Andrade Talavera, YunieskyBenito, ItziarCasañas, Juan JoséRodríguez-Moreno, AntonioMontesinos, María Luz2025-04-022025-04-022015Neurobiology of Disease 82 (2015) 516–52510.1016/j.nbd.2015.09.005https://hdl.handle.net/10433/23690Down'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.application/pdfenAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/BDNF-LTPBarnes mazeERKMTORPharmacotherapyRapamycinSynaptic plasticityTrisomy 21Ts1Cjejournal articlerestricted access