McLean Hospital – 115 Mill Street, Belmont, MA 02478
Penny Hallett, PhD, is an assistant professor of psychiatry at Harvard Medical School and director of the Neuroregeneration Research Institute. She received her PhD from the University of Manchester, UK, before completing post-doctoral studies at Massachusetts General Hospital, moving in 2006 to McLean Hospital to join the Neuroregeneration Research Institute, founded by Dr. Ole Isacson.
Dr. Hallett’s research interests focus on understanding early neuronal dysfunction and degeneration in neurodegenerative diseases with a focus on Parkinson’s disease, and testing therapeutic interventions using regenerative and neuroprotective strategies. Her research aims to understand neurodegenerative diseases not only as central nervous system disorders, but also as systemic diseases involving the periphery, and also tests how aging processes can modulate cellular function and vulnerability. Since 2009, Dr. Hallett has been an editor for Molecular and Cellular Neuroscience.
The Neuroregeneration Research Institute, founded in 1989 by Dr. Ole Isacson and now led by Dr. Hallett, is accelerating the treatment of Parkinson’s disease and other degenerative brain disorders. The lab’s novel research team has a keen focus on improving individuals’ lives, and their work has been the basis for numerous innovations that are creating hope for patients and their families.
The lab works to move the field forward by approaching new treatments using novel findings in the modeling of synaptic and neuroplasticity responses. This effort includes new basic neuroscience models for neurodegenerative diseases, such as Parkinson’s disease, as well as cognitive models for aging research and neuropsychiatrically linked diseases.
Over the past two decades, the lab’s discoveries have significantly advanced the knowledge base to the point that Dr. Hallett and her staff are currently exploring viable therapies aimed at both protecting vulnerable neurons and replacing those destroyed by disease.
The lab has made numerous landmark discoveries in the area of novel treatments for Parkinson’s disease. In 2002, the lab proved that transplanting embryonic stem cells in animal models of Parkinson’s disease yielded functional new dopamine neurons that restored motor function. Taking this work a step further, in 2008, they were the first to show that skin cells could be reprogrammed into stem cells (becoming induced pluripotent stem cells, or iPS cells), then differentiated into specific dopamine neurons. These new dopamine neurons were effectively transplanted into the brain, again in animal models. In 2010, the lab made the exciting breakthrough that dopamine neurons could be grown from human iPS cells and transplanted effectively to mitigate disease, setting the stage for forthcoming clinical trials in humans.
By understanding how certain brain cells are either vulnerable or resistant to neurodegenerative diseases, the lab has also discovered specific “profiles” of vulnerable cell types, thus advancing neuroprotective strategies for Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis (ALS).
In addition, the lab coordinates with other local and international training programs within the areas of psychiatry, neurology, neuroregeneration, stem cell biology, and regenerative medicine.
Rocha EM, Smith GA, Park E, Cao H, Brown E, Hayes MA, Beagan J, McLean JR, Izen SC, Perez-Torres E, Hallett PJ, Isacson O. Glucocerebrosidase gene therapy prevents α-synucleinopathy of midbrain dopamine neurons. Neurobiology of Disease 2015;82:495-503.
Hallett PJ, Deleidi M, Astradsson A, Smith GA, Cooper O, Osborn T, Sundberg M, Moore MA, Perez-Torres E, Brownell A-L, Schumacher J, Spealman RD, Isacson O. Successful function of autologous iPSC-derived dopamine neurons following transplantation in a non-human primate model of Parkinson’s disease. Cell Stem Cell 2015;16:269-74.
Smith GA, Jansson J. Rocha EM, Osborn T, Hallett PJ, Isacson O. Fibroblast biomarkers of sporadic Parkinson’s disease and LRRK2 kinase inhibition. Molecular Neurobiology 2016; 53(8):5161-77.
Belmont campus - Mailman Research Center, Room 103