TY - JOUR T1 - ADAP1/Centaurin-α1 Negatively Regulates Dendritic Spine Function and Memory Formation in the Hippocampus JF - eneuro JO - eNeuro DO - 10.1523/ENEURO.0111-20.2020 VL - 8 IS - 1 SP - ENEURO.0111-20.2020 AU - Erzsebet M. Szatmari AU - Corey Moran AU - Sarah Cohen AU - Amanda Jacob AU - Paula Parra-Bueno AU - Naomi Kamasawa AU - Debbie Guerrero-Given AU - Michael Klein AU - Robert Stackman, Jr AU - Ryohei Yasuda Y1 - 2021/01/01 UR - http://www.eneuro.org/content/8/1/ENEURO.0111-20.2020.abstract N2 - ADAP1/Centaurin-α1 (CentA1) functions as an Arf6 GTPase-activating protein highly enriched in the brain. Previous studies demonstrated the involvement of CentA1 in brain function as a regulator of dendritic differentiation and a potential mediator of Alzheimer’s disease (AD) pathogenesis. To better understand the neurobiological functions of CentA1 signaling in the brain, we developed Centa1 knock-out (KO) mice. The KO animals showed neither brain development nor synaptic ultrastructure deficits in the hippocampus. However, they exhibited significantly higher density and enhanced structural plasticity of dendritic spines in the CA1 region of the hippocampus compared with non-transgenic (NTG) littermates. Moreover, the deletion of Centa1 improved performance in the object-in-place (OIP) spatial memory task. These results suggest that CentA1 functions as a negative regulator of spine density and plasticity, and of hippocampus-dependent memory formation. Thus, CentA1 and its downstream signaling may serve as a potential therapeutic target to prevent memory decline associated with aging and brain disorders. ER -