In sum, it appears that the preponderance of the data can be most consistently interpreted as showing that the brain inflammatory protein apoE plays a catalytic role in the AD/DS amyloid cascade and consequent cognitive decline, with binding and clearance differences between the apoE isoforms reflecting their differing abilities to bind to Aβ and catalyze its conversion into neurotoxic macromolecular species (Figure 2). The gene discussed is PROS1; the disease is Alzheimer disease.