| First Author | Andrade-Talavera Y | Year | 2015 |
| Journal | Neurobiol Dis | Volume | 82 |
| Pages | 516-525 | PubMed ID | 26388397 |
| Mgi Jnum | J:227661 | Mgi Id | MGI:5702374 |
| Doi | 10.1016/j.nbd.2015.09.005 | Citation | Andrade-Talavera Y, et al. (2015) Rapamycin restores BDNF-LTP and the persistence of long-term memory in a model of Down's syndrome. Neurobiol Dis 82:516-25 |
| abstractText | Down's syndrome (DS) is the most prevalent genetic intellectual disability. Memory deficits significantly contribute to the cognitive dysfunction in DS. Previously, we discovered that mTOR-dependent local translation, a pivotal process for some forms of synaptic plasticity, is deregulated in a DS mouse model. Here, we report that these mice exhibit deficits in both synaptic plasticity (i.e., BDNF-long term potentiation) and the persistence of spatial long-term memory. Interestingly, these deficits were fully reversible using rapamycin, a Food and Drug Administration-approved specific mTOR inhibitor; therefore, rapamycin may be a novel pharmacotherapy to improve cognition in DS. |
