Key points:
- A new paper connects cognitive and behavioral symptoms to protein buildup in the brain that marks CTE.
- The research team measured the amount of p-tau pathology across 11 different brain regions in 364 brains with autopsy-confirmed CTE, in combination with behavioral assessment forms completed by families.
- The team hopes these findings validate CTE symptom criteria, providing the opportunity to help living CTE patients obtain a diagnosis and treatment plan.
Since chronic traumatic encephalopathy (CTE) can only be formally diagnosed after a person dies, researchers have found it difficult to track how it impacts mental well-being during life.
Now, a new study from the foremost experts at Boston University’s CTE Center edges closer to being able to diagnose the disease in the living.
In a paper published in Molecular Neurodegeneration, researchers show a clear relationship between the amount of CTE pathology—meaning the accumulation of a protein called p-tau in specific regions of the brain—and the severity of a person’s cognitive and behavioral symptoms during their life. CTE is characterized by an accumulation of misfolded tau protein—that presents differently from aging-related changes or other neurodegenerative diseases like Alzheimer’s.
For the study, the research team measured the amount of p-tau pathology across 11 different brain regions in 364 brains with autopsy-confirmed CTE that were donated to BU’s UNITE Brain Bank. They also asked family and friends of the brain donors to complete several standardized assessments to assess their loved one’s cognitive, functional, mood and behavioral symptoms. The researchers then examined the relationship between the p-tau pathology and results of the behavior assessments.
They found that p-tau pathology across the brain, most predominantly in the frontal lobe, was associated with more reported cognitive functional symptoms, including difficulties in attention, memory, perception, and psychomotor abilities. P-tau in the frontal lobe was associated with some neurobehavioral symptoms, like the reduced ability to control impulses and self-monitor behavior, but overall, there was a higher correlation between cognition than neurobehavior.
The BU team hopes these latest findings validate CTE symptom criteria, giving them and other clinicians the opportunity to help living CTE patients obtain a diagnosis and treatment plan.
“These findings provide a clear step forward toward diagnosing CTE in life,” said study coauthor Jesse Mez, a CTE Center co-director of clinical research. “Diagnosis is crucial before we can test therapies. With validated in-life diagnostic criteria, we will be able to design clinical trials for therapies.”