Olga Ciccarelli1, Ahmed Toosy1,
Nicola De Stefano2, Claudia Angela Michela Wheeler-Kingshott3,
David H. Miller3, Alan J. Thompson1
1NMR Unit, Department of Brain Repair
and Rehabilitation, UCL Institute of Neurology, London, United Kingdom; 2Department
of Neurological and Behavioural Sciences, University of Siena, Siena, Italy; 3NMR
Unit, Department of Neuroinflammation, UCL Institute of Neurology, London,
United Kingdom
Mitochondrial
dysfunction is central to the pathogenesis of many neurological diseases,
including MS. We propose a methodology to estimate in-vivo neuronal
mitochondrial metabolism and its relatice contribution to disability. We
modelled N-acetyl-aspartate (NAA), measured by spinal cord 1H-MR
spectroscopy, which reflects axonal integrity and mitochondrial metabolism,
together with measures of axonal integrity, such as axial diffusivity and
cord area, in patients with MS studied six months after a spinal cord
relapse. The residual variance in NAA concentration after accounting for the
structural measures should reflect mitochondrial metabolism. A lower mitochondrial
metabolism was associated with greater disability indipendent of structural
damage.
Keywords