Abstract: Microglial cells are the key immunocompetent cells in the central nervous system (CNS) and play a crucial role in CNS health and disease (Paolicelli et al., 2022). Under the homeostatic conditions, microglial cells assume diverse and dynamic states, depending upon interactions with neighboring cells and structures in local contextual settings, continuously patrol brain parenchyma utilizing their highly mobile fine processes, phagocytize protein aggregates, unwanted synapses and cells to maintain CNS health, and secrete neurotrophic factors to support neuronal function (Colonna and Butovsky, 2017; Paolicelli et al., 2022). In response to damage or infection, microglial cells change to different functional states, in many cases accompanied with distinct morphology characterized by an enlarged cell body with short and thick processes. Mechanistically, such changes in the states of microglial cells, commonly referred to microglial activation, are initiated upon ligation of pattern recognition receptors to damage-associated molecular patterns from host cells, or pathogen-associated molecular patterns from invading pathogens, and enable microglial cells to coordinate an immune response to reinstate CNS homeostasis (Colonna and Butovsky, 2017; Paolicelli et al., 2022). However, incomplete resolution of the immune response leading to chronic inflammation or, more specifically, unwanted production of neurotoxic inflammatory mediators that can damage synapses and neurons and thereby impair CNS function. Such microglial cell-mediated action is an important factor driving the progression of age-related neurodegenerative diseases, including Alzheimer’s disease (AD) (Takata et al., 2021).