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- W3030540729 abstract "ABSTRACT While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of cortical injury that does not directly damage subcortical structures, we found a chronic increase in C1q expression specifically in the corticothalamic circuit. Increased C1q expression co-localized with neuron loss and chronic inflammation, and correlated with altered cortical rhythms. Blocking C1q counteracted most of these outcomes, suggesting that C1q is a disease modifier in TBI. Since the corticothalamic circuit is important for sensory processing, attention, cognition, and sleep, all of which can be impaired by TBI, this circuit could be a new target for treating TBI-related disabilities." @default.
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- W3030540729 date "2020-05-31" @default.
- W3030540729 modified "2023-10-15" @default.
- W3030540729 title "Complement factor C1q mediates chronic neuron loss and inflammation post-brain injury" @default.
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- W3030540729 doi "https://doi.org/10.1101/2020.05.29.120220" @default.
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