CPEB1 is overexpressed in neurons derived from Down syndrome IPSCs and in the hippocampus of the mouse model Ts1Cje

• Published in: Molecular and cellular neuroscience 2019-03, Vol.95, p.79-85
• Main Authors: Casañas, Juan José, González-Corrales, Macarena, Urbano-Gámez, Jesús David, Alves-Sampaio, Alexandra, Troca-Marín, José Antonio, Montesinos, María Luz
• Format: Article
• Language: English
• Subjects: CPEB1; Dendritic mRNA; Down syndrome; MAP1B; Trisomy 21; α-CaMKII
• ISSN: 1044-7431; 1095-9327
• DOI: 10.1016/j.mcn.2019.02.002

Trisomy 21, also known as Down syndrome (DS), is the most frequent genetic cause of intellectual impairment. In mouse models of DS, deficits in hippocampal synaptic plasticity have been observed, in conjunction with alterations to local dendritic translation that are likely to influence plasticity, learning and memory. Here we show that expression of a local translational regulator, the Cytoplasmic Polyadenylation Element Binding Protein 1 (CPEB1), is enhanced in hippocampal neurons from the Ts1Cje DS mouse model. Interestingly, this protein, which is also involved in dendritic mRNA transport, is overexpressed in dendrites of neurons derived from DS human induced pluripotent stem cells (hIPSCs). Moreover, there is an increase in the mRNA levels of α-Calmodulin Kinase II (α-CaMKII) and Microtubule-associated protein 1B (MAP1B), two dendritic mRNAs, in Ts1Cje synaptoneurosomes. Taking into account the fundamental role of CPEB1 protein and its target mRNAs in synaptic plasticity, these data could be relevant to the intellectual impairment in the context of DS. •CPEB1 (a regulator of mRNA transport) is overexpressed in a Down syndrome model.•Dendritic levels of α-CaMKII and MAP1B mRNAs are increased in that model.•CPEB1 is overexpressed in dendrites of neurons derived from Down syndrome IPSCs.•These data could be relevant to the trisomy 21 intellectual impairment.