Once called “punch-drunk” syndrome or “dementia pugilistica”, chronic traumatic encephalopathy (CTE) has come to public attention in recent years through its association with professional football players in America. CTE results from blows to the head over a period of time which cause mild traumatic brain injury (concussion). The injuries sustained by the brain lead to progressive degeneration of brain function, seen as difficulties with thinking, emotions and behaviors. The symptoms may not become noticeable until many years later.
Previously only diagnosable at autopsy, neurology researchers showed in 2013 that brain damage consistent with CTE could be detected by PET scanning in some living, retired NFL players. CTE reached the headlines in the same year when the NFL provided $765 million in medical assistance for players suffering from severe neurological diseases who had a CTE diagnosis. As one commentator observed, CTE has subsequently become “the lynchpin for the brain injury conversation in America”.
However, in a series of recent papers, respected researchers (Faden & Loane, Department of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine) argue that there is a widespread misunderstanding about the true nature of traumatic brain injury and how it causes chronic degenerative problems. They are concerned that the focus on CTE is deflecting attention from other mechanisms, which they believe may be more important and treatable. While acknowledging that CTE is a serious problem, they claim that relatively few people have been diagnosed with the condition. The key culprit, they contend, is inflammation.
The researchers propose that inflammation’s role in the neurological problems ( such as brain atrophy, depression and cognitive decline) which occur after traumatic brain injury has been under-emphasised. Citing evidence from animal studies, recent brain imaging studies of professional football players, as well as larger studies, the researchers suggest that it is persistent brain inflammation after a single moderate head injury or repeated milder traumatic brain injury that is the likely cause of cognitive problems. The research also notes that brain inflammation can persist for many months or years in many people with TBI and may remain treatable long after injury has been sustained.
The researchers conclude
Manifested by extensive microglial and astroglial activation, such chronic traumatic brain inflammation may be the most important cause of post-traumatic neurodegeneration in terms of prevalence. Critically, emerging preclinical studies indicate that persistent neuroinflammation and associated neurodegeneration may be treatable long after the initiating insult(s).
The findings of Faden and Loane provide encouraging support for Neuren’s use of trofinetide in treating TBI. From yesterday’s Annual Report
Summarising, trofinetide helps to correct four of the hallmark pathological features of many central nervous system disorders: inflammation, over-activation of microglia, dysfunction of synapses and reduced levels of IGF-1.
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