DP1受体阻断可减轻老年脑组织外泌体PTGDS引起的小胶质细胞衰老和认知能力下降

核心信息

• 论文英文标题: DP1 Receptor Blockade Attenuates Microglial Senescence and Cognitive Decline Caused by PTGDS in Exosomes From Aged Brains
• 期刊: Aging Cell
• 发表年份: 2025
• DOI: 10.1111/acel.70228
• PMID/PMCID: 40974022; PMC12610410

研究概览

Aging leads to neurodegenerative diseases, such as cognitive decline, which are induced by persistent chronic low-grade inflammation in the brain driven by microglial activation. Our findings reveal a systemic mechanism underlying the sustained activation of microglia following brain aging, paving the way for improving chronic neuroinflammation, cellular senescence, and cognitive decline associated with aging.

核心发现

Aging leads to neurodegenerative diseases, such as cognitive decline, which are induced by persistent chronic low-grade inflammation in the brain driven by microglial activation.

However, whether and how brain-derived exosomes from aged mice (A-exo) induce a pro-inflammatory state and cellular senescence in microglia within the aging brain is poorly understood.

Here, we report that brain-derived exosomes from aged mice (A-exo) cause cognitive decline in normal young mice, inducing microglial overactivation, lipid droplet accumulation, and senescence-associated secretory phenotype (SASP) secretion.

This abnormal microglial activity arises from the elevated expression of PTGDS in A-exo due to mouse aging, resulting in increased central and peripheral D-prostanoid receptor 1 (DP1) ligand PGD2 levels, which subsequently leads to sustained DP1 signaling activation.

Echo Biotech 角色

组织外泌体分离 & 4D-labelfree蛋白组

关联平台: Exoomics®

关联服务与能力: Tissue EV Isolation & Purification

关联产品或试剂: 无明确产品引用

参考文献

原始论文: DP1 Receptor Blockade Attenuates Microglial Senescence and Cognitive Decline Caused by PTGDS in Exosomes From Aged Brains Aging cell. 2025. DOI: 10.1111/acel.70228. PMID/PMCID: 40974022; PMC12610410.