RT Journal Article
T1 Rapamycin restores BDNF-LTP and the persistence of long-term memory in a model of Down's syndrome
A1 Andrade Talavera, Yuniesky
A1 Benito, Itziar
A1 Casañas, Juan José
A1 Rodríguez-Moreno, Antonio
A1 Montesinos, María Luz
K1 BDNF-LTP
K1 Barnes maze
K1 ERK
K1 MTOR
K1 Pharmacotherapy
K1 Rapamycin
K1 Synaptic plasticity
K1 Trisomy 21
K1 Ts1Cje
AB 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.
PB Elsevier
YR 2015
FD 2015
LK https://hdl.handle.net/10433/23690
UL https://hdl.handle.net/10433/23690
LA en
NO Neurobiology of Disease 82 (2015) 516–525
NO Departamento de Fisiología, Anatomía y Biología Celular
DS RIO
RD May 26, 2026