The goal of our laboratory is to prevent the causes of brain degeneration and loss of neuronal function. In addition, we aim to repair brain function by restoration of new neurons and glia in the brain. We have three major lines of research:

(1) Lipid storage and lysosomal enzyme deficiencies create massive risk for Parkinson's disease. In our laboratory we are testing disease-provoking genetic and age-related changes in enzymes and molecules that control lipid levels inside neurons and glia. Specifically, the so-called GBA enzyme has been found to be altered in both genetic and all forms of age-induced Parkinson's disease in our studies. Our team and collaborators have found several key components in pathways of lysosomal and lipid function to be defective in Parkinson's disease cells and tissues. New research in this laboratory aims to elucidate which molecules can solve the lipid problem that causes Parkinson's disease and some forms of dementia.

(2) Inflammation in the brain prevents function and leads to nerve cell degeneration. Our team provided early scientific findings that showed how the development of inflammation around neurons and glia in the brain results in cell death and loss of brain connection as in Parkinson's disease, Alzheimer's disease and other dementias. This research has progressed to a stage where a refined understanding of the inflammatory mechanisms that cause degeneration of the brain can be identified and potentially reversed by novel treatments. We have recently begun new projects to prevent nerve cell and glial degeneration caused by inflammatory disarray in the brain. These projects have potential to provide specific and novel therapies for many patients at risk for Parkinson's disease and dementias.

(3) Restoring function and reducing symptoms. Cell-based therapies to provide new nerve cells and glia to the Parkinson's disease patients and related disorders. By the time movement symptoms emerge, a Parkinson patient has usually lost over 60% of dopamine neurons due to the disease process. Our lab has developed cell-based restoration by transplantation in Parkinson's disease, using the patient's own cells which are reprogrammed into new dopamine neurons. This approach can restore all dopaminergic function lost by the disease. A potentially curative treatment for the well-established loss of dopamine neurons in the midbrain of patients with Parkinson's disease is underway in the lab and collaborative clinical institutions.