“…Furthermore, whereas the ERK/Elk-1, JAK/STAT, and AKT/ CREB pathways have all been correlated to neuroprotection, it is today widely admitted that IGF-1-mediated neuroprotection occurs through activation of the AKT/CREB pathway (D'Mello et al, 1997;Párrizas et al, 1997;Yadav et al, 2005). Furthermore, in the specific case of cerebellar granule neurons, IGF-1-induced neuroprotection results from both the activation of AKT and the inhibition of MEK-ERK1/2 through the AKT pathway (Subramaniam et al, 2005). Similarly, the neuroprotection induced by IGF-1R reduction in SMA spinal cords, as evidenced by the relative persistence of the motor neuron population and the reduced activation of caspase-3, might result from both an increased SMN protein expression and the presence of the two powerful antiapoptotic molecules, AKT and CREB, at the activated state.…”