Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury
Author(s) -
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 AndrewsZwilling,
Andrea J. Tenner,
Anita Lüthi,
Eleonora Aronica,
M. Ryan Corces,
Ted Yednock,
Jeanne T. Paz
Publication year - 2021
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.abj2685
Subject(s) - complement (music) , neuroscience , sleep (system call) , complement system , epilepsy , complement factor i , factor (programming language) , psychology , medicine , chemistry , computer science , immunology , biochemistry , phenotype , immune system , gene , complementation , programming language , operating system
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. Holdenet 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
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