OBJECTIVES To image amyloid deposition in patients with traumatic brain injury (TBI) using carbon 11-labeled Pittsburgh Compound B ([C-11] PiB) positron emission tomography (PET) and to validate these findings using tritium-labeled PiB ([H-3] PiB) autoradiography and immunocytochemistry in autopsy-acquired tissue.
DESIGN, SETTING, AND PARTICIPANTS In vivo PET at tertiary neuroscience referral center and ex vivo immunocytochemistry of autopsy-acquired brain tissue from a neuropathology archive. [C-11] PiB PET was used to image amyloid deposition in 11 controls (median [range] age, 35 [24-60] years) and in 15 patients (median [range] age, 33 [21-50] years) between 1 and 361 days after a TBI. [H-3] PiB autoradiography and immunocytochemistry for beta-amyloid (A beta) and beta-amyloid precursor protein in brain tissue were obtained from separate cohorts of 16 patients (median [range] age, 46 [21-70] years) who died between 3 hours and 56 days after a TBI and 7 controls (median [range] age, 61 [29-71] years) who died of other causes.
MAIN OUTCOMES AND MEASURES We quantified the [C-11] PiB distribution volume ratio and standardized uptake value ratio in PET images. The distribution volume ratio and the standardized uptake value ratio were measured in cortical gray matter, white matter, and multiple cortical and white matter regions of interest, as well as in striatal and thalamic regions of interest. We examined [H-3] PiB binding and A beta and beta-amyloid precursor protein immunocytochemistry in autopsy-acquired brain tissue.
RESULTS Compared with the controls, the patients with TBI showed significantly increased [C-11] PiB distribution volume ratios in cortical gray matter and the striatum (corrected P
CONCLUSIONS AND RELEVANCE [C-11] PiB shows increased binding following TBI. The specificity of this binding is supported by neocortical [H-3] PiB binding in regions of amyloid deposition in the postmortem tissue of patients with TBI. [C-11] PiB PET could be valuable in imaging amyloid deposition following TBI.
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