M. Paul Murphy

TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.

TL;DR: A subsequent cleavage by γ-secretase that releases the ErbB-4 intracellular domain from the membrane and facilitates its translocation to the nucleus is reported.

TL;DR: Transgenic models that express Abeta1-40 or Abeta2-42 in the absence of human amyloid beta protein precursor (APP) overexpression establish that Abeta 1-42 is essential for amyloids deposition in the parenchyma and also in vessels.

TL;DR: The findings indicate that the AICD regulates phosphoinositide-mediated calcium signaling through a γ-secretase-dependent signaling pathway, suggesting that the intramembranous proteolysis of APP may play a signaling role analogous to that of Notch.

TL;DR: It is concluded that after Aβ immunization, the effects of anti-Aβ antibodies on Aβ deposition in APP Tg2576 transgenic mice are not dependent on FcR-mediated phagocytic events.