Artículo
Rapamycin restores BDNF-LTP and the persistence of long-term memory in a model of Down's syndrome
Autor/es | Andrade-Talavera, Yuniesky
Benito, Itziar Casañas, Juan José Rodríguez Moreno, Antonio Montesinos Gutiérrez, María Luz |
Departamento | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica |
Fecha de publicación | 2015 |
Fecha de depósito | 2021-04-15 |
Publicado en |
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Resumen | 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 ... 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. |
Cita | Andrade-Talavera, Y., Benito, I., Casañas, J.J., Rodríguez Moreno, A. y Montesinos, M.L. (2015). Rapamycin restores BDNF-LTP and the persistence of long-term memory in a model of Down's syndrome. Neurobiology Of Disease, 82, 516-525. |
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