Alzheimer’s disease (AD) is a neurodegenerative disease with a high incidence rate. The main pathological features of AD are β-amyloid plaques (APs), which are formed by β-amyloid protein (Aβ) deposition, and neurofibrillary tangles (NFTs), which are formed by the excessive phosphorylation of the tau protein. Although a series of studies have shown that the accumulation of metal ions, including calcium ions (Ca²⁺), can promote the formation of APs and NFTs, there is no systematic review of the mechanisms by which Ca²⁺ affects the development and progression of AD. In view of this, the current review summarizes the mechanisms by which Ca²⁺ is transported into and out of cells and organelles, such as the cell, endoplasmic reticulum, mitochondrial and lysosomal membranes to affect the balance of intracellular Ca²⁺ levels. In addition, dyshomeostasis of Ca²⁺ plays an important role in modulating the pathogenesis of AD by influencing the production and aggregation of Aβ peptides and tau protein phosphorylation and the ways that disrupting the metabolic balance of Ca²⁺ can affect the learning ability and memory of people with AD. In addition, the effects of these mechanisms on the synaptic plasticity are also discussed. Finally, the molecular network through which Ca²⁺ regulates the pathogenesis of AD is introduced, providing a theoretical basis for improving the clinical treatment of AD.