Brain-derived exosomes from aged mice accelerate cognitive decline in repeated mild traumatic brain injury by activating neuronal Tnfrsf25
Quick Facts
- Publication title: Brain-derived exosomes from aged mice accelerate cognitive decline in repeated mild traumatic brain injury by activating neuronal Tnfrsf25
- Journal: Exp Gerontol
- Year: 2025
- DOI: 10.1016/j.exger.2025.112931
- PMID/PMCID: 41109644
Research overview
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.
Key findings
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 Role
Echo Biotech contributed EV isolation and purification.
Related platforms: Exoomics®
Related services and capabilities: Tissue EV Isolation & Purification
References
Original publication: 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.