IL1B and Alzheimer disease: As for astrocytes, EAAT and astrocyte-neuron lactate shuttle are impaired, leading to the production and accumulation of Aβ and tau protein under the stimulation of cytokines, such as TGF-β and IL-1β, while the risk gene ApoE4 regulates cerebrovascular functions, resulting in neuronal energy metabolism dysfunction, glutamate excitatory toxicity, and the development of AD [96].