Contributions
Abstract: 137
Type: Oral
While inflammation, demyelination and axon degeneration are well established neuropathological features of MS, recent studies acknowledge changes in metabolism and energy deficient states driven by mitochondrial defects in progressive MS. Oligodendrocytes metabolically support axons and, following demyelination, functional mitochondria gather in increased numbers and size within demyelinated axons. This compensatory phenomenon is not completely reversed by remyelination and is perturbed in a subset of demyelinated aaxons in progressive MS. I will discuss the mechanisms of energy failure in progressive MS as well as potential therapeutic options, that target energy production and oxidative injury, to preserve axons and improve neurological function in progressive MS.
Disclosure: I have received research grants from Biogen, Genzyme and MedDay.
Abstract: 137
Type: Oral
While inflammation, demyelination and axon degeneration are well established neuropathological features of MS, recent studies acknowledge changes in metabolism and energy deficient states driven by mitochondrial defects in progressive MS. Oligodendrocytes metabolically support axons and, following demyelination, functional mitochondria gather in increased numbers and size within demyelinated axons. This compensatory phenomenon is not completely reversed by remyelination and is perturbed in a subset of demyelinated aaxons in progressive MS. I will discuss the mechanisms of energy failure in progressive MS as well as potential therapeutic options, that target energy production and oxidative injury, to preserve axons and improve neurological function in progressive MS.
Disclosure: I have received research grants from Biogen, Genzyme and MedDay.