We sought to biochemically validate the proteomics-based observation of increased C1qa and C1qb expression in PS190/+;Pyk2−/− hippocampal synaptosomes and assessed whether genetic Pyk2 deletion modulated Tau-induced C1q deposition in a manner that reflects Pyk2’s role in suppressing Tau-associated memory impairment in PS190/+ mice. Here, C1QB is linked to memory impairment.