APOLIPOPROTEIN-E EPSILON-4 ASSOCIATED WITH CHRONIC TRAUMATIC BRAIN INJURY IN BOXING

Context.-Given the similarities between Alzheimer disease and dementia pugilistica, we evaluated the relationship between apolipoprotein E ( APOE) genotype and chronic traumatic brain injury (CTBI) in boxers to determine whether there is a genetic susceptibility to the effects of head trauma. Objective.-To assess the relationship between CTBI and AP OE genotype in boxers. Design and Setting.-Clinical characterization o f 24 volunteer and 6 referred boxers in an outpatient setting. Partici pants.-Thirty professional boxers aged 23 to 76 years underwent neurol ogic and behavioral assessment in conjunction with APOE genotyping. Ma in Outcome Measures.-Apolipoprotein E genotype was examined in relatio nship to measures of CTBI. A 10-point clinical rating scale (0-9), the Chronic Brain Injury (CBI) scale, was devised to assess the severity of traumatic encephalopathy associated with boxing, Boxers with abnorm al CTBI scores were further classified on the basis of whether their i mpairments were possibly or probably related to boxing. Scores were an alyzed in relation to boxing exposure (number of bouts) and APOE genot ype. Results.-Among the 30 boxers, 11 were found to be normal (CBI sco re=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impa ired (CBI score=3-4), and 3 showed signs of severe impairment (CBI sco re >4). High-exposure boxers tie, those with greater than or equal to 12 professional bouts) had significantly higher CBI scores (mean [SD], 2.6 [1.9]) than low-exposure boxers (mean [SD], 0.3 [0.7]) (P<.001), indicating that neurologic impairment as measured by the CBI scale see ms related to boxing exposure. The APOE genotype frequencies of the st udy population were approximately the same as those found in the gener al population. Boxers with low exposure had mean CBI scores of 0.33, i rrespective of APOE genotype. However, high-exposure boxers with an AP OE epsilon 4 allele had significantly greater CBI scores (mean [SD], 3 .9 [2.3]) than high-exposure boxers without APOE epsilon 4 (mean [SD], 1.8 [1.2]) (P=.04), All boxers with severe impairment possessed at le ast 1 APOE epsilon 4 allele. The tendency for greater CTBI among those with both high exposure and an epsilon 4 allele was statistically sig nificant at the P<.001 level. ConcIusions.-These preliminary findings suggest that possession or an APOE epsilon 4 allele may be associated with increased severity of chronic neurologic deficits in high-exposur e boxers.