C3 and early-onset autosomal dominant Alzheimer disease: Among them, the classical pathway is particularly attractive since it is activated by the interaction of C1q with triggering elements (i.e., the Fc domain of immunoglobulins or peptides) that typify neurodegenerative (i.e., the amyloid β1-42 oligomers in Alzheimer disease) [83] or autoimmune diseases (i.e., the anti-GluN or anti-GluA antibodies in autoimmune encephalitis) [84] and leads to a sustained overproduction of this component and downstream constituents (i.e., C3).