| First Author | Dengler-Crish CM | Year | 2018 |
| Journal | Neurobiol Aging | Volume | 67 |
| Pages | 148-158 | PubMed ID | 29660685 |
| Mgi Jnum | J:264770 | Mgi Id | MGI:6196691 |
| Doi | 10.1016/j.neurobiolaging.2018.03.021 | Citation | Dengler-Crish CM, et al. (2018) Evidence of Wnt/beta-catenin alterations in brain and bone of a tauopathy mouse model of Alzheimer's disease. Neurobiol Aging 67:148-158 |
| abstractText | Low bone mineral density (BMD) is a significant comorbidity in Alzheimer's disease (AD) and may reflect systemic regulatory pathway dysfunction. Low BMD has been identified in several AD mouse models selective for amyloid-beta or tau pathology, but these deficits were attributed to diverse mechanisms. In this study, we identified common pathophysiological mechanisms accounting for bone loss and neurodegeneration in the htau mouse, a tauopathy model with an early low BMD phenotype. We investigated the Wnt/beta-catenin pathway-a cellular signaling cascade linked to both bone loss and neuropathology. We showed that low BMD persisted in male htau mice aged from 6 to 14 months, remaining significantly lower than tau-null and C57BL/6J controls. Osteogenic gene expression in female and male htau mice was markedly reduced from controls, indicating impaired bone remodeling. In both the bone and brain, htau mice showed alterations in Wnt/beta-catenin signaling genes suggestive of increased inhibition of this pathway. These findings implicate dysfunctional Wnt signaling as a potential target for addressing bone loss in AD. |
