NeuroImage: Clinical (Jan 2020)

Interaction of APOE4 alleles and PET tau imaging in former contact sport athletes

  • Anna Vasilevskaya,
  • Foad Taghdiri,
  • Charles Burke,
  • Apameh Tarazi,
  • Seyed Ali Naeimi,
  • Mozghan Khodadadi,
  • Ruma Goswami,
  • Christine Sato,
  • Mark Grinberg,
  • Danielle Moreno,
  • Richard Wennberg,
  • David Mikulis,
  • Robin Green,
  • Brenda Colella,
  • Karen D. Davis,
  • Pablo Rusjan,
  • Sylvain Houle,
  • Charles Tator,
  • Ekaterina Rogaeva,
  • Maria C. Tartaglia

Journal volume & issue
Vol. 26

Abstract

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Background: Genetic polymorphisms like apolipoprotein E (APOE) and microtubule-associated protein tau (MAPT) genes increase the risk of neurodegeneration. Methods: 38 former players (age 52.63±14.02) of contact sports underwent neuroimaging, biofluid collection, and comprehensive neuropsychological assessment. The [F-18]AV-1451 tracer signal was compared in the cortical grey matter between APOE4 allele carriers and non-carriers as well as carriers of MAPT H1H1 vs non-H1H1. Participants were then divided into the high (N = 13) and low (N = 13) groups based on cortical PET tau standard uptake value ratios (SUVRs) for comparison. Findings: Cortical grey matter PET tau SUVR values were significantly higher in APOE4 carriers compared to non-carriers (p = 0.020). In contrast, there was no significant difference in SUVR between MAPT H1H1 vs non-H1H1 carrier genes (p = 1.00). There was a significantly higher APOE4 allele frequency in the high cortical grey matter PET tau group, comparing to low cortical grey matter PET tau group (p = 0.048). No significant difference in neuropsychological function was found between APOE4 allele carriers and non-carriers. Interpretation: There is an association between higher cortical grey matter tau burden as seen with [F-18]AV-1451 PET tracer SUVR, and the APOE4 allele in former professional and semi-professional players at high risk of concussions. APOE4 allele may be a risk factor for tau accumulation in former contact sports athletes at high risk of neurodegeneration. Funding: Toronto General and Western Hospital Foundations; Weston Brain Institute; Canadian Consortium on Neurodegeneration in ageing; Krembil Research Institute. There was no role of the funders in this study.

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