Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Intracranial administration of deglycosylated C-terminal-specific anti-Aβ antibody efficiently clears amyloid plaques without activating microglia in amyloid-depositing transgenic mice | Journal of Neuroinflammation BioMed Central Research Open Access Intracranial administration of deglycosylated C-terminal-specific anti-Ap antibody efficiently clears amyloid plaques without activating microglia in amyloid-depositing transgenic mice Niki C Carty1 Donna M Wilcock1 Arnon Rosenthal2 Jan Grimm2 Jaume Pons2 Victoria Ronan1 Paul E Gottschall1 Marcia N Gordon1 and Dave Morgan 1 Address 1Alzheimer s Research Laboratory University of South Florida Department of Molecular Pharmacology and Physiology 12901 Bruce B Downs Blvd Tampa FL 33612 USA and 2Rinat Neuroscience Corp. 3155 Porter Drive Palo Alto California 94304 USA Email Niki C Carty - ncarty@ Donna M Wilcock - dwilcock@ Arnon Rosenthal - ar@ Jan Grimm - grimm@ Jaume Pons - jaume@ Victoria Ronan - victoria@ Paul E Gottschall - pgottsch@ Marcia N Gordon - mgordon@ Dave Morgan - dmorgan@ Corresponding author Published 10 May 2006 Received 03 January 2006 Journal of Neuroinflammation 2006 3 11 doi 1742-2094-3-11 Accepted 10 May 2006 This article is available from http content 3 1 1 1 2006 Carty et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Antibodies against the AB peptide clear AB deposits when injected intracranially. Deglycosylated antibodies have reduced effector functions compared to their intact counterparts potentially avoiding immune activation. Methods Deglycosylated or intact C-terminal specific high affinity anti-AP antibody 2H6 were intracranially injected into the right frontal cortex and hippocampus of amyloid precursor protein APP transgenic mice. The untreated left hemisphere was
