Core Viewpoint - The research on Alzheimer's disease (AD) has shifted focus from the traditional view of amyloid-beta (Aβ) accumulation and tau protein tangles as the primary causes of dementia, highlighting the role of dysfunctional microglia and chronic neuroinflammation in disease progression [2][3]. Group 1: Research Findings - Recent studies indicate that abnormal protein deposition is a pathological feature of AD rather than its causative mechanism, emphasizing the harmful effects of these proteins on disease progression [2]. - The study published by Xu Peisheng's team at the University of South Carolina introduces a ceria nanocluster-based therapy that targets activated microglia and reduces Aβ deposition [3][4]. Group 2: Innovative Treatment Approach - The developed brain-targeted ceria nanoparticles (T-CeNP) effectively penetrate the blood-brain barrier (BBB) and alleviate neuroinflammation while reducing Aβ accumulation [4][6]. - T-CeNP operates through a triple-function mechanism: it crosses the BBB via RAGE-targeting peptides, regulates pathological processes by enhancing microglial phagocytosis of Aβ, and exhibits multi-pathway synergistic effects in AD mouse models [6][7]. Group 3: Implications for Future Research - The study's findings suggest that T-CeNP can effectively block the pathological cascade of Alzheimer's disease by modulating the neuroinflammatory microenvironment and amyloid metabolism, providing a new paradigm for multi-target therapies in neurodegenerative diseases [9].