| First Author | Späni C | Year | 2015 |
| Journal | Acta Neuropathol Commun | Volume | 3 |
| Pages | 71 | PubMed ID | 26558367 |
| Mgi Jnum | J:281484 | Mgi Id | MGI:6355546 |
| Doi | 10.1186/s40478-015-0251-x | Citation | Spani C, et al. (2015) Reduced beta-amyloid pathology in an APP transgenic mouse model of Alzheimer's disease lacking functional B and T cells. Acta Neuropathol Commun 3:71 |
| abstractText | INTRODUCTION: In Alzheimer's disease, accumulation and pathological aggregation of amyloid beta-peptide is accompanied by the induction of complex immune responses, which have been attributed both beneficial and detrimental properties. Such responses implicate various cell types of the innate and adaptive arm of the immunesystem, both inside the central nervous system, and in the periphery. To investigate the role of the adaptive immune system in brain beta-amyloidosis, PSAPP transgenic mice, an established mouse model of Alzheimer's disease, were crossbred with the recombination activating gene-2 knockout (Rag2 ko) mice lacking functional B and T cells. In a second experimental paradigm, aged PSAPP mice were reconstituted with bone marrow cells from either Rag2 ko or wildtype control mice. RESULTS: Analyses from both experimental approaches revealed reduced beta-amyloid pathology and decreased brain amyloid beta-peptide levels in PSAPP mice lacking functional adaptive immune cells. The decrease in brain beta-amyloid pathology was associated with enhanced microgliosis and increased phagocytosis of amyloid beta-peptide aggregates. CONCLUSION: The results of this study demonstrate an impact of the adaptive immunity on cerebral beta-amyloid pathology in vivo and suggest an influence on microglia-mediated amyloid beta-peptide clearance as a possible underlying mechanism. |
