| First Author | Wang Q | Year | 2012 |
| Journal | Brain Res | Volume | 1459 |
| Pages | 15-26 | PubMed ID | 22560596 |
| Mgi Jnum | J:186448 | Mgi Id | MGI:5432323 |
| Doi | 10.1016/j.brainres.2012.04.011 | Citation | Wang Q, et al. (2012) Stromal cell-derived factor 1alpha decreases beta-amyloid deposition in Alzheimer's disease mouse model. Brain Res 1459:15-26 |
| abstractText | beta-amyloid (Abeta) aggregates are known to induce neuronal and synaptic dysfunction, and thus are involved in learning and memory deficits in Alzheimer's disease (AD), making Abeta deposits a potential target for prevention or treatment. Microglia, especially bone marrow-derived microglia (BMDM), has been recently thought to play important roles in internalizing and phagocytozing Abeta. BMDM originate in the bone marrow, migrate into the blood as hematopoietic progenitor cells (HPCs) and enter the brain in a chemokine-dependent manner. An effective chemoattractant for HPCs is stromal cell-derived factor 1 (SDF-1), which is also involved in regulating HPCs differentiation. Therefore, we hypothesize that SDF-1 might have influence on the migration of BMDM from peripheral cycle to brain. To explore whether treatment with SDF-1alpha can decrease Abeta burden, APP/PS1 double transgenic mice were given intracerebroventricular injection of SDF-1alpha weekly from the age of 28 to 32 weeks (4 weeks of injections) or from 28 to 36 weeks (8 weeks of injections). The results of our study showed that SDF-1alpha treatment decreased the area and the number of Abeta deposits, increased the level of Iba-1, a marker of microglia, and increased the number of plaque associated microglia in the parenchyma of APP/PS1 transgenic mice. These results suggest that SDF-1 could provide a novel and promising target for the purpose of lowering Abeta pathology in AD. |
