Cell重磅：鲁友明团队揭示癌症对抗阿尔茨海默病的机制，带来全新治疗思路

Core Viewpoint - The research reveals a surprising link between peripheral cancers and a reduced risk of Alzheimer's disease, suggesting that certain cancer patients may possess a protective mechanism against Alzheimer's through the protein cystatin-c [2][6]. Group 1: Research Findings - The study published in Cell demonstrates that tumor cells secrete cystatin-c, which acts as a "molecular glue" to activate TREM2 receptors on microglial cells, facilitating the clearance of amyloid plaques associated with Alzheimer's disease [3][5]. - In experiments with Alzheimer's model mice implanted with peripheral cancer cells, a significant reduction in amyloid plaques and improved cognitive function were observed [6][12]. Group 2: Mechanism of Action - Cystatin-c binds to toxic amyloid oligomers in the brain, activates microglial cells via TREM2, and enhances the clearance of existing amyloid plaques [9][15]. - The protective effect of cystatin-c was confirmed through gene knockout experiments, where the absence of cystatin-c eliminated the protective benefits, which were restored upon reintroduction of normal cystatin-c [13][14]. Group 3: Therapeutic Implications - This research opens new avenues for Alzheimer's treatment by focusing on the removal of existing amyloid plaques rather than solely preventing their formation [17][21]. - Direct injection of recombinant cystatin-c into Alzheimer's model mice successfully reduced amyloid burden and improved learning and memory capabilities [18][20].