BU CTE Center post-mortem presentation on Aaron Hernandez: stage 3 CTE

This past Thursday, Boston University CTE Center director Ann McKee presented the specific findings of the brain examination of New England Patriots’ player Aaron Hernandez. Mr. Hernandez was serving a life sentence for murder when he committed suicide in his Massachusetts prison cell. The family donated his brain after his death. At age 27, his brain was determined to have Stage 3 (of 4) chronic traumatic encephalopathy (CTE), with severe deposition of tau protein in the frontal lobes of the brain.

Dr. McKee noted, “These are very unusual findings for someone so young”, stating that this level of damage usually is found in players at least 20 years older. In a 2016 New York Times interview after the death of Oakland Raiders quarterback Ken Stabler, Dr. McKee correlated long careers plus the increasing age of the player with the severity of CTE.

Dr. McKee confined herself to presenting the pathology, but the CTE Center’s research has associated CTE with aggressiveness, explosiveness, impulsivity, depression, memory loss and other cognitive changes. The CTE Center has pioneered research in the prevalence of CTE in NFL players’ brains [TTA 26 July] and is conducting longitudinal research on the relationship between concussive and sub-concussive head trauma and behavioral change [TTA 21 Sept] in the living. More details and video available here: Boston Herald, CNN. The September BU CTE Center diagnosis of Mr. Hernandez.

The importance to health tech is in the prevention, mitigation, and early diagnosis (not possible yet) of the end result of repeated concussive and sub-concussive damage, sustained in contact sports, military service (usually combat), and in civilian trauma from, for instance, car and industrial accidents. TTA’s long-standing coverage of CTE and brain trauma can be gleaned from searches on these terms.

CTE found in 99% of former, deceased NFL players’ brains: JAMA study (updated)

click to enlargeUpdated for additional information and analysis at conclusion. In the largest-ever case study published of CTE–chronic traumatic encephalopathyVA Boston Healthcare System (VABHS) and the Boston University School of Medicine’s CTE Center found mild to severe CTE pathology in nearly all of the brains of former football players studied. Jesse Mez, MD, BU Medical assistant professor of neurology and lead author on the JAMA study, said that “The data suggest that there is very likely a relationship between exposure to football and risk of developing [CTE].” The CTE is marked by defective tau (stained red in the brain sample pictures, click to expand), which is also evident in Parkinson’s and Alzheimer’s Disease.

Of the 202 brains donated to the VA-BU-CLF (Concussion Legacy Foundation) Brain Bank:

  • The most dramatic finding is the detection of CTE in 110 of 111 donated former NFL players’ brains (defined as having played one play in a regular NFL season game).
  • In addition, the brains of other football players were studied. CTE was detected in seven of eight Canadian Football League former players (88 percent), nine of 14 semi-professional players (64 percent), 48 of 53 college players (91 percent), and three of 14 high school players (21 percent).
  • The severity increased with length of play, with the majority of former college, semi-professional and professional players having severe pathology. The deceased high school players diagnosed with CTE had mild pathology findings. Age at death ranged from 23 to 89.
  • Player position mattered. Linemen, running backs, defensive backs, and linebackers, who take most of the punishment in football, were the bulk of the donated brains with CTE.

Separately, and with no knowledge of the pathology, backgrounds on each donor were compiled to gather medical history and symptoms. What was striking were the personality changes evident with even mild CTE. Dr. Mez: “We found cognitive, mood and behavioral symptoms were very common, even among players with mild CTE tau pathology. This suggests that tau pathology is only the tip of the iceberg and that other pathologies, such as neuroinflammation and axonal damage, contribute to the clinical symptoms.” 

Preliminary to the current study was UNITE (more…)