Abstract: Chronic inflammation has increasingly been acknowledged as a hallmark feature of several progressive neurodegenerative disorders. Accruing evidence indicates that sustained inflammation compromises the core neuroprotective mechanisms underlying neural injury in Alzheimer’s disease (AD) and retinal neurodegenerative disorders. Innate immunity and activation of the classical complement pathways are suggested to play important roles in normal central nervous system physiology and complex tissue remodeling during the disease process (Gasque et al., 2000). The pathway is implicated in normal brain development and is also involved in the inflammatory response in a wide range of neurodegenerative conditions either directly or indirectly through recruitment and activation of immune cells. The classical, alternative and lectin complement pathways, together encompass about 30 plasma and membrane-bound proteins. The classical pathway is comprised of about 20 proteins including several serine proteinases and proteinase inhibitors connected as part of an amplifying cascade. Activation of the classical pathway is triggered once C1q is attached to the immune complexes containing IgG or IgM leading to production of the C3 convertase