9 research outputs found
Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage
Quantitation of adenosine A2A receptors availability in Parkinson's Disease patients with and without dyskinesias with [11C]SCH442416 PET using spectral analysis
Adenosine A(2A) Receptor Availability in Parkinson's Disease Patients with and without Levodopa Induced Dyskinesias Studied with [C-11]SCH442416 PET
Kinetic modeling of the adenosine A2A subtype receptor radioligand [11C]SCH442416 in humans
none9noneIlaria Boscolo Galazzo;Subrata K. Bose;Anil F. Ramlackhansingh;Imtiaz Ahmed;Nicola Pavese;Gaia Rizzo;David J. Brooks;Federico E. Turkheimer;Alessandra BertoldoIlaria Boscolo, Galazzo; Subrata K., Bose; Anil F., Ramlackhansingh; Imtiaz, Ahmed; Nicola, Pavese; Rizzo, Gaia; David J., Brooks; Federico E., Turkheimer; Bertoldo, Alessandr
Kinetic modeling of the adenosine A2A subtype receptor radioligand [11C]SCH442416 in humans
Amyloid pathology and axonal injury after brain trauma
OBJECTIVE: To image β-amyloid (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer disease (AD). METHODS: Patients 11 months to 17 years after moderate–severe TBI underwent (11)C-Pittsburgh compound B ((11)C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BP(ND)) images of (11)C-PiB, which index Aβ plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BP(ND) were assessed. In TBI, a measure of white matter integrity, fractional anisotropy, was estimated and correlated with (11)C-PiB BP(ND.) RESULTS: Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased (11)C-PiB BP(ND) was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy of associated white matter tracts and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum. CONCLUSIONS: Increased Aβ burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathologic features of dementia, which may relate to axonal damage produced by the injury