These post-translationally modified proteins are significantly overexpressed in AD where pGlu-Aβ has been shown to be synaptotoxic, proinflammatory, promoting of self-aggregation into oligomers, and resistant to degradation [1], while pGlu-CCL2 has been linked to the presence and severity of neuroinflammation [2]. Here, CCL2 is linked to Alzheimer disease.