Early synapse loss is a hallmark of nearly all neurodegenerative diseases. Published studies indicate that C1q and early components of the classical complement cascade are involved in the aberrant elimination of synapses during neurodegenerative processes. Through targeted inhibition of the classical complement pathway, Annexon is developing novel approaches to protect against synapse loss and inflammatory nerve damage in brain and retinal cells.
CMND in eye disease
C1q accumulates on synapses with normal age in many parts of the CNS, including the retina. In animal models of glaucoma, C1q activation leads to synapse loss, neuronal damage and loss of the optic nerve. Inhibition of C1q is protective in several animal models of glaucoma.