Microglia are the primary cells responsible for neuroimmune. The roles of microglia include phagocytosis, scavenging, the release of cytokines, and antigen presentation to T cells. Furthermore, microglia help to form efficient neural circuits by removing excess neurons and synapses during neurodevelopment. After maturity, microglia also have an essential role in memory formation and elimination by using a complement‐dependent system. In degenerative diseases such as Alzheimer’s disease, microglia have the capacity to clean pathological changes like amyloid‐β and abnormal tau protein. Moreover, microglia attack and remove normal neurons and synapses, resulted in cognitive decline. In patients with Alzheimer’s disease, synaptic pathology and abnormalities of presynaptic proteins were reported. The reductions of presynaptic proteins were associated with cognitive declines in the patients. Presynaptic proteins, complexin‐1, mainly distributed in inhibitory neurons, were reported to be associated with cognitive functions in early dementia. Complexin‐2, dominantly distributed in excitatory nerves, was shown to be correlated with cognitive functions during the progression of dementia. We plan to evaluate the distribution of complexin and microglia by quantitative immunohistochemistry of older adults’ hippocampal tissues with and without dementia.