Alzheimer's disease (AD) is the most common type of neurodegenerative disorder in the world. Although both amyloid beta peptide deposition and neurofibrillary tangle (NFT) formation in the AD brain have been established as pathological hallmarks of the disease, many other factors contribute in a complex manner to the pathogenesis of AD. Longitudinal pathophysiological processes cause patients' brains to exist in a state of chronic neuroinflammation; additionally, reactive glial cells contribute to AD pathogenesis. However, the detailed molecular and cellular mechanisms underlying this pathogenesis are still unclear. Such disease complexities make it difficult for the pathogenesis of AD to be understood, and impede the development of effective therapeutic strategies to combat the disease. Relevant AD animal models are thus likely to serve as a key resource to overcome many of these issues. In this symposium, I will introduce current situation of research and share perspectives for understanding glial pathophysiology.