
Movement Disorders Basic & Translational Research
Investigators in the Kellar Family Division of Movement Disorders lead basic and translational research projects designed to advance our understanding of conditions such as Parkinson’s disease and improve our ability to provide effective treatments.
Basic Research
At the Fresco Institute for Parkinson’s and Movement Disorders, we research the molecular and cellular mechanisms that groups of neurons in the basal ganglia use to select, motivate, and reinforce voluntary motor actions. We also investigate the dopamine effects on downstream neural signaling and animal behavior. Taking advantage of the rich clinical and basic research environments at NYU Langone Health, we employ a combination of advanced molecular, genetic, optical, neurochemical, and electrophysiological approaches to tackle fundamental questions about the function of the basal ganglia, as well as identify novel therapeutic targets for Parkinson’s disease and other movement disorders.
We also study the molecular pathogenesis of neurodegeneration, focusing on repetitive genetic elements, mitochondrial metabolism, and nonneuronal brain cells. We collaborate with investigators at the Institute for Translational Neuroscience, including Molly C. Gale Hammell, PhD, Biyu J. He, PhD, Shane A. Liddelow, PhD, Esteban O. Mazzoni, PhD, Michael E. Pacold, MD, PhD, Margaret E. Rice, PhD, Richard Tsien, PhD, and others.
Translational Research
Our goal is to translate basic research findings toward clinical applications. Our laboratory studies are uncovering the mechanisms by which dopamine loss perturbs brain circuitry to Parkinson’s disease symptoms, how prolonged pharmacological dopamine replacement therapy causes abnormal basal ganglia activity that can lead to motor complications (including levodopa-induced dyskinesia), how adaptive plasticity in striatal neurons can prolong the motor benefit of dopamine replacement therapy (the long-duration response), and how other brain regions, such as the pedunculopotine nucleus, interact with the basal ganglia to produce Parkinson's disease symptoms and/or motor complications such as abnormal gait and freezing. These studies will instruct future therapeutic approaches for symptomatic treatment of Parkinson's disease.
We are also working to understand the mechanisms that cause neurodegeneration in Parkinson's disease and multiple system atrophy (MSA). With Dr. Horacio Kaufmann’s team at the NYU Dysautonomia Center, we are identifying and developing disease-specific biomarkers that may allow for earlier diagnosis, better monitoring of disease progression, and assessment of target engagement in therapeutic trials. Moreover, these studies allow us to understand the heterogeneity in Parkinson’s disease and related disorders, allowing us to better individualize therapeutic approaches.
The genetic program at the Fresco Institute offers comprehensive assessments for rare genetic movement disorders and genetic forms of Parkinson’s disease, from clinical assessment to advanced research based genomic analysis. Our genetic research program aims to understand of undiagnosed genetic movement disorders through the discovery of new causal genes and the characterization of new clinical presentation of genetic forms of movement disorders leveraging a dedicated team at NYU Langone as well as national and international collaborations.
As cornerstone members of the Parekh Center for Interdisciplinary Neurology, we coordinate and collaborate with other Department of Neurology divisions and the broader NYU neuroscience community on research efforts to find common mechanisms underlying disparate neurologic disorders, including peripheral immune dysfunction. We are particularly interested in understanding how the peripheral system contributes to central nervous system pathogenesis, other peripheral manifestations of neurodegenerative disease, and identifying prodromal stages prior to overt neurodegeneration. Identification of biomarkers at these stages and discovering stage-appropriate treatments would allow us to forestall the disease process early when therapy is likely to have the most impact.