• Olga Ciccarelli, Frederik Barkhof, Benedetta Bodini, Nicola De Stefano, Xavier Golay, Klaas Nicolay, Daniel Pelletier, Petra J W Pouwels, Seth A Smith, Claudia A M Wheeler-Kingshott, Bruno Stankoff, Tarek Yousry, and David H Miller.
• Queen Square MS Centre, University College London Institute of Neurology, London, UK; NIHR UCL/UCLH Biomedical Research Centre, London, UK. Electronic address: o.ciccarelli@ucl.ac.uk.
• Lancet Neurol. 2014 Aug 1;13(8):807-22.

AbstractThe mechanisms underlying the pathogenesis of multiple sclerosis induce the changes that underpin relapse-associated and progressive disability. Disease mechanisms can be investigated in preclinical models and patients with multiple sclerosis by molecular and metabolic imaging techniques. Many insights have been gained from such imaging studies: persisting inflammation in the absence of a damaged blood-brain barrier, activated microglia within and beyond lesions, increased mitochondrial activity after acute lesions, raised sodium concentrations in the brain, increased glutamate in acute lesions and normal-appearing white matter, different degrees of demyelination in different patients and lesions, early neuronal damage in grey matter, and early astrocytic proliferation and activation in lesions and white matter. Clinical translation of molecular and metabolic imaging and extension of these techniques will enable the assessment of novel drugs targeted at these disease mechanisms, and have the potential to improve health outcomes through the stratification of patients for treatments.Copyright © 2014 Elsevier Ltd. All rights reserved.

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