An analysis of complement activation at the node of Ranvier in mouse models of Guillain-Barré syndrome

Guillain-Barré syndrome (GBS) is a severe paralytic neurological disorder affecting the peripheral
nervous system that follows minor infections. It can induce complete paralysis, often with
permanent untreatable disability. The causative mechanisms in GBS involve antibodies formed in
response to infections that injure nerves by activating the inflammation response in the body. This
project aims to explore the mechanisms underlying this nerve injury in experimental models of the
disease. In particular, an inflammation pathway called the complement cascade will be examined in
detail, using a new experimental drug that blocks the activation of the cascade. If effective, this
study will bring the drug closer to clinical trials in man.