For that we use a combination of biochemical, molecular biology, electrophysiology, advanced microscopy and other imaging techniques. Since Ng levels and cognitive performance are positively correlated in the human brain, we are interested to understand the mechanisms underlying the regulation of Ng transcription and its local translation in dendrites. We propose Ng as a molecular target for strategies designed to prevent, treat or alleviate conditions and pathologies associated to impaired cognitive function. We justify this objective on the following premises. First, Ng function is quite restricted to its action in the brain. Thus, Ng deficiency in mice does not cause apparent anatomical or physiological abnormalities, but severe cognitive impairments. And second, targeting Ng expression to improve cognition is very likely devoid of side-effects, since Ng expression is tightly regulated in space and time (only expressed in the postnatal forebrain) and specifically associated to cognitive performance. In summary, a broader and deeper understanding of the role of Ng and other CaM-sequestering proteins in the mechanisms of neuronal plasticity will contribute to the development of newer therapies to improve the cognitive function and quality of life of aging individuals and patients suffering from neurological diseases.