Basic Science Program
Preclinical dysarthria in Parkinson Disease
The hallmark pathology of PD, loss of dopamine, has guided therapy for decades; however, dopamine-centered treatments do not improve vocal communication, cognition, or affect. In fact, during the early stages of PD prior to dopamine loss, there is significant degeneration in the locus coeruleus, a brainstem region rich in norepinephrine, another neurotransmitter. This region is vital to communicative and cognitive behaviors, indicating the importance of norepinephrine in controlling communication and cognitive processes. This research will examine three different therapeutic approaches that modulate norepinephrine: exercise, drugs, and social interaction. The rationale is that modulating noradrenergic brain systems will improve PD-related communication deficits, as well as cognition and affect.
Relating  deficits to pathology in models of Parkinson Disease
The pathology of Parkinson disease is complex and the pathogenesis underlying cranial sensorimotor behaviors, such as voice and swallowing deficits, are virtually unknown. Further, the onset of these deficits may occur in the preclinical periods. To address these issues in the basic science laboratory, we employ neurotoxin and genetic rat and mouse models of Parkinson diseases and test the onset and progression of vocalization, tongue use, chewing, functional swallowing, olfaction, forelimb use, and gait deficits. Our primary goals are to relate these behavioral deficits to the complex pathology of PD in order to improve behavioral, pharmacologic and surgical interventions.
PD as a whole body disease
Recent evidence shows that Parkinson disease affects not only the central nervous system, but also affects autonomic function and peripheral nerves and muscles. Our research efforts are aimed at determining the timing and progression of pathology in peripheral nerves and muscles that affect communication and ingestive behaviors.
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