Journal
NEUROBIOLOGY OF DISEASE
Volume 20, Issue 2, Pages 541-549Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2005.04.007
Keywords
Alzheimer's disease; Tg2576 mouse; beta-amyloid peptide (A beta); F(ab ')(2) fragment; IgG1 isotype; anti-A beta monoclonal antibody; passive immunization; amyloid plaque; microglia
Categories
Ask authors/readers for more resources
This work examines whether administering the F(ab')(2) fragment of an IgG1 monoclonal antibody (mAb) targeting the N-terminal 1-13 amino acids of the beta-amyloid peptide (A beta mAb) reduces amyloid deposition in Alzheimer's disease (AD). The F(ab')(2) fragment was injected intraperitoneally or intracranially into Tg2576 mice, a murine model of human AD. Both routes of administration significantly reduced A plaque formation in the brain, as determined immunohistochemically and by monitoring levels of A beta(1-40) and A beta(1 -42) peptide. Use of the F(ab')(2) fragment significantly reduced phagocytic infiltration in the CNS when compared to intact mAb. Since IgG1 Abs do not fix complement, these findings suggest that effective in vivo clearance of amyloid deposits can be achieved without stimulation of FcR-reactive phagocytes or activation of the complement cascade. (c) 2005 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available