Accelerated cellular senescence in a model of multiple sclerosis (S50.004)

Conclusions:Our study provides evidence of accelerated CS in demyelinating lesions. The accelerated CS along with the ongoing axonal damage and functional impairment seen in our model support the role of CS in the pathogenesis of disability progression under conditions chronic demyelination.Study Supported by:This work is supported by a research grant from the Multiple Sclerosis Trials Collaboration (MSTC), UKDisclosure: Dr. Papadopoulos has received personal compensation for activities with Bayer Hellas, Novartis, Genesis Pharma, and Sanofi-Genzyme as a speaker and for serving on scientific advisory boards. Dr. Karamita has nothing to disclose. Dr. Mitsikostas received personal compensation for activities with Allergan, Amgen, Bayer Schering, Eli Lilly, EMD Serono, Novartis, and Teva as a consultant. Dr. Gorgoulis has nothing to disclose. Dr. Probert has nothing to disclose. Dr. Nicholas has received personal compensation for activities with Genzyme, Roche, Novartis, and Biogen.
Source: Neurology - Category: Neurology Authors: Tags: MS Novel Therapeutics and Animal Models Source Type: research