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Cognitive Decline and Neurodegenerative Conditions Cognitive decline and neurodegenerative conditions show substantial preclinical evidence across multiple pathologies: Stroke models: BPC-157 given during reperfusion counteracted neuronal damage and produced full functional recovery in spatial memory, motor coordination, and balance tests Parkinsons models: MPTP-induced models showed reduced motor symptoms (tremor, rigidity, akinesia), protection of nigrostriatal dopaminergic neurons, and near-complete prevention of mortality Multiple sclerosis models: Cuprizone-induced demyelination resulted in significantly less brain damage and reduced clinical abnormalities when BPC-157 was given in drinking water or intragastrically Traumatic brain injury: Falling weight model studies demonstrated reduced hemorrhage, decreased brain lacerations and edema, and improved early outcomes These diverse models share common mechanisms

This is in line with the fact that, although some studies have shown the presence of the GLP-1R in other parts of the heart ( Apart from the chronotropic effects, direct effects of GLP-1 specifically on the heart have not been comprehensively documented, although evidence exists to suggest that GLP-1 RAs may improve cardiac output as well as cardiomyocyte survival ( It should be noted that one of the two major DPP-IV-generated truncated forms of GLP-1 (GLP-1 [9-36amide]) has been shown to have direct beneficial cardiac effects in mice, which is representative of the hypothesis that a GLP-1R-associated response can be elicited also by these metabolites and thus not only via the classic incretin pathway ( Future perspectives In summary, the cardiovascular safety of all currently marketed GLP-1 RAs has been thoroughly established in large CVOTs ( As noted by others ( Of note, the finding of a markedly greater benefit on HF of efpeglenatide amongst trial participants using SGLT2 inhibitors at enrolment in the AMPLITUDE-O CVOT highlights another important point ( Another drug class widely used to treat type 2 diabetes is inhibitors of the enzyme dipeptidyl peptidase-4 (DPP4), which mediates enzymatic breakdown of GLP-1

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