| First Author | Xu Z | Year | 2015 |
| Journal | Mol Neurodegener | Volume | 10 |
| Pages | 58 | PubMed ID | 26526066 |
| Mgi Jnum | J:323015 | Mgi Id | MGI:6819300 |
| Doi | 10.1186/s13024-015-0056-1 | Citation | Xu Z, et al. (2015) Deletion of aquaporin-4 in APP/PS1 mice exacerbates brain Abeta accumulation and memory deficits. Mol Neurodegener 10:58 |
| abstractText | BACKGROUND: Preventing or reducing amyloid-beta (Abeta) accumulation in the brain is an important therapeutic strategy for Alzheimer's disease (AD). Recent studies showed that the water channel aquaporin-4 (AQP4) mediates soluble Abeta clearance from the brain parenchyma along the paravascular pathway. However the direct evidence for roles of AQP4 in the pathophysiology of AD remains absent. RESULTS: Here, we reported that the deletion of AQP4 exacerbated cognitive deficits of 12-moth old APP/PS1 mice, with increases in Abeta accumulation, cerebral amyloid angiopathy and loss of synaptic protein and brain-derived neurotrophic factor in the hippocampus and cortex. Furthermore, AQP4 deficiency increased atrophy of astrocytes with significant decreases in interleukin-1 beta and nonsignificant decreases in interleukin-6 and tumor necrosis factor-alpha in hippocampal and cerebral samples. CONCLUSIONS: These results suggest that AQP4 attenuates Abeta pathogenesis despite its potentially inflammatory side-effects, thus serving as a promising target for treating AD. |
