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Alzheimer's disease (AD) is a multifactorial and socioeconomically burdensome disease. In view of the failures of anti-AD candidates, we should try to rethink what we did before and what we should do next, in part at least. Research shows that the more neurotoxic factor, pyroglutamate-Aβs, and the more important inflammatory mediators, pyroglutamate-CCL2, both contribute to the initiation of AD specifically and the generation of N-terminal intramolecular cyclization catalyzed by glutaminyl cyclase quality control, the over-expression of which correlates positively with the severity of AD. Subsequently, lowering pyroglutamate-Aβs and pyroglutamate-CCL2 levels by quality control inhibition using small molecule inhibitors could be expected as an amazing strategy for the prevention and treatment of AD.

Can small molecule inhibitors of glutaminyl cyclase be used as a therapeutic for Alzheimer's disease?