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In human iPSC-derived dopaminergic neurons from PD patients with SNCA mutations, exendin-4 restored insulin signaling, improved mitochondrial function, and reduced -synuclein aggregation via PI3K/Akt/mTOR activation (26)

Recent improvements in molecular modeling have enabled the design of new inhibitors with higher selectivity for DPP-4 than for other dipeptidyl peptidases, thus minimizing side effects [28]