BU Research: It May Be Possible to Diagnose CTE in Living Patients
The discovery could open the door to new treatments.
Researchers from Boston University School of Medicine and VA Boston Healthcare System may have found a way to diagnose chronic traumatic encephalopathy (CTE) in living patients, a potentially huge breakthrough for scientists who study the trauma-related brain disease.
Currently, CTE can only be diagnosed posthumously, through an autopsy. If the disease could be identified while a patient is still alive, it would greatly improve research efforts—potentially even opening the door to new therapies.
“Once we can successfully diagnose CTE in living individuals, we will be much closer to discovering treatments for those who suffer from it,” senior study author Ann McKee says in a statement.
Just last week, Boston University confirmed that Aaron Hernandez had CTE before he died, making the former Patriots tight end the latest in a string of football players to receive that diagnosis after death.
In the latest study, published Tuesday in PLOS ONE, McKee, who is the director of BU’s CTE Center, and her team studied the post-mortem brains of 23 former college and professional football players, 50 non-athlete Alzheimer’s patients, and 18 non-athlete controls. They found that levels of a biomarker called CCL11 were significantly elevated in the brains of CTE patients, but not among members of the other two groups. CCL11 levels also correlated with the length of time the individual had played football.
While that finding alone suggests that CCL11 is linked with CTE, it was the study’s next step that holds diagnostic promise. The team tested the cerebrospinal fluid of seven subjects with CTE, four controls, and four Alzheimer’s patients, and again found an association between the biomarker and CTE. That, the researchers explain in the statement, suggests that CTE could be identified in living patients through a spinal fluid test.
“Not only did this research show the potential for CTE diagnosis during life, but it also offers a possible mechanism for distinguishing between CTE and other diseases,” first author Jonathan Cherry says. “By making it possible to distinguish between normal individuals, individuals with Alzheimer’s disease, and CTE, therapies can become more targeted and hopefully more effective.”
More research will be necessary to fully understand the link between CCL11 and CTE, and to translate the findings into a patient-ready diagnostic test. Even still, the research represents some of the first good news to enter the often-bleak discussion around CTE.