Professor Alan Faden M.D. hosts next CBR Seminar Event as iCalendar

02 February 2017

10:30 - 12pm

Venue: Clinical Education Centre

Location: Auckland City Hospital

Host: Professor Alan Faden

Contact info: Frankie Favero

Contact email:


About Professor Alan Faden M.D.

Dr. Alan Faden received his medical degree from the University of Chicago and neurology training at the University of California at San Francisco (UCSF).

Professor Faden is currently the David S. Brown Professor in Trauma, and Professor of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurosurgery and Neurology at the University of Maryland School of Medicine, as well as University of Maryland Professor; he has additional Professorship appointments in the School of Nursing, School of Pharmacy, and at the University of Maryland at College Park (Kinesiology). 

He serves as Director of the Shock, Trauma and Anesthesiology Research (STAR) Organized Research Center; as Scientific Co-Director for the Center for Sports Medicine Health & Human Performance (UMB and UMCP); and as Associate Dean for Trans-Campus Research Advancement in the School of Medicine.

Dr. Faden has published 380+ refereed research papers, more than 50 book chapters and proceedings, and edited 9 books or dedicated volumes.  His present work focuses on the pathobiology and treatment of traumatic brain and spinal cord injuries, mechanisms of cell death, neuroinflammation, central pain and drug discovery.

Professor Faden was the founding Editor-in-Chief of Neurotherapeutics  He served as President of the American Society for Experimental NeuroTherapeutics, first President of the National Neurotrauma Society and as President of the San Francisco Neurological Society. 



Traumatic brain injury (TBI) has been linked to chronic neurodegeneration. Described initially in boxers and subsequently recognized in contact sports, the association between repeated concussion (mild TBI) and progressive neuropsychiatric abnormalities has recently received widespread attention.

Less well appreciated are cognitive changes associated with neurodegeneration in the brain after isolated spinal cord injury. Also under-recognized is the role of sustained neuroinflammation after brain or spinal cord trauma, even though this relationship has been known since the 1950s and is supported by more recent preclinical and clinical studies.

These pathological mechanisms, manifested by extensive microglial and astroglial activation and appropriately termed chronic traumatic brain inflammation or chronic traumatic inflammatory encephalopathy, may be among the most important causes of post-traumatic neurodegeneration in terms of prevalence.

Importantly, emerging experimental work demonstrates that persistent neuroinflammation can cause progressive neurodegeneration that may be treatable even weeks after traumatic injury. 


CBR Seminars are supported by the Neurological Foundation of New Zealand.