Consistent head impacts in sports can compromise the blood-brain barrier and lead to chronic traumatic encephalopathy (CTE), a neurodegenerative disorder affecting numerous retired athletes from soccer, rugby, and boxing. This crucial finding raises hopes for new diagnostic and therapeutic approaches, as CTE is typically diagnosed only post-mortem.

“Numerous drugs are being developed to restore the blood-brain barrier for neurological treatment, which may offer promising futures if they receive approval,” notes Matthew Campbell from Trinity College, Dublin.

Campbell and his team conducted brain scans on 47 former athletes from contact sports, retired an average of 12 years ago, and compared them with those from non-contact sports like rowing and individuals without sports backgrounds.

Participants underwent magnetic resonance imaging (MRI), utilizing a contrast agent that reveals blood-brain barrier breaches. Results showed that 17 athletes experienced significant contrast dye leakage, indicating severe damage, while non-contact athletes exhibited minimal leakage.

Those former athletes displaying greater blood-brain barrier impairment performed worse on cognitive assessments, pointing to a potential early link to CTE characterized by memory difficulties, emotional instability, and depression. “Previous evidence has shown that breaches in the blood-brain barrier correlate with CTE, and this supports that notion,” says Michael Buckland from the University of Sydney.

Mechanics of head impacts and whiplash during contact sports can physically damage the blood-brain barrier, explains Chris Greene from the Royal College of Surgeons in Ireland. “It’s better to view the blood-brain barrier as a dynamic system rather than a rigid wall,” he states, noting that impact forces can disrupt the cellular seal within the barrier, leading to increased permeability.

Once compromised, proteins, immune cells, and inflammatory mediators may invade the brain, causing inflammation and cell damage. Their study also analyzed brain tissue from individuals who succumbed to CTE, revealing prominent immune and blood protein infiltration within affected regions. The characteristics of CTE resemble those of Alzheimer’s disease, suggesting similar underlying mechanisms involving blood-brain barrier degradation with age.

Like in Alzheimer’s, CTE is marked by abnormal tau protein accumulation in the brain, with head trauma potentially triggering incorrect tau folding and aggregation.

If a head injury concurrently endangers the blood-brain barrier, blood proteins and inflammatory agents may enter the brain, exacerbating tau misfolding, further complicating the cognitive issues associated with CTE, according to Greene. His previous findings suggested that patients who died from CTE displayed a genetic signature linked to breaches in the blood-brain barrier, corroborating recent research.

Currently, CTE diagnosis is limited to post-mortem examinations revealing tau abnormalities. Nevertheless, Campbell and Greene assert that their MRI advancements could facilitate earlier diagnosis for individuals exhibiting cognitive or mood-related changes. In the future, this imaging technique might also evaluate CTE risk among active athletes, pending further research confirmation.

If deterioration of the blood-brain barrier signifies an initial CTE risk factor, adapting existing or developing new medications aimed at reinforcing the barrier could help prevent or slow its progression, suggests Greene. A compound like bevacizumab, known for diminishing blood vessel permeability, could be explored further. Additionally, other anti-inflammatory medications like minocycline are gaining traction amid ongoing developments.

“By focusing on strengthening vascular integrity and suppressing harmful signals before tau pathology solidifies, we may shift towards preventive measures,” concludes Professor Greene.