C1q dependency of retinal ganglion cell death in blast-mediated traumatic brain injury

Adam Hedberg-Buenz; Laura M Dutca; Nickolas A Boehme; Ashelyn R Mann; Matthew M Harper; Mona K Garvin; Michael G Anderson

doi:10.1016/j.exer.2026.111192

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C1q dependency of retinal ganglion cell death in blast-mediated traumatic brain injury

Journal article

Peer reviewed

C1q dependency of retinal ganglion cell death in blast-mediated traumatic brain injury

Adam Hedberg-Buenz, Laura M Dutca, Nickolas A Boehme, Ashelyn R Mann, Matthew M Harper, Mona K Garvin and Michael G Anderson

Experimental eye research, Vol.272, 111192

11/2026

DOI: 10.1016/j.exer.2026.111192

PMID: 42556773

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Abstract

Traumatic brain injury is a widespread health concern that annually affects millions of people worldwide, with blast-mediated TBI (bTBI) being of particular relevance to military personnel and civilians in war zones. Current treatments primarily target symptoms, rather than the underlying neuropathology, and are ultimately limited by the need for an improved etiological understanding of TBI. Here, we utilized a pre-clinical mouse model of bTBI, previously shown to evoke a high susceptibility to retinal ganglion cell (RGC) death, to investigate whether neuroinflammatory pathways associated with the complement factor 1q (C1q) complex contribute to RGC death. To test this, C57BL/6J (B6) mice with genetic knock-out of C1qa (B6.C1qako) were exposed to bTBI, or sham control, with subsequent comparisons of RGC survival at durations of 5- and 16-weeks following exposure. Survival metrics consisted of quantifying RGC somas from immunostained retinal flat-mounts and axons from histochemically stained optic nerve cross sections. Relative to sham controls, no significant differences in the abundance of RGC somas in retina or axons in the optic nerve were detected in B6.C1qako mice at either 5- or 16-weeks after bTBI exposure. These results demonstrate that loss of C1qa confers robust and persistent neuroprotection of RGCs and identify a C1q-dependent neuroinflammatory mechanism that contributes to pathways of neuronal death that are similar to other forms of neurodegeneration, particularly glaucoma.

Retinal ganglion cells

Neuroinflammation

AxonDeep

C1q

Blast-mediated TBI

Details

Title: Subtitle: C1q dependency of retinal ganglion cell death in blast-mediated traumatic brain injury
Creators: Adam Hedberg-Buenz - University of Iowa, Molecular Physiology and Biophysics
Laura M Dutca - Iowa City VA Health Care System
Nickolas A Boehme - Iowa City VA Health Care System
Ashelyn R Mann - University of Iowa
Matthew M Harper - Iowa City VA Health Care System
Mona K Garvin - University of Iowa, Electrical and Computer Engineering
Michael G Anderson - University of Iowa
Resource Type: Journal article
Publication Details: Experimental eye research, Vol.272, 111192
DOI: 10.1016/j.exer.2026.111192
PMID: 42556773
NLM abbreviation: Exp Eye Res
ISSN: 1096-0007
eISSN: 1096-0007
Publisher: Elsevier
Grant note: NIH/NEI: EY017673, EY034492 US Dept. of Veterans Affairs/RR D: I01RX001481, IK2 RX002003 NIH/NEI: P30EY025580
This work was supported by grants from the NIH/NEI (EY017673, MGA; EY034492, MGA) and US Dept. of Veterans Affairs/RR & D (I01RX001481, MGA; IK2 RX002003, LD) . We also acknowledge NIH/NEI Center Support from Grant P30EY025580 to the University of Iowa. The contents do not represent the views of the U.S. Department of Veterans Affairs or the U.S. Government.
Language: English
Electronic publication date: 08/05/2026
Date published: 11/2026
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Electrical and Computer Engineering; Molecular Physiology and Biophysics; Ophthalmology and Visual Sciences
Record Identifier: 9985217830102771

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