Risk of chronic traumatic encephalopathy in rugby union is associated with length of playing career.
Risk of chronic traumatic encephalopathy in rugby union is associated with length of playing career.
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DOI:
10.1007/s00401-023-02644-3
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发表时间:
2023-12
影响因子:
12.7
通讯作者:
中科院分区:
文献类型:
--
作者:
There is concern over late, adverse brain health outcomes associated with contact sports participation, with high neurodegenerative disease risk reported in studies of former American football [3, 8], soccer [9, 16] and rugby union players [15]. In parallel, autopsy studies of former athletes from a range of contact sports describe a frequent finding of chronic traumatic encephalopathy (CTE), a neuropathology uniquely associated with prior history of traumatic brain injury (TBI) and repetitive head impact (RHI) exposure [7, 12–14]. Among contact sports, rugby union (hereafter ‘rugby’) is documented as having high risk of concussion/mild TBI, with reported injury rates ranging 4.1 concussions/1000 player hours at community level [2] to 22.2 concussions/1000 player hours in professional rugby [4]. Nevertheless, despite its popularity, with a reported 8.46 million active participants globally [20], there have been relatively few case descriptions of CTE in former rugby players [7, 17, 18]. To address this, we collated and analyzed neuropathological data from autopsy brain examinations on individuals with rugby as primary sport exposure submitted to three international brain banks with specific interest in contact sport and brain health. Case records of the Understanding Neurologic Injury and Traumatic Encephalopathy Brain Bank (UNITE; Boston University School of Medicine, US), the Glasgow TBI Archive (GTBI; University of Glasgow, UK) and the Australian Sports Brain Bank (ASBB; Royal Prince Alfred Hospital and University of Sydney, Australia) were surveyed to identify case donations in which primary sport exposure was recorded as ‘rugby union’. Each archive employs standardized procedures for case accrual, clinical history acquisition and tissue processing, with neuropathological evaluations conducted blind to demographic and clinical information and employing established, consensus protocols for assessment of neurodegenerative disease pathologies, including CTE [1, 11, 13]. For the purposes of this study, existing
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影响因子:
3.2
作者:
Bieniek KF;Cairns NJ;Crary JF;Dickson DW;Folkerth RD;Keene CD;Litvan I;Perl DP;Stein TD;Vonsattel JP;Stewart W;Dams-O'Connor K;Gordon WA;Tripodis Y;Alvarez VE;Mez J;Alosco ML;McKee AC;TBI/CTE Research Group
通讯作者:
TBI/CTE Research Group
影响因子:
29
作者:
Russell ER;Mackay DF;Stewart K;MacLean JA;Pell JP;Stewart W
通讯作者:
Stewart W
影响因子:
12.7
作者:
通讯作者:
--
影响因子:
29
作者:
Mckee, Ann C.;Mez, Jesse;Abdolmohammadi, Bobak;Butler, Morgane;Huber, Bertrand Russell;Uretsky, Madeline;Babcock, Katharine;Cherry, Jonathan D.;Alvarez, Victor E.;Martin, Brett;Tripodis, Yorghos;Palmisano, Joseph N.;Cormier, Kerry A.;Kubilus, Caroline A.;Nicks, Raymond;Kirsch, Daniel;Mahar, Ian;Mchale, Lisa;Nowinski, Christopher;Cantu, Robert C.;Stern, Robert A.;Daneshvar, Daniel;Goldstein, Lee E.;Katz, Douglas I.;Kowall, Neil W.;Dwyer, Brigid;Stein, Thor D.;Alosco, Michael L.
通讯作者:
Alosco, Michael L.
影响因子:
14.5
作者:
McKee, Ann C.;Stein, Thor D.;Cantu, Robert C.
通讯作者:
Cantu, Robert C.