Mild Traumatic Brain Injury Increases Risk of Parkinson's

There's a clear link between mTBI and later development of Parkinson Disease.

Posted May 25, 2018

Recent research by Raquel Gardner and colleagues at the University of California in San Francisco shows that there are long-term effects of mild traumatic brain injury (mTBI) on the potential expression of neurodegenerative disease. Their study, “Mild TBI and risk of Parkinson Disease,” just published in the journal Neurology, is the most comprehensive to date to examine the chronic effects of brain injury on later development of the neurodegenerative disorder Parkinson disease.

They assessed of records of military veterans from Operation Enduring Freedom and Operation Iraqi Freedom available in the Veterans Health Administration database. Screening whittled the initial sample of over 325 000 veterans to a total sample of 182,634 folks. Those with mTBI had more than 50% increased risk for development of Parkinson Disease and 65 percent of those who were later diagnosed with Parkinson’s Disease had a prior mTBI.

With severe brain injury there is an increased expression of a protein called alpha-synuclein. The neurophysiological function of alpha-synuclein remains to be unraveled. But we do know that the neurobiological mechanism of degradation and dysfunction of neurons in Parkinson’s is strongly related to formation of Lewy bodies that arise from accumulation of alpha-synuclein.  So, elevated levels of alpha-synuclein are related to impaired brain function.

The study by Gardner and her colleagues provides critical evidence of the relationship between exposure to mild traumatic brain injury and later neurodegeneration. Along with the evidence showing increased risk of depression after mTBI and the potential for multiple exposures to lead to chronic traumatic encephalopathy, the relationship to Parkinson Disease underscores the need to prevent mTBI; to track, monitor, and follow up those so injured; and to develop strategies to minimize exposure in the first place. In truth, there is nothing mild about the lived experience of “mild traumatic brain injury.”

When considering the broader implications of the Gardner paper, what stands out is the gap that exists in research into mild traumatic brain injury across disciplines. Different approaches are taken based on the contextual cause of the injury: mTBI is studied in a sport injury context, as a blast injury in military contexts, and as a regular injury that just happens to normal folks. Much of the discussion about research takes place independently within sports medicine, clinical neurology, and neuroscience specialists.

However, the axons in your nervous system and the neurons to which they are connected do not differentiate the cause of the damage they experience and then express alpha-synuclein accordingly. Regardless whether the injury is caused by an improvised explosive device, a fall from a chair while putting up Christmas lights, or a heavy helmet-to-helmet hit between NFL players, the so-called mild traumatic brain injury is experienced the same way at the cellular level.

Appreciating common ground is critical for moving the field forward and uniting all the different research approaches that are taken to address the different health concerns. A hot topic related to mTBI is the potential relationship between accumulation of subconcussive events and concussion exposure and subsequent disease. Building together on common ground across different research and clinical agendas will truly be critical in improving prevention, diagnosis and treatment in “mild” traumatic brain injury.