Journal
JOURNAL OF NEUROINFLAMMATION
Volume 12, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12974-015-0445-y
Keywords
Microglia; Translocator protein; Positron emission tomography; Traumatic brain injury; Traumatic axonal injury; PK11195; Thalamus
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Funding
- Wellcome Trust-GlaxoSmithKline Translational Medicine Training Programme
- MS Society of Great Britain
- Progressive MS Alliance
- MRC
- GlaxoSmithKline
- Edmund J. Safra Foundation
- Lily Safra
- MRC (UK) Clinician Scientist Fellowship
- National Institute for Health Research (NIHR) Imperial Biomedical Research Centre
- MRC [G0701951, G1100810, MC_U120036861, G0900897, MR/L022141/1] Funding Source: UKRI
- Medical Research Council [G0900897, MR/K501013/1, G1100810, G0701951, MR/L022141/1, MC_U120036861] Funding Source: researchfish
- National Institute for Health Research [NIHR-RP-011-048, NF-SI-0514-10022] Funding Source: researchfish
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Background: Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo. Findings: Using [C-11]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage. Conclusions: These findings support a link between axonal damage and persistent inflammation after brain injury.
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