Name
#59 Trauma-Induced Complement Activation Precedes CNS Damage in Traumatic Spinal Cord Injury
Speakers
Content Presented On Behalf Of:
International Delegates
Session Type
Poster
Date
Tuesday, March 3, 2026
Start Time
5:00 PM
End Time
7:00 PM
Location
Prince Georges Expo Hall E
Focus Areas/Topics
Clinical Care
Learning Outcomes
- Neurological recovery after TSCI depends on a balanced complement response.
Early but controlled activation of the alternative pathway (Bb elevation with timely Factor I recovery) promotes reparative remodeling, while uncontrolled overactivation impairs recovery.
- Persistent complement dysregulation marks maladaptive immune–neuronal crosstalk.
Sustained elevations of Ba, C3a, and C5a with low Factor H indicate defective inhibitory control, linking chronic inflammation to poor neurological outcomes.
- Distinct neuroaxonal biomarker patterns reflect divergent injury trajectories.
High admission NFL and α-synuclein levels identify severe early axonal injury, whereas transient Aβ42 increases in remitters signal adaptive neuronal regeneration.
- Combined complement and neurodegenerative profiling offers a mechanistic signature of recovery potential.
Integrating immune and neuronal markers enables early differentiation between regenerative versus non-reparative trajectories, guiding personalized therapeutic strategies after spinal cord injury.
Early but controlled activation of the alternative pathway (Bb elevation with timely Factor I recovery) promotes reparative remodeling, while uncontrolled overactivation impairs recovery.
- Persistent complement dysregulation marks maladaptive immune–neuronal crosstalk.
Sustained elevations of Ba, C3a, and C5a with low Factor H indicate defective inhibitory control, linking chronic inflammation to poor neurological outcomes.
- Distinct neuroaxonal biomarker patterns reflect divergent injury trajectories.
High admission NFL and α-synuclein levels identify severe early axonal injury, whereas transient Aβ42 increases in remitters signal adaptive neuronal regeneration.
- Combined complement and neurodegenerative profiling offers a mechanistic signature of recovery potential.
Integrating immune and neuronal markers enables early differentiation between regenerative versus non-reparative trajectories, guiding personalized therapeutic strategies after spinal cord injury.
Session Currently Live
Description
Background: Complement activation and neuroaxonal injury are pivotal determinants of neurological recovery after traumatic spinal cord injury (TSCI). This study compared temporal dynamics of complement cascade activity and neurodegenerative biomarkers between patients with and without neurological recovery, defined as positive AIS conversion within 3 months after the injury.
Methods: Eighteen patients with acute TSCI were prospectively sampled at 11 predefined timepoints (admission, 4h, 9h, 12h, 24h, 3d, 7d, 14d, 1m, 2m, and 3m after the injury). Serum concentrations of eight complement proteins (Ba, Bb, C3a, C4a, Factor I, Factor H, C5a, SC5b-9) and five neuroaxonal markers
(α-synuclein, Tau, Aβ40, Aβ42, NFL) were analyzed across acute, subacute, and intermediate/chronic phases.
Results: Alternative-pathway components Ba and Bb remained elevated compared with controls. Bb was significantly higher in remitters at 3 d (p = 0.042),
indicating controlled amplification during reparative remodeling. Regulators Factor I and H started below control medians; Factor I increased after 24 h, whereas
Factor H stayed low throughout, reflecting partial restoration of inhibitory control. C5a and SC5b-9 increased from 12 h onward and were significantly higher in remitters at 24 h (C5a, p = 0.031), and 7 d (SC5b-9, p = 0.042), consistent with balanced terminal-pathway activity during recovery. C3a and C4a were constantly
above control levels, with a pronounced rise in remitters during the transition from acute to chronic injury from 3 days to 3 months after the injury. Neuroaxonal
markers showed distinct trajectories. NFL levels were higher in non-remitters at admission (p = 0.012) and equalized thereafter, reflecting early axonal damage.
α-Synuclein peaked within 24 h, being higher in non-remitters, then normalized. Aβ42 increased transiently in remitters, whereas the Aβ40/Aβ42 ratio was higher
in non-remitters in the acute phase.
Conclusions: Neurological remission after TSCI is characterized by a regulated complement response with early Bb-driven activation and timely recovery of
Factor I, accompanied by transient neuronal regeneration. The convergence of persistent complement overactivation and defective regulation (persistent Ba/C3a/C5a
elevation, low Factor H) with downstream axonal and amyloid injury implies maladaptive immune–neuronal crosstalk to potentially contribute causally to neurological
non-recovery after TSCI.