Imperial College London

Professor Paul M. Matthews

Faculty of MedicineDepartment of Brain Sciences

Edmond and Lily Safra Chair. Head of Department
 
 
 
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Contact

 

+44 (0)20 7594 2855p.matthews

 
 
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Assistant

 

Ms Siobhan Dillon +44 (0)20 7594 2855

 
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Location

 

E502Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Scott:2016:10.​1212/​WNL.​0000000000002413,
author = {Scott, GPT and Ramlackhansingh, A and Edison, P and Hellyer, PJ and Cole, J and Veronese, M and Leech, R and Greenwood, RJ and Turkheimer, F and Gentleman, S and Heckemann, RA and Matthews, PM and Brooks, D and Sharp, DJ},
doi = {10.1212/WNL.0000000000002413},
journal = {Neurology},
pages = {821--828},
title = {Amyloid pathology and axonal injury after brain trauma},
url = {http://hdl.handle.net/10044/1/27749},
volume = {86},
year = {2016}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Objective: To image amyloid-β (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’s disease.Methods: Patients 11 months to 17 years after moderate-severe TBI had 11C-Pittsburgh compound-B (PIB) PET, structural and diffusion MRI and neuropsychological examination. Healthy aged controls and AD patients had PET and structural MRI. Binding potential (BPND) images of 11C-PIB, which index Aβ 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 (FA), was estimated and correlated with 11C-PIB BPND.Results: 28 participants (9 TBI, 9 controls, 10 AD) were assessed. Increased 11C-PIB BPND was found in TBI versus controls in the posterior cingulate cortex (PCC) and cerebellum. Binding in the PCC increased with decreasing FA 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 neuropathological features of dementia, which may relate to axonal damage produced by the injury.
AU - Scott,GPT
AU - Ramlackhansingh,A
AU - Edison,P
AU - Hellyer,PJ
AU - Cole,J
AU - Veronese,M
AU - Leech,R
AU - Greenwood,RJ
AU - Turkheimer,F
AU - Gentleman,S
AU - Heckemann,RA
AU - Matthews,PM
AU - Brooks,D
AU - Sharp,DJ
DO - 10.1212/WNL.0000000000002413
EP - 828
PY - 2016///
SN - 0028-3878
SP - 821
TI - Amyloid pathology and axonal injury after brain trauma
T2 - Neurology
UR - http://hdl.handle.net/10044/1/27749
VL - 86
ER -