Astrocytes are a type of glial cells in the central nervous system, play a critical role in protecting neuronal signaling by regulating brain homeostasis, synaptic plasticity and transmission, and blood brain barrier functioning in central nervous system. Accumulating evidence has indicated that abnormal behaviors of astrocytic functions, including astrodegeneration and astrogliosis, are implicated as the primary factors contributing to a number of chronic neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Kir4.1 is an inwardly rectifying K+ channel expressed on the projections of astrocytes, which serve important roles in the neuroprotective function of astrocytes, such as maintaining K+ homeostasis and regulating extracellular glutamate. Abnormal expression of Kir4.1 has been reported in certain neurodegenerative diseases, including Amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), suggesting a vital role in the development of pathophysiology. However, the association between the molecular mechanism and expression of Kir4.1 and the underlying pathogenesis of AD and PD has been largely uninvestigated. In this study, we have had the critical opportunity to access human post-mortem brain tissue, provided by the University of Washington Alzheimer’s Disease Research Center, and conducted confocal microscopy studies. Through a quantitative immunofluorescense staining approach, we expect to demonstrate a distinct expression pattern of Kir4.1 in various brain regions of AD and PD post-mortem tissues when compared to control subjects. Determining the role this protein has in neurodegeneration may provide new insight into the development of therapeutic targets to ameliorate the progression of AD and PD.