The role of the complement pathway in post-traumatic sleep disruption and epilepsy
Schedule
Wednesday, June 16, 2021
16:00 UTC
Jeanne Paz
Prof
UCSF
Host: Clinical and Experimental Epilepsy
Recording
Open recording
Event Information
Recording
Available
Host
Clinical and Experimental Epilepsy
Duration
70 minutes
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 mild cortical injury that does not directly damage subcortical structures (mTBI), 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 disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are the source of thalamic C1q. Since the corticothalamic circuit is important for cognition and sleep, which can be impaired by TBI, this circuit could be a new target for treating TBI-related disabilities
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