Is Amyloid Imaging Useful in Traumatic Brain Injury?

Laurie L. Barclay, MD


December 18, 2013

Amyloid Imaging With Carbon 11-Labeled Pittsburgh Compound B for Traumatic Brain Injury

Hong YT, Veenith T, Dewar D, et al
JAMA Neurol. 2013 Nov 11. [Epub ahead of print]

Study Summary

Beta-amyloid plaques are not only characteristic of Alzheimer disease, but they are also found in up to 30% of patients who die with acute traumatic brain injury, in which they occur predominantly in gray matter. After traumatic brain injury, the beta-amyloid deposition seen in "normal" aging may be subsequently accelerated, but it has been difficult to quantify amyloid binding in vivo.

The goal of this study was to image amyloid deposition in patients with traumatic brain injury using carbon 11-labeled Pittsburgh compound B ([11C]PiB) PET and to validate these findings using tritium-labeled PiB ([3H]PiB) autoradiography and immunocytochemistry in tissue obtained at autopsy.

At a tertiary neuroscience referral center, participants underwent imaging of amyloid deposition using [11C]PiB PET. Eleven control individuals with a median age of 35 years (range, 24-60 years) and 15 patients with a median age of 33 years (range, 21-50 years) were imaged between 1 and 361 days after traumatic brain injury.

The investigators also performed [3H]PiB autoradiography and immunocytochemistry for beta-amyloid and a beta-amyloid precursor protein on autopsy-acquired brain tissue from a neuropathology archive. These samples were from 16 patients who died at a median age of 46 years (range, 21-70 years) between 3 hours and 56 days after a traumatic brain injury, and from 7 controls with a median age of 61 years (range, 29-71 years) who died of other causes.

Compared with controls, patients with traumatic brain injury had significantly increased [11C]PiB distribution volume ratios in the cortical gray matter and the striatum (corrected P < .05 for both), but not in the thalamus or white matter. Autoradiography showed [3H]PiB binding in neocortical gray matter, in regions corresponding to areas of amyloid deposition seen on immunocytochemistry. In the white matter, immunocytochemistry revealed beta-amyloid and beta-amyloid precursor protein, but no [3H]PiB binding.

Cerebellar gray matter in autopsy-acquired tissue from either controls or patients with traumatic brain injury did not show any plaque-associated amyloid immunoreactivity or [3H]PiB binding. However, a single sample of cerebellar tissue from a patient with traumatic brain injury showed amyloid angiopathy affecting meningeal vessels.


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