One research challenge is the identification of early signals indicated risk for remote cognitive decline and dementia.
For example, repeated concussions at age 20 with brain injury may not produce clinical cognitive deficits for 20 or 30 years. Early identification of risk and counseling of individuals may reduce trauma exposure and cognitive decline.
There are no valid tests of brain imaging in high-risk populations for trauma-related cognitive decline.
PET or positron emission tomography of the brain holds promise in assessment of Alzheimer's and other dementia. A recent study examined PET brain finding is a former NFL football player and contrasted the findings with that of a subject with frontotemporal dementia and head trauma. The key findings from the study included:
* The 71 year old ex-NFL player had subjective memory decline. Neuropsychological testing revealed significant impairment in memory function in visual, auditory and delayed memory domains.
* The ex-NFL player lacked evidence of amyloid plaque development ruling out a diagnosis of dementia of the Alzheimer's type
* A novel PET approach to assess tau protein deposition in the brain was performed on the ex-NFL player. Tau protein deposition was found in the brain striatum, substantia nigra and hippocampal regions.
* In the second case of traumatic brain injury in a physician with frontotemporal dementia, neuropsychological testing showed impairment in memory and language function.
* PET imaging revealed no amyloid deposition and ruled out Alzheimer's disease in case 2.
* The previous TBI occuring one year earlier in the second case resulted in evidence of tau protein deposition limited to the area of brain trauma.
The authors conclude that PET imaging may be a valuable tool in the assessment of brain trauma in NFL and other football players. However, unlike Alzheimer's dementia where amyloid plaque is present and diagnostic, amyloid plaque appears absent in cases now being classified as chronic traumatic encephalopathy or CTE.
Use of PET tau protein imaging may be better in assessing effects of trauma. The authors note they are in the process of testing more subjects with chronic brain trauma with tau protein PET imaging. Their results will be an important addition to this clinical dilemma.
Interested readers can access the free full-text manuscript of this study by clicking on the DOI link in the citation below.
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Mitsis, E., Riggio, S., Kostakoglu, L., Dickstein, D., Machac, J., Delman, B., Goldstein, M., Jennings, D., D’Antonio, E., Martin, J., Naidich, T., Aloysi, A., Fernandez, C., Seibyl, J., DeKosky, S., Elder, G., Marek, K., Gordon, W., Hof, P., Sano, M., & Gandy, S. (2014). Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: studies of a retired NFL player and of a man with FTD and a severe head injury Translational Psychiatry, 4 (9) DOI: 10.1038/tp.2014.91
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