Abstract: Astrocytes, a major class of glial cells, have emerged as crucial regulators of synaptic function, neuronal homeostasis, and cognitive processes (Cabral-Miranda et al., 2024). These star-shaped cells not only provide structural and metabolic support to neurons but also actively participate in modulating synaptic transmission, neurovascular coupling, and inflammatory responses in the brain. Among the diverse array of astrocytic proteins implicated in neural function, Hevin (also known as SPARCL-1) has gained increasing attention due to its pivotal role in synapse formation and plasticity (Strunz et al., 2019; Gan and Südhof, 2020). Hevin has been shown to act as an extracellular matrix protein that promotes synaptic organization by bridging pre- and postsynaptic partners, thereby facilitating synaptic maturation and stability (Kucukdereli et al., 2011). Additionally, emerging evidence suggests that Hevin may influence neurodegenerative processes, particularly in Alzheimer ’s disease (AD), where synaptic dysfunction is a hallmark feature. However, despite these advances, the precise mechanisms by which Hevin contributes to age-related cognitive decline and AD progression, including its interactions with amyloid-β, tau pathology, or neuroinflammatory pathways, remain poorly understood.