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IR can disrupt this NAD + metabolism, diminishing sirtuin activity and weakening mitochondrial function and neuronal cell survival (Figure 1) ( FIGURE 1 6 GLP-1 and incretin mimetics in PD The incretin hormones known as GLP-1 and GIP are released from enteroendocrine L-cells and K-cells in the small intestine in response to nutrient ingestion, where they play a key role in regulating glucose metabolism and maintaining systemic nutrient homeostasis ( (Heloderma suspectum) saliva as a stable GLP-1 mimetic enabled appetite suppression and glycemic control in metabolic disease, driving the development of long-acting GLP-1 analogues and unimolecular agents that co-activate GLP-1 and GIP receptors ( Although direct involvement of GLP-1/GIP system abnormalities in PD remains uncertain, growing evidence shows that incretin-based therapies can improve cognitive function and exert neuroprotective effects, positioning them as promising candidates for treating neurodegenerative disorders ( In PD models, Agonists of GLP-1 receptor have also been shown to restore impaired GLUT expression and stabilize glucose uptake in brain that supports improvement in metabolic flexibility ( GLP-1 receptor agonists (e.g., exenatide, liraglutide, lixisenatide) and dual GLP-1/GIP agonists (e.g., tirzepatide) have been also reported to reduce microglial and astrocytic hyperactivation and suppress the release of inflammatory mediators such as TNF-, IL-1, and NF-B

[1] However, the clinical significance of these modest elevations remains uncertain, as they occurred in the context of substantial weight loss and improvements in other cardiovascular risk factors, including blood pressure, lipid profiles, and glycemic control in patients with type 2 diabetes

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Costello, P., Bresnihan, B., OFarrelly, C

Immune Support: Antioxidant-containing fruits like berries and citrus contribute to a varied diet