Evidences revealed that QCs are responsible for the formation of pGlu-modified Aβ peptides in AD, which are more neurotoxic, hydrophobic, and resistant to aminopeptidase degradation compared to unmodified Aβ peptides and, thus, accumulating in AD patients’ brains [130] Therefore, inhibition of QCs may have therapeutic potential for treatment of disorders associated with protein aggregation and (neuro) inflammation and, therefore, might be considered as one of therapeutic approaches in treatment of AD [131]. This evidence concerns the gene CPQ and Alzheimer disease.