Evidence indicates that cognitive deficits in SAMP8 can be observed as early as four months after birth, which is earlier than those in SAMR1 and that the deficits appear to be due to dysfunction of the neurobiological signaling mediated by some key proteins such as Ca2+/calmodulin-dependent kinase II (CaMKII), cyclic AMP responsive element binding protein (CREB) and N-methyl-D-aspartate receptor (NMDAR), which are important for synaptic plasticity [13,15,19,20]. This evidence concerns the gene CAMK2G and Cognitive impairment.