Thursday, 28 March, 2024
HomeWeekly RoundupEngland's football authorities invite research into brain disease risk

England's football authorities invite research into brain disease risk

England's football authorities have invited applications for independent research into whether playing the sport heightens the risk of degenerative brain disease in later life.

Sport24 reports that this follows a campaign by the family of former West Bromwich Albion striker Jeff Astle, whose 2002 death from chronic traumatic encephalopathy (CTE) was linked to repeatedly heading heavy leather footballs.

The Football Association and players' union the Professional Footballers' Association made the call for research following 18 months of consultation and analysis. "This is a crucial issue for the FA and one that we feel passionately about addressing," the FA's head of medicine, Charlotte Cowie, is quoted in the report as saying.

"Dementia is a debilitating disease, which places extraordinary emotional and physical burdens on both sufferers and those close to them. Player welfare is paramount and it is increasingly important that the football authorities investigate further whether there are any potential risks associated with heading the ball, as this is a unique feature of our game."

The report says the focus of the independent study will be the question: "Is the incidence of degenerative neurocognitive disease more common in ex-professional footballers than in the normal population?" The FA and PFA will jointly fund the project. The closing date for the submission of research proposals is May this year.

The report says research into links between football and brain damage in later life is thin on the ground. A recent British study found the brains of four out of six former players with dementia showed signs of CTE, far in excess of the average rate of 12%.

World governing body Fifa says there is no conclusive proof that heading a ball or other sub-concussive impacts increase the risk of brain disease.

Abstract
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild impact traumatic brain injury from contact sports. Recently, a consensus panel defined the pathognomonic lesion for CTE as accumulations of abnormally hyperphosphorylated tau (p-tau) in neurons (neurofibrillary tangles), astrocytes and cell processes distributed around small blood vessels at sulcal depths in irregular patterns within the cortex. The pathophysiological mechanism for this lesion is unknown. Moreover, a subset of CTE cases harbors cortical β-amyloid plaques. In this study, we analyzed postmortem brain tissues from five institutionalized patients with schizophrenia and history of surgical leucotomy with subsequent survival of at least another 40 years. Because leucotomy involves severing axons bilaterally in prefrontal cortex, this surgical procedure represents a human model of single traumatic brain injury with severe axonal damage and no external impact. We examined cortical tissues at the leucotomy site and at both prefrontal cortex rostral and frontal cortex caudal to the leucotomy site. For comparison, we analyzed brain tissues at equivalent neuroanatomical sites from non-leucotomized patients with schizophrenia, matched in age and gender. All five leucotomy cases revealed severe white matter damage with dense astrogliosis at the axotomy site and also neurofibrillary tangles and p-tau immunoreactive neurites in the overlying gray matter. Four cases displayed p-tau immunoreactivity in neurons, astrocytes and cell processes encompassing blood vessels at cortical sulcal depths in irregular patterns, similar to CTE. The three cases with apolipoprotein E ε4 haplotype showed scattered β-amyloid plaques in the overlying gray matter, but not the two cases with apolipoprotein E ε3/3 genotype. Brain tissue samples from prefrontal cortex rostral and frontal cortex caudal to the leucotomy site, and all cortical samples from the non-leucotomized patients, showed minimal p-tau and β-amyloid pathology. These findings suggest that chronic axonal damage contributes to the unique pathology of CTE over time.

Authors
Sharon B Shively, Sarah L Edgerton, Diego Iacono, Dushyant P Purohit, Bao-Xi Qu, Vahram Haroutunian, Kenneth L Davis, Ramon Diaz-Arrastia, Daniel P Per

[link url="http://www.sport24.co.za/Soccer/International/english-fa-invites-brain-disease-research-20170330"]Sport24 report[/link]
[link url="http://link.springer.com/article/10.1007/s00401-016-1649-7"]Acta Neuropathologica abstract[/link]

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