Chronic inflammation has increasingly been acknowledged as a hallmark feature of several progressive neurodegenerative disor-ders. Accruing evidence indicates that sustained inflammation compromises the core neuroprotective mechanisms underlying neural injury in Alzheimer’s disease (AD) and retinal neurodegen-erative disorders. Innate immunity and activation of the classical complement pathways are suggested to play important roles in nor-mal central nervous system physiology and complex tissue remod-eling 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, altative 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 protein-ase inhibitors connected as part of an amplifying cascade. Activa-tion 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 (Merle et al., 2015).