Ontology highlight
ABSTRACT:
SUBMITTER: Schattling B
PROVIDER: S-EPMC5111507 | biostudies-literature | 2016 Nov
REPOSITORIES: biostudies-literature
Schattling Benjamin B Fazeli Walid W Engeland Birgit B Liu Yuanyuan Y Lerche Holger H Isbrandt Dirk D Friese Manuel A MA
JCI insight 20161117 19
Counteracting the progressive neurological disability caused by neuronal and axonal loss is the major unmet clinical need in multiple sclerosis therapy. However, the mechanisms underlying irreversible neuroaxonal degeneration in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) are not well understood. A long-standing hypothesis holds that the distribution of voltage-gated sodium channels along demyelinated axons contributes to neurodegeneration by increasin ...[more]