Specifically, transgenic overexpression of miR-132 increases dendritic spine density while causing significant deficits in novel object recognition (Hansen et al. 2010) via suppression of a specific miR-132 target, the p250 GTPase-activating protein (P250GAP) (Wayman et al. 2008); also, miR-132 controls dendritic plasticity by modulating the expression of the stress-sensitive transcription factor methyl CpG-binding protein 2 (MECP2) (Fyffe et al. 2008; Klein et al. 2007) known for its role in the Rett syndrome (Amir et al. 1999). This evidence concerns the gene MECP2 and atypical Rett syndrome.