Complement proteins C3 and C1q are thought to bind to amyloid-beta proteins in the brain in the early stages of the Alzheimer's syndrome, and subsequent complementmediated lysis of neurons may further exacerbate the syndrome. In ischemia/reperfusion injury of tissues, complement activation during the reperfusion phase is thought to contribute to the ensuing inflammation. Age-related macular degeneration is thought to occur due to excessive complement activation (Zipfel et al. 2007 ) and appears to be related to defective Factor H attachment to the Bruch's membrane in the retina, leading to protein deposits on the membrane known as Drusen. Excessive complement activation has also been associated with disease severity in patients infected with malaria (reviewed in Silver et al. 2010) . Interestingly, C5 deficiency or intercepting C5a and C5aR interaction has a protective effect in an animal model of cerebral malaria (Patel et al. 2008) .