| First Author | Santuccione AC | Year | 2013 |
| Journal | Mol Psychiatry | Volume | 18 |
| Issue | 3 | Pages | 358-68 |
| PubMed ID | 22688190 | Mgi Jnum | J:278130 |
| Mgi Id | MGI:6355886 | Doi | 10.1038/mp.2012.70 |
| Citation | Santuccione AC, et al. (2013) Active vaccination with ankyrin G reduces beta-amyloid pathology in APP transgenic mice. Mol Psychiatry 18(3):358-68 |
| abstractText | Serum antibodies against amyloid-beta peptide (Abeta) in humans with or without diagnosis of Alzheimer's disease (AD) indicate the possibility of immune responses against brain antigens. In an unbiased screening for antibodies directed against brain proteins, we found in AD patients high serum levels of antibodies against the neuronal cytoskeletal protein ankyrin G (ankG); these correlated with slower rates of cognitive decline. Neuronal expression of ankG was higher in AD brains than in nondemented age-matched healthy control subjects. AnkG was present in exosomal vesicles, and it accumulated in beta-amyloid plaques. Active immunization with ankG of arcAbeta transgenic mice reduced brain beta-amyloid pathology and increased brain levels of soluble Abeta(42). AnkG immunization induced a reduction in beta-amyloid pathology, also in Swedish transgenic mice(.) Anti-ankG monoclonal antibodies reduced Abeta-induced loss of dendritic spines in hippocampal ArcAbeta organotypic cultures. Together, these data established a role for ankG in the human adaptive immune response against resident brain proteins, and they show that ankG immunization reduces brain beta-amyloid and its related neuropathology. |
