Figure 2.

A ‘frustrated innate immune system’ in the inflamed Alzheimer’s disease brain. This contribution is from multiple sources including the polymorphic complement component genes [26–28], the APOE variant [8], blood-brain barrier defects [30], pathogen entry, and Aβ as a defense peptide released in response to infections [24]. All these contribute to complement activity, cell activation, defective phagocytosis and chronic inflammation [15]. There would be clinical value in inhibiting all three main pathways of complement at the C3 stage