MAR 15, 2017 07:30 AM PDT

Exercise Targeting Neuroplasticity in Parkinson's disease

Presented At Neuroscience 2017
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  • Associate Professor and Clinical Scholar in Neurology and Movement Disorders, University of Southern California, Keck School of Medicine
      Giselle M. Petzinger, MD, is an Associate Professor and Clinical Scholar in Neurology and Movement Disorders at The University of Southern California, Keck School of Medicine in the department of neurology. She completed her MD degree at University of Southern California, her neurology residency at Yale University, and her Fellowship in movement disorders at Columbia University. Her research primarily focuses on elucidating the underlying molecular mechanisms by which different forms of exercise target and facilitate repair of cognitive and motor circuitry, through processes collectively termed neuroplasticity. Her research involves both animal models of PD and clinical studies with patients thus providing the foundation for a translational research program spanning the spectrum from bench to bedside. She has been funded by national Parkinson foundation, NIH and US Army and has published extensively in the field of PD and exercise and repair. Dr. Petzinger is also committed to promoting education of wellness and lifestyle practices to facilitate disease prevention and to improve the quality of life for individuals of all ages. Towards this goal she has participated in developing as well as teaching educational health and wellness programs at universities both within the United States and abroad.


    Parkinson’s disease (PD) is characterized by the loss of dopamine and the disruption of brain circuits (basal ganglia and cortex) that are responsible for normal cognitive and motor performance.  Investigations utilizing animal models of PD serve as an important first translational research step for identifying therapeutic targets that can be used to identify and guide novel therapeutic treatments for modifying disease progression in PD. Studies from our lab and others have demonstrated that exercise can improve motor and cognitive function in PD.  Using animal models of PD, our lab has also shown evidence of exercise-induced neuroplasticity through modulating dopaminergic and glutamatergic neurotransmission and enhancing basal ganglia synaptic connections. Animal studies in our lab also suggest that the type of exercise performed, e.g. aerobic vs. skill based exercise, may play differential roles on these repair mechanisms.  Specifically, using a rodent model of striatal dopamine depletion we have provided the first evidence that skilled exercise compared to simple aerobic exercise increases functional recruitment of prefrontal cortex (PFC), a brain region central to cognition, and in particular executive function.  Ongoing studies in our lab investigate the molecular mechanisms that underlie exercise-induced alterations of regional blood flow and neuronal metabolic demand including the transcription factor hypoxia inducible factor HIF-1α.  Findings from these studies will elucidate mechanism(s) of exercise-induced neuroplasticity and repair and help guide exercise interventions in PD.


    Learning Objectives:

    1. Define Neuroplasticity and understand it’s potential role in mechanisms of repair of Parkinson’s disease.
    2. Understand the role that exercise may play in modulating dopamine and glutamate neurotransmission within the basal ganglia.
    3. Understand the role of exercise on synaptogenesis in animal models of PD.
    4. Describe different types of exercises that may be beneficial in enhancing cognitive function in PD.

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