| First Author | Kusakari S | Year | 2018 |
| Journal | J Neurochem | Volume | 144 |
| Issue | 2 | Pages | 218-233 |
| PubMed ID | 29164613 | Mgi Jnum | J:257300 |
| Mgi Id | MGI:6116184 | Doi | 10.1111/jnc.14258 |
| Citation | Kusakari S, et al. (2018) Calmodulin-like skin protein protects against spatial learning impairment in a mouse model of Alzheimer disease. J Neurochem 144(2):218-233 |
| abstractText | Humanin and calmodulin-like skin protein (CLSP) inhibits Alzheimer disease (AD)-related neuronal cell death via the heterotrimeric humanin receptor in vitro. It has been suggested that CLSP is a central agonist of the heterotrimeric humanin receptor in vivo. To investigate the role of CLSP in the AD pathogenesis in vivo, we generated mouse CLSP-1 transgenic mice, crossed them with the APPswe/PSEN1dE9 mice, a model mouse of AD, and examined the effect of CLSP over-expression on the pathological phenotype of the AD mouse model. We found that over-expression of the mouse CLSP-1 gene attenuated spatial learning impairment, the loss of a presynaptic marker synaptophysin, and the inactivation of STAT3 in the APPswe/PSEN1dE9 mice. On the other hand, CLSP over-expression did not affect levels of Abeta, soluble Abeta oligomers, or gliosis. These results suggest that the CLSP-mediated attenuation of memory impairment and synaptic loss occurs in an Abeta-independent manner. The results of this study may serve as a hint to the better understanding of the AD pathogenesis and the development of AD therapy. |
