| Literature DB >> 34516796 |
Stephanie S Holden1,2,3,4,5, Fiorella C Grandi2,3,6,4, Oumaima Aboubakr2,4, Bryan Higashikubo2,4, Frances S Cho1,2,3,6,4, Andrew H Chang2,4, Alejandro Osorio Forero6,7, Allison R Morningstar2,4, Vidhu Mathur2,8, Logan J Kuhn2,8, Poojan Suri2,8, Sethu Sankaranarayanan2,8, Yaisa Andrews-Zwilling2,8, Andrea J Tenner1,4, Anita Luthi6,7, Eleonora Aronica3,7,5, M Ryan Corces2,3,6,4, Ted Yednock2,8, Jeanne T Paz1,2,3,8,5,9.
Abstract
Although 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 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.Entities:
Mesh：
Substances：
Year: 2021 PMID： 34516796 PMCID： PMC8750918 DOI： 10.1126/science.abj2685
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 63.714