Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury

Author:

Holden Stephanie S.12345ORCID,Grandi Fiorella C.2364ORCID,Aboubakr Oumaima24ORCID,Higashikubo Bryan24,Cho Frances S.12364ORCID,Chang Andrew H.24ORCID,Forero Alejandro Osorio67ORCID,Morningstar Allison R.24ORCID,Mathur Vidhu28,Kuhn Logan J.28ORCID,Suri Poojan28,Sankaranarayanan Sethu28ORCID,Andrews-Zwilling Yaisa28,Tenner Andrea J.14ORCID,Luthi Anita67ORCID,Aronica Eleonora375ORCID,Corces M. Ryan2364ORCID,Yednock Ted28ORCID,Paz Jeanne T.12385ORCID

Affiliation:

1. Neurosciences Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA.

2. Gladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.

3. Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.

4. Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA.

5. Stichting Epilepsie Instellingen Nederland (SEIN), 2103 SW Heemstede, Netherlands.

6. Department of Fundamental Neurosciences, University of Lausanne, CH-1005 Lausanne, Switzerland.

7. Department of Neuropathology, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, Netherlands.

8. Annexon Biosciences, South San Francisco, CA 94080, USA.

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

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference80 articles.

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3. The neuropathology of traumatic brain injury

4. Emerging views of corticothalamic function

5. Sleep-Wake Disturbances After Traumatic Brain Injury: Synthesis of Human and Animal Studies

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