We have shown in the Alzheimer's diseases mouse models that subcutaneously injected AmyTrap significantly reduced the Aβ plaque burden in the brain, and improved the cognitive parameters of these mice. Our preliminary studies also suggest that AmyTrap does not enter the brain. Undetectable levels of AmyTrap in the brain and reduction of the Aβ burden in the brain suggest that the AmyTrap possibly exerts its therapeutic activity by acting as peripheral sink for circulatory Aβ.
Such a mechanism of action has been proposed for anti-Aβ antibodies. Similar to AmyTrap these antibodies reduced the Aβ plaque size in the brain without entering the brain. Based on these observations it has been hypothesized that Aβ exists in equilibrium between the brain and in circulation. Sequestration of the circulatory Aβ in the periphery creates an imbalance in this equilibrium driving efflux of Aβ from the brain into the circulation.