AKT1 and Alzheimer disease: In pre-symptomatic and middle-aged APPSwe/PS1ΔE9 (APP/PS1) mice, generation of reactive oxygen species was found to lead to oxidative modification of Akt1 in the synapse resulting in reduction of Akt1-mTOR signaling and deficiency in activity-dependent protein translation; moreover, a similar attenuation of synaptoneurosomal protein translation was found in postmortem AD brains (Ahmad et al., 2017).