Core Viewpoint - The research highlights that Alzheimer's disease (AD) is not solely characterized by the accumulation of amyloid-beta (Aβ) plaques and tau tangles, but also involves a disruption in communication between neurons and glial cells, particularly astrocytes and microglia, which is crucial for disease progression [2][3][5]. Group 1: Research Findings - The study published in Cell provides a comprehensive view of how brain cells interact in Alzheimer's patients, revealing that the disruption of information exchange between neurons and glial cells is closely related to the development of AD [3][5]. - A protein named AHNAK has been identified as a key driver protein in the disrupted protein networks associated with Alzheimer's disease, suggesting a new avenue for innovative treatment strategies [3][9]. - The research team conducted deep proteomic analysis on the parahippocampal gyrus (PHG) of 198 deceased Alzheimer's patients, mild cognitive impairment (MCI) patients, and normal controls to understand molecular dysregulation in AD [6][7]. Group 2: Key Protein Networks - The analysis revealed over 300 key driver proteins (KDPs) that play significant roles in triggering or accelerating Alzheimer's disease, with AHNAK being one of the most prominent proteins found in astrocytes [8][11]. - The study indicates that in Alzheimer's disease, the balance between neurons and glial cells is disrupted, leading to hyperactivity of glial cells and diminished neuronal function, which correlates with increased inflammation [8][11]. - Different biological factors, such as sex and genetic background, can influence the expression of these protein networks, with carriers of the APOE4 gene showing distinct patterns of protein network disruption compared to non-carriers [11].