However, in brain injury or pathological states such as Alzheimer’s disease, the C1q expression is significantly upregulated in the injured region, and By integrating multi-omics analyses, it was shown that complement proteins (e.g., C1q) are co-localized with the postsynaptic PSD95 dot in an AD mouse model, which suggests that C1q can act as a molecular label on synapses in preparation for microglia phagocytosis (192). Here, VTN is linked to Alzheimer disease.