Complement C3

Complement C3 (C3) is a central hub protein of the complement cascade, serving as a precursor for multiple complement pathways (classical, alternative, lectin, and GZMK) (UniProt: P01024). Upon cleavage, C3b acts as an opsonin marking pathogens for removal and participates in C5 convertase formation, while C3a functions as a pro-inflammatory mediator and chemoattractant for immune cells. The protein also exhibits adipogenic hormone activity, promoting triglyceride synthesis and glucose transport in adipocytes.

C3 is broadly expressed and participates in immune defense and inflammatory signaling. Deficiency of C3 results in severe pyogenic infections and potential autoimmune complications. The protein has been associated with age-related macular degeneration and atypical hemolytic uremic syndrome through genetic studies (UniProt: P01024).

In Alzheimer's Disease, C3 is significantly up-regulated in post-mortem AD brain tissue compared to age-matched controls (mean log2 fold-change: 1.09) (Chaparral AD proteomics). This up-regulation suggests enhanced complement pathway activation in the AD brain, potentially contributing to neuroinflammatory processes characteristic of the disease.