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Rejuvenating aged microglia increases amyloid-β clearance in Alzheimer's disease
Writer 고홍숙
Date 2024-04-11 08:34:17.0
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The National Research Foundation of Korea has disclosed a potential breakthrough in dementia treatment. Collaborative research between Professor Kim, Dong Woon's team from Kyung Hee University and Dr. Shin, Hyo Jung of the Brain Science Research Institute at Chungnam National University suggests a novel approach to address dementia by reversing the aging process of microglial cells using nanoparticles.

   

Alzheimer's disease, the most prevalent form of dementia, is primarily characterized by the accumulation of amyloid beta plaques in the brain, triggering the activation of adjacent glial cells and subsequent neuroinflammation. Recent studies have revealed that as microglial cells age, their ability to engulf and remove these plaques diminishes, exacerbating neuroinflammation and cognitive decline. Unlike neurons, glial cells undergo slow cell division, which inevitably leads to a decline in their phagocytic function with aging. Aged microglial cells often accumulate plaques without effectively clearing them.

   

In response, Professor Kim’s team developed a strategy to target microglial cell cycle mediator using PLGA nanoparticles and tested it on an Alzheimer's disease animal model. By inhibiting the p16ink4a gene, a key driver of cellular senescence, the researchers successfully reversed the aging process in old microglia, rejuvenating their phagocytic function and cognitive abilities. The microglia-targeting PLGA nanoparticles were directly synthesized by Nanoglia Co., Ltd., a laboratory affiliated with Professor Kim team.




Rejuvenating aged microglia by p16ink4a-siRNA-loaded nanoparticles increases amyloid-β clearance 

in animal models of Alzheimer's disease



[Reference] 1: Shin HJ, Kim IS, Choi SG, Lee K, Park H, Shin J, Kim D, Beom J, Yi YY, Gupta DP, Song GJ, Chung WS, Lee CJ, Kim DW. Rejuvenating aged microglia by p16<sup>ink4a</sup>-siRNA-loaded nanoparticles increases amyloid-β clearance in animal models of Alzheimer's disease. Mol Neurodegener. 2024 Mar 16;19(1):25. doi: 10.1186/s13024-024-00715-x. PMID: 38493185; PMCID: PMC10943801.

   

[Main Author] Dong Woon Kim (Kyung Hee University), Hyo Jung Shin (Chungnam National University)

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