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Michael Whalen, MD., Ph.D.
Neuroscience Center at Massachusetts General Hospital

Massachusetts General Hospital – East
Building 149
13th Street
Charlestown, MA 02129

Telephone: 617-724-4380


Dr. Whalen received his M.D. degree from the University of Vermont, Burlington, VT and residency training in Pediatrics at Medical College of Virginia, VA. He also trained in Pediatric Critical Care at the Pittsburgh Children's Hospital, Pittsburgh, PA before joining the Massachusetts General Hospital.

Research Program

My translational neuroscience laboratory is made up of a group of physicians and research scientists dedicated to finding specific treatments to improve outcome after traumatic brain injury (TBI).  We use mouse models of concussion and contusion traumatic brain injury to study mechanisms involved in cell death and cognitive dysfunction.  A major area of effort is dedicated to developing models of single and repetitive concussion brain injury in children and adults.  One major area of interest is the role of programmed necrosis mediated by RIPK1, also known as necroptosis, in cell death and cognitive outcome after cerebral contusion.  Recently we have discovered that RIPK1 may also mediate cognitive dysfunction after concussion TBI in which cell death does not occur, suggesting multiple functions for RIPK1 in addition to cell death that may be TBI model specific.  A second major area of interest is the role of plasma membrane damage in cell death and secondary damage after contusion TBI.  This line of investigation has led to the discovery that membrane resealing agents reduce blood brain barrier damage and improve a number of clinically relevant outcome measures after cerebral contusion in mice.  A third major research area is the effect of near infrared light on cell death and cognitive outcome after TBI.  Near infrared light interacts with cytochrome C oxidase and improves respiration, increases ATP and reduces inflammation.  We have found that near infrared laser light applied 80 minutes after controlled cortical impact reduces cognitive deficits at 1-2 weeks after injury.  We are hoping to bring this promising therapy to clinical trials in children and adults with TBI.  A fourth major area of study is how repeated concussions lead to development of traumatic encephalopathy, Alzheimer’s disease, and cognitive dysfunction, using newly developed mouse models of repetitive concussive TBI.  A fifth area of interest is the role of microglia in the pathogenesis of cell death and cognitive dysfunction in TBI, and how the peripheral and CNS immune systems interact to modify outcome after injury.  We use models of adult and childhood TBI and are focused on understanding mechanisms of secondary injury and finding new treatments to reduce cognitive and other neurological sequelae of TBI in children and adults.  Another major area of interest is the study of mechanisms of cell death after intracerebral hemorrhage.  We have a wide range of collaborators in the Boston area including scientists at Massachusetts General Hospital, Children’s Hospital Boston, Tufts University, and Harvard Medical School. 

We accept high school and college students in summer research programs and medical students year round, as well as physicians in KO8 track research training.  We are funded by NIH/NINDS, the National Football League Charities, and the Charles Hood Foundation.  Those interested in providing philanthropic support for a specific area of interest, especially concussion studies, should contact Dr. Whalen at

Thank you for your interest in our laboratory.


Click here to access a full PubMed search on Dr. Whalen

Khuman J, Meehan WP 3rd, Zhu X, Qiu J, Hoffmann U, Zhang J, Giovannone E, Lo EH, Whalen MJ, Tumor necrosis factor alpha and Fas receptor contribute to cognitive deficits independent of cell death after concussive traumatic brain injury in mice. J Cereb Blood Flow Metab 2011;31(2):778-89

• Qiu J, Whalen M, Lowenstein P, Fiskum G, Fahy B, Darwish R, Aarabi B, Yuan J, and Moskowitz M, Upregulation of the Fas receptor death-inducing signaling complex after traumatic brain injury in mice and humans. J Neurosci, 2002. 22(9): p. 3504-11.

Yoshimura S, Teramoto T, Whalen M, Irizarry M, Takagi Y, Qiu J, Harada J, Waeber C, Breakefield X, and Moskowitz M. FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice. J Clin Invest, 2003. 112(8): p. 1202-1210.

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