1. Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury
- Author
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Stephanie S. Holden, Frances S. Cho, Ted A. Yednock, Oumaima Aboubakr, Eleonora Aronica, Yaisa Andrews-Zwilling, Fiorella C. Grandi, Andrea J. Tenner, M. Ryan Corces, Bryan Higashikubo, Allison R. Morningstar, Sethu Sankaranarayanan, Logan J. Kuhn, Jeanne T. Paz, Poojan Suri, Anita Lüthi, Andrew H Chang, Alejandro Osorio Forero, Vidhu Mathur, Pathology, and ANS - Cellular & Molecular Mechanisms
- Subjects
Sleep Wake Disorders ,Physical Injury - Accidents and Adverse Effects ,General Science & Technology ,Traumatic brain injury ,Thalamus ,Sleep spindle ,chemical and pharmacologic phenomena ,Complement factor I ,Traumatic Brain Injury (TBI) ,Article ,Mice ,Cortex (anatomy) ,Animals ,Medicine ,Traumatic Head and Spine Injury ,Epilepsy ,Multidisciplinary ,Animal ,business.industry ,Complement C1q ,Neurosciences ,Injuries and accidents ,medicine.disease ,Brain Disorders ,Disease Models, Animal ,medicine.anatomical_structure ,nervous system ,Brain Injuries ,Disease Models ,Neurological ,Microglia ,Sleep Stages ,Sleep Research ,business ,Neuroscience - Abstract
Neuroinflammation after brain injury 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. —PRS
- Published
- 2021
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