Attention has been paid to the occurrence of neuroinflammation in the early stages of Alzheimer’s disease (AD), acting as a key factor in promoting the progression of AD. Neuroinflammation is generally characterized by the activation of microglia and astroglia, and the associated expression of proinflammatory cytokines and chemokines, which damage the nervous system. Numerous pieces of evidence prove that formaldehyde is closely related to learning, memory, and cognitive impairment in AD patients. Formaldehyde has been shown to elicit amyloid β (Aβ) deposition and Tau hyperphosphorylation, leading to cognitive impairment based on animal and clinical studies. Changes in concentrations of formaldehyde can be observed in general inflammation in different organs such as lung, liver, kidney, and circulating immune of brain. Furthermore, formaldehyde is usually used as an agent to induce pain, resulting in a marked inflammatory process in central and peripheral nervous system. As an inflammation-inducing factor, formaldehyde is able to activate microglia and astrocytes, leading to the release of proinflammatory cytokines and chemokines, by deteriorating the permeability of the blood–brain barrier (BBB), eliciting Aβ deposition and inducing Tau hyperphosphorylation in brain. In other words, formaldehyde participates not only in the general inflammation but may also in neuroinflammation, although the mechanisms by which formaldehyde-induced inflammation activates microglia and astroglia in central nervous system (CNS) still need further investigation.