions with other cells within the SN milieu (astrocytes and microglia) can alter sensitivity to environmental agents known to induce parkinsonism. Later studies, which she led, have examined the mechanisms underlying exercise-induced neuroprotection. She and her team demonstrated the need for induction of hypoxia prior onset of exercise-induced neuroprotection and the key role for the transcription factor Hypoxia-Inducible factor 1alpha (HIF1a) in this process. Together, this work has provided useful experimental approaches for studying dopamine-neuron vulnerability, neuron–glia interactions, and the cellular mechanisms underlying parkinsonian neurodegeneration and neuroprotection.

Elena Kozina’s research focuses on the neuroimmune mechanisms contributing to Parkinson’s disease, particularly how genetic susceptibility, peripheral inflammation, and infection influence the vulnerability of substantia nigra dopamine neurons. She earned her PhD in Physiology and Neuroscience from the Russian Academy of Sciences in Moscow where she examined progressive degeneration and compensatory plasticity within the nigrostriatal dopamine system in experimental models of Parkinson’s disease. She also completed advanced training at CNRS–Pierre and Marie Curie University in Paris. In 2013, she joined the Smeyne’s lab at St. Jude Children’s Research Hospital as a postdoctoral fellow and moved to Thomas Jefferson University in 2016. 

In the Smeyne lab, Elena Kozina has made important contributions to defining the role of LRRK2-dependent immune dysfunction in Parkinson’s disease. Her research demonstrated that inflammatory stress interacts with pathogenic LRRK2 mutations to produce exaggerated peripheral and central immune responses and dopaminergic-neuron loss. Using bone-marrow chimeric models, she further showed that mutant LRRK2 expression in peripheral lymphocytes can drive neurodegeneration following inflammatory challenge. This work also identified circulating interleukin-6 as a critical mediator, because neutralizing peripheral IL-6 prevented dopamine-neuron loss. Her current research seeks to identify the specific immune-cell populations responsible for LRRK2-associated neurodegeneration and determine how peripheral immune signals are transmitted to the brain. She is also investigating immune-cell exhaustion and biological immune aging as contributors to Parkinson’s disease risk and clinical heterogeneity through the ASAP Collaborative Research Network.

Elena Kozina also contributes to neuroscience education, mentoring, peer review, and scientific advocacy. She teaches neuropharmacology at Thomas Jefferson University, mentors graduate and postdoctoral researchers, and reviews manuscripts for several neuroscience and Parkinson’s disease journals. In 2024, she was selected as a Society for Neuroscience Early Career Policy Ambassador, recognizing her commitment to scientific advocacy and public support for biomedical research.

Matthew Byrne’s research focuses on experimental models of neurodegenerative disease, particularly Parkinson’s disease, with an emphasis on α-synuclein pathology, neuroinflammation, genetic susceptibility, and environmental contributors to dopamine-neuron degeneration. He earned a B.A. in Health and Societies from the University of Pennsylvania and a PhD in Neuroscience from Thomas Jefferson University. He has more than a decade of experience developing and characterizing rodent models of Parkinson’s disease and related synucleinopathies. His technical expertise includes stereotactic intracranial surgery, genetic disease models such as LRRK2, quantitative neuroanatomy, unbiased stereology, and measurement of central and peripheral immune responses. 

A major focus of  Matthew Byrne’s work has been determining how α-synuclein contributes to neurodegeneration. His studies have examined the biological compatibility and pathogenicity of α-synuclein fibrils and demonstrated that monomeric α-synuclein, previously considered relatively benign, can initiate inflammation and substantia nigra dopamine-neuron death in a susceptible genetic background. His work has also contributed to studies showing that LRRK2-dependent peripheral immune signaling, circulating interleukin-6, and viral infections can increase vulnerability to parkinsonian neurodegeneration. He has additionally advanced rigorous methods for quantifying neuropathology in both experimental models and human tissue. His contributions include stereological assessment, automated and semi-automated image analysis, and approaches that integrate spatial and temporal immune changes with neurodegenerative outcomes. He has applied these methods to studies of Parkinson’s disease, frontotemporal lobar degeneration, tauopathy, and amyloid pathology. 

In addition to his research, Matthew Byrne contributes to interdisciplinary team science and trainee development. He has completed certificates in Teaching in the Sciences and Science Communication and has actively mentored trainees within his laboratory, department, and the broader regional neuroscience community.

Her doctoral research examines how voluntary exercise alters the microvascular, anatomical, and epigenetic environment of the substantia nigra and whether these changes provide lasting protection against dopaminergic-neuron injury. Her broader interests include neurovascular biology, exercise-induced plasticity, epigenetic regulation, and the translation of exercise biology into therapeutic strategies for neurodegenerative disease. Tabitha Rodriguez earned a B.A. in Biological Foundations of Behavior with a concentration in neuroscience from Franklin & Marshall College and entered the Neuroscience PhD Program at Thomas Jefferson University. Her dissertation, Exercise-Induced Neuroprotection: Anatomical and Epigenetic Contributions in a Mouse Model of Parkinson’s Disease, integrates neuroanatomical, vascular, molecular, and computational approaches to understand the sustained effects of exercise on the nigrostriatal system. In this work, she is determining whether exercise-induced remodeling of the substantia nigra microvascular network contributes to dopamine-neuron resilience. She has also investigated whether neuroprotection persists after exercise is discontinued and has examined exercise-induced changes in the substantia nigra methylome using sequencing, R-based analysis, gene-ontology networks, protein-interaction networks, and transcription-factor motif analysis. 

In addition to her research, Tabitha Rodriguez has developed substantial experience in teaching, mentorship, scientific communication, and institutional service. She has taught neuroanatomy and advanced neurobiology, served as a laboratory teaching assistant and graduate peer mentor, and held leadership roles in Jefferson Neuroscience Mentoring, Development, and Advocacy and Jefferson Business and Biotechnology. Her work has been recognized through a Society for Neuroscience Trainee Professional Development Award, a Carl Storm Fellowship for the Gordon Research Summit, and graduate travel support from Thomas Jefferson University.

Sachi Gunesakara is an immunologist and virologist whose research focuses on innate immune responses to viral infection and how these may contribute to the development of parkinsonism. Sachithra Gunasekara earned a B.Sc. with honors in Immunology and Integrative Molecular Biology from the University of Colombo in Sri Lanka. She subsequently pursued doctoral training in Biomedical Sciences at the Oklahoma State University College of Veterinary Medicine and completed a graduate certificate in bioinformatics.

A major focus of Dr. Gunasekara’s doctoral studies defined the neutrophil response to SARS-CoV-2 infection using the domestic cat as a translational model of human COVID-19. Her studies characterized neutrophil activation, neutrophilia, neutrophil extracellular trap formation, and differences in immune responses to viral variants including Delta and Omicron. This work demonstrated the value of comparative animal models for understanding the immunopathogenesis of emerging viral diseases and for evaluating neutrophil-directed therapeutic strategies. She is using these skills in the Smeyne lab to define the role of peripheral immune responses to viral stimuli as an initiator of the signals that lead to development of Parkinson’s disease.

Her scientific accomplishments have been recognized through multiple research, presentation, fellowship, and travel awards, including an American Society for Virology Student Travel Award, the Robberson Summer Dissertation Fellowship, and awards for oral presentations at the INTERACT and Phi Zeta symposia and a recent postdotiral travel award at TJU. She has also taught immunology, virology, bacteriology, mycology, and molecular biology.