| Abstract |
The work described in this thesis dissertation demonstrates that complement is involved in the pathology of chronic multiple sclerosis. The early complement components C1q and C3 mediate the phagocytosis of synapses or partly myelinated axons in the brains of patients with chronic multiple sclerosis. In addition, the membrane attack complex, the terminal complex of complement activation, is linked to neuroinflammation and neuroaxonal damage in the chronic relapsing experimental autoimmune encephalomyelitis, a model of chronic neuroinflammation.
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