P3‐416: Differential TGF‐β‐Smad 2/3 and BMP‐Smad 1/5/8 pathway activation promotes macrophage Aβ phagocytosis

impairment of cognitive function. Conclusions: Our studies provide strong evidence that the N-termini of amyloid peptides influence their characteristics. This is primarily caused by a loss of N-terminal charge and solubility which increases aggregation propensity and, interestingly, influence on LTP. Likewise, novel transgenic animal models overproducing N-truncated Abeta develop an early phenotype. Thus, an accumulation of N-truncated amyloid as described for human AD might contribute to the pathogenesis due to the changes in the molecular properties. The data suggest that suppression of QC-catalyzed pGlu-formation provides potential for development of a treatment paradigm to prevent Aband inflammation-driven pathophysiology in AD, FDD and FBD.