TY - JOUR
AU - Miles, Luke
AB - Acta Neuropathol (2014) 128:611–614 DOI 10.1007/s00401-014-1333-8 COrrespONDeNCe Andrew D. Watt · Gabriela A. N. Crespi · Russell A. Down · David B. Ascher · Adam Gunn · Keyla A. Perez · Catriona A. McLean · Victor L. Villemagne · Michael W. Parker · Kevin J. Barnham · Luke A. Miles received: 6 August 2014 / Accepted: 7 August 2014 / published online: 15 August 2014 © springer-Verlag Berlin Heidelberg 2014 We have read with interest the commentary by siemers engagement with brain Aβ, consistent with published clini- et al. [28] regarding our paper describing the ability of cal data”. To reiterate, we reported data showing that bap- the three anti-Aβ antibodies, bapineuzumab, crenezumab ineuzumab was capable of binding soluble Aβ with a low and solanezumab to engage Aβ in both a synthetic and a nanomolar affinity and demonstrated that the antibody biological setting. We appreciate the opportunity to clarify could detect Aβ species in buffer and in brain homogen- any misunderstandings and here provide a brief response to ate and plasma from transgenic animal models of AD. Fur- their concerns. thermore, in agreement with the phase 3 clinical data [23], siemers et al. [28] begin their commentary by stat- 
TI - Anti-Aβ antibody target engagement: a response to Siemers et al.
JF - Acta Neuropathologica
DO - 10.1007/s00401-014-1333-8
DA - 2014-08-15
UR - https://www.deepdyve.com/lp/springer-journals/anti-a-antibody-target-engagement-a-response-to-siemers-et-al-lJV4TRWOSE
SP - 611
EP - 614
VL - 128
IS - 4
DP - DeepDyve
ER -