老年小鼠脑组织外泌体通过激活神经元Tnfrsf25加速反复轻度创伤性脑损伤的认知能力下降

核心信息

• 论文英文标题: Brain-derived exosomes from aged mice accelerate cognitive decline in repeated mild traumatic brain injury by activating neuronal Tnfrsf25
• 期刊: Exp Gerontol
• 发表年份: 2025
• DOI: 10.1016/j.exger.2025.112931
• PMID/PMCID: 41109644

研究概览

This study investigated how brain-derived exosomes from aged mice (A-Exo) worsen rm-TBI outcomes. Our further investigations demonstrated that A-Exo could upregulate the expression of tumor necrosis factor receptor superfamily member 25 (Tnfrsf25) in neurons.

核心发现

Aging increases vulnerability to cognitive decline after repetitive mild traumatic brain injury (rm-TBI), yet mechanisms linking age-related factors to neurodegeneration remain poorly understood.

This study investigated how brain-derived exosomes from aged mice (A-Exo) worsen rm-TBI outcomes.

In a murine rm-TBI model, intranasal A-Exo administration significantly exacerbated spatial memory deficits and hippocampal neuronal apoptosis compared to brain-derived exosomes from young mice (Y-Exo) or controls.

Proteomic analysis revealed the enrichment of Tnfrsf21 in brain-derived exosomes from aged mice, and these exosomes were closely associated with the neuronal death pathway.

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: Brain-derived exosomes from aged mice accelerate cognitive decline in repeated mild traumatic brain injury by activating neuronal Tnfrsf25 Experimental gerontology. 2025. DOI: 10.1016/j.exger.2025.112931. PMID/PMCID: 41109644.