| First Author | Wang F | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 1 | Pages | 111-22 |
| PubMed ID | 25085784 | Mgi Jnum | J:218109 |
| Mgi Id | MGI:5616681 | Doi | 10.1016/j.neurobiolaging.2014.06.029 |
| Citation | Wang F, et al. (2015) Combined treatment of amyloid-beta(1)(-)(4)(2)-stimulated bone marrow-derived dendritic cells plus splenocytes from young mice prevents the development of Alzheimer's disease in APPswe/PSENldE9 mice. Neurobiol Aging 36(1):111-22 |
| abstractText | Anti-amyloid-beta (Abeta) immunotherapy is a potential therapeutic strategy to reduce amyloid plaques and amyloid-associated pathologies in Alzheimer's disease (AD). Immune senescence with aging has also played a crucial role in AD pathogenesis and influences the effect of anti-Abeta immunotherapy. In this study, a combined treatment of Abeta(1)(-)(4)(2)-bone marrow-derived dendritic cells (BMDCs) with intraperitoneal injection of splenocytes from young mice was designed as a novel immunotherapy for AD in APPswe/PSEN1de9 transgenic mice models. The results showed that the combined treatment not only elevated the level of anti-Abeta antibodies but also reduced amyloid plaques in brain and finally ameliorated deterioration of spatial learning and memory in AD mice. Additionally, the results revealed an increase of CD68 positive microglial cells in the vicinity of amyloid plaques in the mouse brain, which was responsible for the enhanced phagocytosis of Abeta plaques. In conclusion, the Abeta(1)(-)(4)(2)-BMDCs plus splenocytes treatment improved the phagocytosis of microglia and prevented AD pathology more effectively. This combined immunotherapy provided a promising treatment in preventing the progression of AD in clinical studies in the near future. |
