In the brains of patients with Alzheimer's disease (AD) or AD animal models, β-amyloid (Aβ), tau protein, presenilin (PS)1, PS2 and apolipoprotein E4 (ApoE4) would affect the calcium channels on neuronal cell membrane, endoplasmic reticulum membrane and mitochondrial membrane, and eventually lead to the imbalance of calcium homeostasis in neurons. Aβ can also act on the endoplasmic reticulum of astrocytes and cause abnormal calcium signal. Abnormal calcium signals in the brain in turn act on neurons and promote Aβ and tau protein phosphorylation, which aggravates the disease. This study focuses on the changes of calcium signals in neurons and astrocytes in AD, in order to clarify the relationship between the calcium dyshomeostasis in neurons and astrocytes and the pathogenesis of AD, thus provides new idea for the prevention and treatment of AD.