CNS-specific expression of C3a and C5a exacerbate demyelination severity in the cuprizone model

Elevation of the terminal complement activation products C5a and C5b-9 in ALS patient blood

“…chemoattractants (Manthey et al, 2009), and is involved in increasing blood-brain barrier breakdown (Flierl et al, 2009;Jacob et al, 2010), as well as the infiltration of leukocytes into the CNS (Ingersoll et al, 2010). Both are key events in the progression of numerous neurodegenerative diseases.…”

Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

“…In this blast model, BBB breakdown occurs early and is limited to the outer layer of the cortex [9], suggesting that systemic complement activation may be the source of complement proteins accumulated in the cortex by crossing a dysfunctional BBB. On the other hand, recent findings revealed that brain cells have the ability to produce complement proteins [15,27,28]. Thus, the complement protein accumulation observed in the hippocampus could have been produced locally after injury.…”

A novel role of complement in retinal degeneration

“…For example, mice lacking C3a and/or C5a signaling have abnormal susceptibility to neuroexcitotoxicity, 23 abnormal neurogenesis, 24 abnormal differentiation and migration of neural progenitor cells, 25 abnormal liver cell survival/regeneration, 26 and abnormal remyelination. 27 Furthermore, the pathology associated with a model of retinopathy of prematurity was exacerbated in mice lacking either C3 or C5aR. 28 To date, the retinas of mice lacking C3aR or C5aR have not been examined.…”