Michael N. Sack MD, PhD trained in South Africa and did his clinical residency and fellowship at Georgetown and Washington Universities, respectively. As chief of the Laboratory of Mitochondrial Biology and Metabolism at the National Heart, Lung and Blood Institute, Dr. Sack and his laboratory found that mutations in PARK2, a gene mutated in young-onset Parkinson’s disease, decreases stability of the CD36 receptor. CD36 plays an important role in immune and metabolic regulation. His team is studying patients at the National Institutes of Health Clinical Center to explore mechanisms whereby PARK2 mutations lead to Parkinson’s disease. These studies include the use of skin biopsy and blood samples donated by trial participants to develop cellular models of Parkinson’s disease through induced pluripotent stem (iPS) cell technology. As Parkin (the PARK2 protein regulates additional immune proteins), Dr. Sack’s laboratory staff are now extending their research to explore the role of Parkin in brain immune repair programs important in preventing damage to dopaminergic neurons.