This study tested whether complement factor C1q drives retinal ganglion cell (RGC) death in a mouse model of blast-mediated traumatic brain injury (bTBI), comparing RGC soma and optic nerve axon survival in C1qa knockout (B6.C1qako) vs. wild-type C57BL/6J mice at 5 and 16 weeks post-blast exposure.
C1qa knockout mice showed no significant RGC soma or optic nerve axon loss relative to sham controls at either 5 or 16 weeks after bTBI, indicating that C1q deletion confers robust and persistent neuroprotection of RGCs.
Pre-clinical mouse model only — direct translation to human bTBI is uncertain. The study does not assess functional visual outcomes (e.g., electroretinography, visual acuity). Only C1qa was knocked out; the broader complement cascade and other neuroinflammatory mediators were not fully characterized.
C1q-mediated complement signaling appears to be a key driver of RGC neurodegeneration after blast TBI, paralleling its role in glaucoma. Targeting C1q may represent a viable neuroprotective strategy for blast-related vision loss, though clinical validation is still needed.
