Alzheimer’ s disease ( AD) is one of the most common neurodegenerative diseases. Its main pathological markers include neurofibrillary tangle and senile plaque formation, and its pathogenesis is extremely complex. As the main factor of the insulin signaling pathway, Akt plays an important role in regulating cell growth, energy utilization, mitochondrial functions, autophagy, oxidative stress, synaptic plasticity and cognitive functions. Studies have shown different post-translational modifications of Akt in the brains of AD patients, which suggests that different post- translational modifications of Akt may be closely related to the pathogenesis of AD. In this review, the possible role of Akt in the pathogenesis of AD was discussed, in order to provide new clues for the prevention and treatment of AD.