Alzheimer's disease (AD) is a progressive neurological disorder mainly affecting the elderly. AD demonstrates a gradual deterioration in cognitive functions. Alzheimer's disease is marked by the existence of intracellular flame-shaped neurofibrillary tangles (NFTs) and extracellular plaques of β-amyloid (Aβ) deposition known as amyloid plaques. Degeneration of synapses correlates to cognitive decline in patients with AD along with two hallmarks of AD. Inhibition in the Wnt signaling pathway contributes to AD pathogenesis by triggering synaptic dysfunction and neuronal degeneration. Suppression of Wnt/β-catenin signaling induced by an increase of GSK-3β activation and degradation of β-catenin. Furthermore, it was suggested that Aβ initiates the deregulation of Wnt signaling with a consequent inhibition of synapses. The binding of Wnt protein to Fzd/LRP causes inhibition of GSK3β and consequent activation of Wnt/β-catenin signalling. The activation of Wnt/β-catenin signaling prevents Aβ deposition and tau hyperphosphorylation in the brain. Therefore, restoring Wnt/β-catenin signaling could be a therapeutic opportunity to prevent the development of AD deterioration.