Increased Amyloid Deposition after TBI Correlates with Cognitive Deficits and Symptom Worsening

BACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer's disease (AD). The primary objective of this case-series study was to conduct early 18F-AV-45 (florbetapir F18) positron emission tomography (PET) imaging in mild-to-moderate TBI subjects after injury to determine if amyloid plaque load predicts cognitive deficits. METHODS: Serial florbetapir F18 PET imaging was conducted in 7 individuals with a mild or moderate TBI (as indicated by their Glasgow Coma Scale [GCS] score between 13 and 15) at day 14 and at 12 months after injury. Of the 7 subjects that were tested, only one had a moderate TBI. Amyloid plaque levels were measured in the cerebral cortex of each individual. To screen for cognitive deficits, the symbol match test was administered at 12 months after TBI. RESULTS: At day 14 after injury, compared to healthy controls, the mild and moderate TBI subjects (N=7) had a 10% increase in amyloid plaque load within the cerebral cortex. When stratified by cognitive outcomes, at day 14 after injury, the subjects with poor outcomes (n=3) experienced a 20% and 13% increase in brain amyloid compared to healthy controls and TBI subjects with good outcomes, respectively. With respect to cognition, at 12 months after injury, the subjects with poor outcomes exhibited a negative correlation (r= -0.71) between amyloid plaque load and cognitive performance. Also, a positive correlation (r=+0.78) was detected between increased brain amyloid load and symptom scores at 12 months. CONCLUSIONS: Individuals with early, substantial increases in brain amyloid experience poor outcomes in the form of memory dysfunction and heightened symptoms (memory deficits, headaches, difficulty concentrating, etc.) at 12 months post-injury. Data presented here suggests that florbetapir F18 PET imaging may be a sensitive biomarker for predicting outcomes within the mild and moderate TBI population.