Authors: Stephanie S. Holden, Fiorella C. Grandi, Oumaima Aboubakr, Bryan Higashikubo, Frances S. Cho, Andrew H. Chang, Alejandro Osorio Forero, Allison R. Morningstar, Vidhu Mathur, Logan J. Kuhn, Poojan Suri, Sethu Sankaranarayanan, Yaisa Andrews-Zwilling, Andrea J. Tenner, Anita Luthi, Eleonora Aronica, M. Ryan Corces, Ted Yednock, Jeanne T. Paz
Summary: Traumatic brain injury affects millions of people every year and is a major cause of disability worldwide. Most of the maladaptive outcomes develop months or years later and are thought to be caused by secondary injuries that are indirect and long-term effects after the initial impact. Holden et al. found that secondary and chronic neuroinflammation and neurodegeneration are caused by the C1q molecule, a mediator of the complement pathway. C1q is responsible for chronic inflammation and secondary neuronal loss specifically in the cortico-thalamo-cortical circuit. Traumatic brain injury also leads to altered brain states that are caused by the C1q complement pathway.
Source: Science, 2021; 373 (6560)