Current models developed to explain memory creation propose that memories are coded in the form of changes in the strength of specific synaptic connections between neurons which, in turn, depend on changes in genic expression in the nucleus of said neurons. Studies carried out on different organisms indicate that the CREB activation pathway forms an essential part of the molecular interrupter that transforms short-term memories into long-term memories. CREB and its co-activator CBP are also involved in other important functions of the central nervous system, such as regulation of neuronal survival, and have been related to diverse pathologies of the nervous system. The development of adequate animal models is key to undertaking the analysis of these complex functions. Our laboratory uses a multidisciplinary approach that combines mouse genetics, molecular biology, physiology and behavioural studies to investigate how malfunction of the gene expression cascade regulated by CREB and deficient histone acetylation in neurons cause defects in cognitive processes. We now propose researching the potential benefits of regulated and restricted overexpression of CREB and CBP activities. To do so, we will test the effectiveness of these genetic manipulations in the reduction of symptoms associated with two important pathological processes of the nervous system in which these activities seem to be reduced: the mental weakness associated with Rubinstein-Taybi Syndrome and the cognitive defects associated with Huntington's Disease, known historically as Huntington's Chorea. We will use mouse models for both diseases.