Figure 2

Relationship between inflammation and the etiology and clinical syndrome of Alzheimer's disease. Schematic diagram showing that interactions between innate immunity-related genetic risk factors and inflammation-inducing events (brain trauma, ischemia and infection) can contribute to the multifactorial etiology of the sporadic late-onset form of AD. The diagram illustrates also that delirium and AD share a neuroinflammatory response as a common pathogenic mechanism that could explain the vulnerability of AD patients to further cognitive worsening after an episode of delirium associated with a systemic inflammatory response. Aβ, amyloid-β peptide; AD, Alzheimer's disease; APOE4, apolipoprotein E4; APP, amyloid precursor protein; CLU, clusterin; CR1, complement receptor-1; PS1, presenilin-1; PS2, presenilin-2.