Parkinson’s disease (PD) is estimated to affect one million Americans. Its incidence increases rapidly with age, so as the average age of the population increases, the morbidity and economic burden which it imposes will grow enormously. PD presents with impairments of motor function, including tremor, rigidity, slowness of movement or postural instability. Patients also often develop non-motor impairments, including dementia, depression and autonomic failure. The motor signs are due to the loss of dopamine neurons in the midbrain. Many effective medical and surgical therapies now exist for the symptomatic treatment of the motor signs of PD, but they lose efficacy with time. Unfortunately, there is no therapy now available which prevents the inexorable worsening of the disease due to progressive neurodegeneration. The primary goal of our Laboratory is to develop such neuroprotective therapies.

While there are many good approaches to developing neuroprotective therapies, we focus on targeting the pathways of programmed cell death (PCD), also known as apoptosis. There is a growing consensus that the degeneration of neurons in PD is not a passive event, but rather it is due to the activation of genes which destroy the cell. These genes are the mediators of PCD. It may be possible to prevent neuron death by blocking these pathways.

We investigate PCD in dopamine neurons in two contexts: (1) During postnatal development, when PCD occurs normally, and (2) In adult rodent models of PD.