| First Author | Morales-Corraliza J | Year | 2013 |
| Journal | Neurobiol Aging | Volume | 34 |
| Issue | 1 | Pages | 137-45 |
| PubMed ID | 22608241 | Mgi Jnum | J:191360 |
| Mgi Id | MGI:5461597 | Doi | 10.1016/j.neurobiolaging.2012.04.007 |
| Citation | Morales-Corraliza J, et al. (2013) Immunization targeting a minor plaque constituent clears beta-amyloid and rescues behavioral deficits in an Alzheimer's disease mouse model. Neurobiol Aging 34(1):137-45 |
| abstractText | Although anti-human beta-amyloid (Abeta) immunotherapy clears brain beta-amyloid plaques in Alzheimer's disease (AD), targeting additional brain plaque constituents to promote clearance has not been attempted. Endogenous murine Abeta is a minor Abeta plaque component in amyloid precursor protein (APP) transgenic AD models, which we show is approximately 3%-8% of the total accumulated Abeta in various human APP transgenic mice. Murine Abeta codeposits and colocalizes with human Abeta in amyloid plaques, and the two Abeta species coimmunoprecipitate together from brain extracts. In the human APP transgenic mouse model Tg2576, passive immunization for 8 weeks with a murine-Abeta-specific antibody reduced beta-amyloid plaque pathology, robustly decreasing both murine and human Abeta levels. The immunized mice additionally showed improvements in two behavioral assays, odor habituation and nesting behavior. We conclude that passive anti-murine Abeta immunization clears Abeta plaque pathology--including the major human Abeta component--and decreases behavioral deficits, arguing that targeting minor endogenous brain plaque constituents can be beneficial, broadening the range of plaque-associated targets for AD therapeutics. |
