Derek Narendra, M.D., Ph.D.

Neurodegeneration is an increasing and unmitigated disease burden in our aging population. Among its causes are damaged mitochondria that accumulate with age, particularly in post-mitotic neurons and myocytes. Our group studies monogenic disorders to uncover mitochondrial stress responses that curb mitochondrial damage in neurodegeneration. Our focus includes PINK1 and Parkin, which form a stress-induced mitophagy pathway that targets damaged mitochondria for degradation. Mutations in these genes are the most common recessive forms of Parkinson's disease, linking mitophagy to neurodegeneration. We are additionally focused on dominant mutations in the paralogs CHCHD2 and CHCHD10, which cause Parkinson's disease, amyotrophic lateral sclerosis, frontotemporal dementia, and myopathy. In addition to enabling precision therapies for neurogenetic disorders, our work is uncovering fundamental mitochondrial stress responses to mitochondrial damage.

Dr. Narendra received his B.A. from Columbia University in 2002, Ph.D. from University of Cambridge in 2012, and M.D. from the University of Michigan in 2012. During his graduate research with mentors Dr. Richard Youle and Professor Sir John Walker, he identified a novel mitophagy pathway involving the coordinated activities of Parkin and PINK1, mutations in which are the leading cause of Early Onset Parkinson's Disease. He completed the Brigham and Women's Hospital & Massachusetts General Hospital Harvard Neurology Residency Program in 2016 and the Movement Disorders fellowship at Penn Neurology in 2020. In 2017, Dr. Narendra received the McFarland Transition to Independence Award for Neurologist-Scientists and joined the NINDS as an Assistant Clinical Investigator within the Neurogenetics Branch (NINDS). He was awarded a Lasker Clinical Research Scholarship and became a tenure track investigator in 2020. In 2022, he was awarded the Grass Foundation - American Neurological Association Award in Neuroscience. His laboratory focuses on mitochondrial dysfunction and stress responses in neurodegeneration.