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2016 ; 86
(9
): 821-8
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Amyloid pathology and axonal injury after brain trauma
#MMPMID26843562
Scott G
; Ramlackhansingh AF
; Edison P
; Hellyer P
; Cole J
; Veronese M
; Leech R
; Greenwood RJ
; Turkheimer FE
; Gentleman SM
; Heckemann RA
; Matthews PM
; Brooks DJ
; Sharp DJ
Neurology
2016[Mar]; 86
(9
): 821-8
PMID26843562
show ga
OBJECTIVE: To image ?-amyloid (A?) plaque burden in long-term survivors of
traumatic brain injury (TBI), test whether traumatic axonal injury and A? are
correlated, and compare the spatial distribution of A? 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 (BPND) images of (11)C-PiB,
which index A? plaque density, were computed using an automatic reference region
extraction procedure. Voxelwise and regional differences in BPND were assessed.
In TBI, a measure of white matter integrity, fractional anisotropy, was estimated
and correlated with (11)C-PiB BPND. RESULTS: Twenty-eight participants (9 with
TBI, 9 controls, 10 with AD) were assessed. Increased (11)C-PiB BPND 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 A? 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.
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