Abstract
Molecular imaging has had little application to multiple sclerosis thus far. However, advances in preclinical studies and proofs-of-principle provided for other inflammatory disorders highlight the potential for using positron emission tomography, single-photon emission computerized tomography or MRI-based molecular imaging methods to define the distribution and trafficking of specific immune effector cells, or to follow changes in specific molecular neuropathology in multiple sclerosis. If this promise can be realized, novel insights into the dynamics of in vivo multiple sclerosis neuropathology can be expected. Furthermore, powerful new approaches to testing the pharmacology of novel therapeutics will become possible. Molecular imaging could also contribute to ‘personalizing’ treatments for better outcomes.
Acknowledgements
The authors wish to thank Rachel Green for editorial support and acknowledge helpful critical input from colleagues in the GlaxoSmithKline Clinical Imaging Centre.
Financial & competing interests disclosure
Both Paul M Matthews and Robert Comley are full-time employees of GlaxoSmithKline, which is developing new therapeutic molecules for multiple sclerosis and other autoimmune diseases. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript
Notes
BMB: 1,4-bis(paminostyryl)-2-methoxy benzene; FAC: 1-(2’-deoxy-2’-[18F]fluoroarabinofuranosyl) cytosine; FDG: [18F]-fluorodeoxyglucose; GABAA: γ-aminobutyric acidA; Gd-DTPA: Gadolinium diethylene triamine pentaacetic acid; MRS: Magnetic resonance spectroscopy; PET: Positron emmission tomography; SPECT: Single-photon emission computerized tomography; TSPO: Translocator protein 18 kDa; USPIO: Ultrasmall paramagnetic iron oxide; VCAM: Vascular cell-adhesion molecule.