Patients with traumatic brain injury (TBI) were found to have increased deposits of β-Amyloid (Aβ) plaques, a signature of Alzheimer Disease (AD), in some areas of the brain, according to a study published online Nov. 11 in JAMA Neurology.
As the acceptance of epidemiological and pathophysiological links between TBI and AD grows, it’s been revealed that up to 30 percent of patients who die in the acute phase post-TBI have Aβ plaques. The plaques appear within hours of the sustained injury and can occur in patients of all ages.
“Recent postmortem evidence suggests that, following TBI, the Aβ deposition associated with ‘normal’ aging may be subsequently accelerated, but our inability to quantify amyloid binding in vivo limits a broader understanding of the temporal profile and outcome of amyloid deposition in TBI,” wrote Young T. Hong, PhD, of the University of Cambridge, U.K., and colleagues.
Hong and colleagues subsequently designed a cross-sectional pilot study in which imaging and brain tissue obtained during autopsies were examined for Aβ deposition in patients with TBI. Autopsy-acquired brain tissues were obtained from 16 people who had a TBI, as well as seven patients with a non-neurological cause of death. They then performed PET imaging using carbon 11-labeled Pittsburgh Compound B ([¹¹C]PiB), a marker for brain amyloid deposition, in 15 participants with TBI and 11 healthy patients.
Findings indicated that patients with TBI experienced increases in [¹¹C] PiB binding, a potential marker of Aβ plaque, in cortical gray matter and the striatum. This increase was not, however, apparent in the thalamus or white matter.
“The use of [¹¹C]PiB PET for amyloid imaging following TBI provides us with the potential for understanding the pathophysiology of TBI, for characterizing the mechanistic drivers of disease progression or suboptimal recovery in the subacute phase of TBI, for identifying patients at high risk of accelerated AD, and for evaluating the potential of antiamyloid therapies,” wrote Hong and colleagues.