Complement proteins: possible predictive biomarker of Alzheimer’s disease

Recent research has uncovered more details about how the brain works. As brains develop, the many initially-formed synapses get pruned. How this occurs is important to understand as synapse pruning also occurs in neurodegenerative disease.

In synapse pruning, many mechanisms are operating together in a systems biology fashion, but one key dynamic is that protein molecules (complement proteins C1q and C3) are tagging weak synapses for elimination. For example, complement protein molecules are massively upregulated in Alzheimer’s disease. The Cq1 genes have been shown to come on very early in the case of glaucoma and are proposed to be a global dynamic of synaptic loss in neurodegenerative disease (e.g.; Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, ALS, etc.).

The early and prominent role of complement genes and proteins suggests the possibility of measuring them as a predictive biomarker of neurodegenerative disease.