Alzheimer’ s disease ( AD) is a chronic progressive neurodegenerative disease characterized by dementia as the main symptom. The main neuropathologic features include senile plaques, neurofibrillary tangles, neuroinflammation, and neuron loss. Deposition of amyloid β-protein and misfolded tau protein in patients with AD induces the activation of microglia; this leads to the secretion of cytokines and chemokines, which jointly induce a neuroinflammatory response and affect the progression of AD. This review briefly summarizes the role of microglial activation and chemokine release in the neuroinflammation of AD and provides new insight into the treatment of AD.