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Cited by 133Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchComplement system in diseases

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

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Holden, Stephanie S., Grandi, Fiorella C., Aboubakr, Oumaima, Higashikubo, Bryan, Cho, Frances S., Chang, Andrew H., Forero, Alejandro Osorio, Morningstar, Allison R. +11 more·2021·Science
DOI 10.1126/science.abj2685PMC PMC8750918

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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

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  • C1qa is associated with microglial activation after traumatic brain injury.

    “For instance, Tmem119 expression is significantly reduced in activated microglia in AD, whereas C1qa is associated with microglial activation after traumatic brain injury[49–51].”

    From Comparative analysis of nuclei isolation methods for brain single-nucleus RNA sequencing (2026) · cites this paper as [49]

  • Tmem119 expression is significantly reduced in activated microglia in AD.

    “For instance, Tmem119 expression is significantly reduced in activated microglia in AD, whereas C1qa is associated with microglial activation after traumatic brain injury[49–51].”

    From Comparative analysis of nuclei isolation methods for brain single-nucleus RNA sequencing (2026) · cites this paper as [49]

    The cited paper’s “Microglia are a source of C1q in the thalamus” section examines C1qa after mild traumatic brain injury, not Tmem119 expression in Alzheimer’s disease. A search for Tmem119 and activated microglia in AD found no passage addressing the claimed reduction. The paper supports the citing sentence’s separate C1qa/TBI clause, but not the quoted Tmem119/AD claim. (LLM, conf=0.76)

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Authors
Holden, S. S., Grandi, F. C., Aboubakr, O., Higashikubo, B., Cho, F. S., Chang, A. H., Forero, A. O., Morningstar, A. R., Mathur, V., Kuhn, L. J., Suri, P., Sankaranarayanan, S., Andrews-Zwilling, Y., Tenner, A. J., Luthi, A., Aronica, E., Corces, M. R., Yednock, T., & Paz, J. T.
Affiliations
  • Gladstone Institutes (US)
  • Department of Fundamental Neurosciences, University of Lausanne, CH-1005 Lausanne, Switzerland.
  • University of California, San Francisco (US)
Corresponding author
Paz, Jeanne T.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2021-09-10
Volume
373
Issue
6560
Pages
eabj2685-eabj2685
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.abj2685
PMC
PMC8750918
OpenAlex
W3196441931
Cited by
133
References
11
Citations by year
2026: 21 · 2025: 35 · 2024: 23 · 2023: 33 · 2022: 14 · 2021: 5 · 2012: 1
FWCI
9.33
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
  • PubMed (publishedVersion)
  • SERVAL (Université de Lausanne) (publishedVersion)
  • Pure Amsterdam UMC (acceptedVersion, cc-by)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
  • HAL (submittedVersion)
  • IRIS (submittedVersion)
Funders
  • National Science Foundation (T32-GM007449, 1608236, 1144247, 310030)
  • U.S. Department of Defense (EP150038)
  • Ford Foundation
  • American Epilepsy Society
  • Gladstone Institutes
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (184759, 310030)
  • Epilepsiefonds
  • Université de Lausanne
  • Epilepsy Society
  • National Institutes of Health (2020-02)
  • University of California, San Francisco
  • Medical Research Council
  • National Institute on Aging (R01AG060148)
  • National Institute of General Medical Sciences (T32GM007449)
  • National Institute of Neurological Disorders and Stroke (K99NS078118, R00NS078118, F31NS111819, NS111819, R01NS096369)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
Keywords
mild traumatic brain injury, sleep spindles, epileptic spikes, corticothalamic circuits, thalamus, microglia, chronic inflammation, neuronal loss, secondary brain injury, disease modifiers, single-nucleus RNA sequencing
MeSH terms
Animals, Brain Injuries, Disease Models, Animal, Epilepsy, Sleep Wake Disorders, Sleep Stages, Thalamus, Complement C1q, Microglia, Mice

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