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Active elite rugby participation predicts alterations in cortical thickness
  1. Thomas Parker1,2,3,
  2. Karl Zimmerman1,2,
  3. Etienne Laverse4,
  4. Niall Bourke1,2,
  5. Neil Graham1,2,
  6. Amanda Hesle-Grave3,5,
  7. Henrik Zetterberg3,4,5,6,7,8,
  8. Simon Kemp9,
  9. Huw Morris4,
  10. David Sharp1,2
  1. 1Department of Brain Sciences, Imperial College London
  2. 2UK Dementia Research Institute Care, Research and Technology Centre, Imperial College London, UK
  3. 3Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK
  4. 4University College London
  5. 5UK Dementia Research Institute at UCL, London, UK
  6. 6Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrens
  7. 7Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
  8. 8Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China
  9. 9Rugby Football Union

Abstract

Background Rugby is a collision sport with high rates of head injury. The effect of rugby participation at the elite level on cerebral grey matter structure is unclear.

Methods Data from 44 active professional rugby players, including 21 acquired within one week of mild traumatic brain injury, and 47 healthy controls were analysed. Whole-cortex and region of interest analyses investigating the effects of rugby participation, sub-acute mild traumatic brain injury, and biomarkers of traumatic brain injury (fractional anisotropy, plasma neurofilament light and glial fibrillary acidic protein) on cortical thickness were performed. Plasma neurofilament light and glial fibrillary acidic protein concen- trations were measured using Single molecule array technology.

Results Whole-cortex analysis revealed evidence of lower right hemisphere precentral cortical thickness in non-injured rugby players compared to controls. In region of interest analyses, there was evidence rugby participation predicted lower cortical thickness in the inferior part of the precentral sulcus (right hemisphere). In the same region, there was evidence sub-acute mild traumatic brain injury predicted higher cortical thickness compared to non-injured players, and that plasma glial fibrillary acidic protein was positively associated with cortical thickness in players with sub-acute mild traumatic brain injury. No associations with neurofilament light concentration were found.

Conclusion We present evidence that elite rugby participation predicts alterations in cortical thickness. Larger scale study with prolonged follow-up to understand the clinical implications of these findings is warranted.

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