| First Author | Lifshitz V | Year | 2012 |
| Journal | Neurobiol Aging | Volume | 33 |
| Issue | 2 | Pages | 432.e1-432.e13 |
| PubMed ID | 21371785 | Mgi Jnum | J:188218 |
| Mgi Id | MGI:5439705 | Doi | 10.1016/j.neurobiolaging.2011.01.006 |
| Citation | Lifshitz V, et al. (2012) Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model. Neurobiol Aging 33(2):432.e1-432.e13 |
| abstractText | Cerebrovascular amyloidosis is caused by amyloid accumulation in walls of blood vessel walls leading to hemorrhagic stroke and cognitive impairment. Transforming growth factor-beta1 (TGF-beta1) expression levels correlate with the degree of cerebrovascular amyloid deposition in Alzheimer's disease (AD) and TGF-beta1 immunoreactivity in such cases is increased along the cerebral blood vessels. Here we show that a nasally administered proteosome-based adjuvant activates macrophages and decreases vascular amyloid in TGF-beta1 mice. Animals were nasally treated with a proteosome-based adjuvant on a weekly basis for 3 months beginning at age 13 months. Using magnetic resonance imaging (MRI) we found that while control animals showed a significant cerebrovascular pathology, proteosome-based adjuvant prevents further brain damage and prevents pathological changes in the blood-brain barrier. Using an object recognition test and Y-maze, we found significant improvement in cognition in the treated group. Our findings support the potential use of a macrophage immunomodulator as a novel approach to reduce cerebrovascular amyloid, prevent microhemorrhage, and improve cognition. |
