Central insulin resistance is a typical trait associated with premature ageing and is shown in neurological illnesses such as Alzheimer’s disease (AD) in its early stages. In this sense, the (phosphoinositide 3 kinase)/Akt pathway mediates insulin signalling in the brain, where defective insulin signalling is a risk factor for developing AD. Several lines of evidence show that integrated coordination of neuronal responses through the PI3K /Akt pathway in the brain has a significant functional impact on key events that are negatively affected in AD. Moreover, the PIK3/Akt pathway is crucial in many biological processes such as proliferation, growth, migration and cell survival and many reports have supported that this pathway is inhibited by Aβ oligomers promoting neuron death and eventually dementia. In the present study, we investigated whether D-Pinitol inositol, which acts as an insulin sensitizer, might affect the progression of the illness in the 5xFAD mouse model of AD. Our results showed not only that D-Pinitol treatment improves cognitive function in the mouse 5xFAD model and ameliorates cognitive spatial flexibility, but also tau and Aβ proteins were downregulated after treatment. Moreover, D-Pinitol affects PI3K /Akt pathway suggesting that it may prevent metabolic dysregulation at early stages. Also, evaluating D-Pinitol effectiveness in the 3xTg genetic tauopathy mouse model, allows us to assert that this compound has a pharmacological profile addressing the treatment of Tauopathies. The present findings suggest that D-Pinitol is an interesting drug for developing treatments for AD.