Principal Investigator Myriam Heiman
other focus in our lab is a collaborative project aimed at understanding how long-term adaptations occur in the brain in response to the loss of a key neurotransmitter, dopamine. Specifically, the motor symptoms of Parkinson’s disease (PD) – including resting tremor, rigidity, akinesia, and postural instability – are seen upon dopamine depletion in the brain, resultant from the death of dopamine-producing cells in the substantia nigra. A standard treatment for PD is administration of levodopa, which can be converted to dopamine, and which works well in the short term to relieve symptoms. However, interestingly, over the long term, patients receiving levodopa develop debilitating side effects and, over time, this drug loses its efficacy. The lab is currently investigating the levodopa-induced changes that occur in one of the major cell classes that levodopa acts upon – medium spiny neurons in the striatum. The goal of this project is to identify the molecular basis of levodopa-induced side effects which may ultimately lead to therapeutic targets for the long-term treatment of a Parkinsonian state.
The mosaic nature of the brain reveals itself in the course of diseases, including Huntington’s and Parkinson’s disease, which preferentially strike particular cell types. Our lab is using cell-type specific profiling to identify the molecular basis of this differential vulnerability, in the hope of making progress towards new disease therapeutics, and continuing to unravel the complexity of the mammalian brain.