Post mortem analyses and studies in animal models show that complement components and activation products, notably C1q, C3b/iC3b, the proinflammatory activation products C3a and C5a and the terminal complement complex, are closely associated with AD pathology, and complement activation is implicated in amyloid clearance and synaptic loss.29, 30, 31, 32, 33, 34, 35, 36. The gene discussed is C5; the disease is amyloidosis.