Alzheimer's disease (AD) is a devastating neurodegenerative disorder that impacts a substantial number of individuals globally. Despite its widespread prevalence, there is currently no cure for AD. It is widely acknowledged that normal synaptic function holds a key role in memory, cognitive abilities, and the interneuronal transfer of information. As AD advances, symptoms including synaptic impairment, decreased synaptic density, and cognitive decline become increasingly noticeable. The importance of glial cells in the formation of synapses, the growth of neurons, brain maturation, and safeguarding the microenvironment of the central nervous system is well recognized. However, during AD progression, overactive glial cells can cause synaptic dysfunction, neuronal death, and abnormal neuroinflammation. Both neuroinflammation and synaptic dysfunction are present in the early stages of AD. Therefore, focusing on the changes in glia-synapse communication could provide insights into the mechanisms behind AD. In this review, we aim to provide a summary of the role of various glial cells, including microglia, astrocytes, oligodendrocytes, and oligodendrocyte precursor cells, in regulating synaptic dysfunction. This may offer a new perspective on investigating the underlying mechanisms of AD.