- Role of the immune system in adaptive and maladaptive neural circuit plasticity after brain injury -
Jeanne PAZ
UCSF Weill Institute for Neurosciences
The Kavli Institute for Fundamental Neuroscienc
San Francisco

Traumatic brain injury (TBI) affects millions of people every year and is a major cause of disability worldwide. Although 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 TBI (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic system. Increased C1q expression colocalized 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 a source of thalamic C1q. The corticothalamic circuit could thus be a new target for treating TBI-related disabilities.
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Zoom Metting – January 17th at 5p.m

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