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Proposed mechanisms include oxidative stress, mitochondrial dysfunction, dyslipidaemia, and genomic modulation of hypertrophic and fibrotic signalling pathways (70)

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 (Wang et al., 2023)

Endogenous sources of ROS Major sites of ROS production are mitochondria, membrane-bound NADPH oxidases (NOXs), peroxisomes, and chloroplasts in the course of the process of respiration and photosynthesis

This also has significant implications for the treatment of abscesses caused by bacterial infections, given that the immune mimicking effects of Mn 2+ , which can be released by MnO 2 NPs, to induce robust immune memory (38)