<p>Parkinson’s Disease (PD) is a neurodegenerative disorder that exacerbates over time and is the result of long-term neuroinflammation and the degeneration of dopaminergic neurons. New research shows that adiponectin, an adipokine with strong anti-inflammatory and neuroprotective effects, could be a useful treatment for PD. This review explores molecular processes by which adiponectin changes important signaling pathways like AMPK, PPAR-γ, and NF-κB to lower oxidative stress, stop microglial activation, and improve neuronal survival. The article additionally addresses adiponectin-based treatments for PD, including as receptor agonists, bioengineered versions, and improved delivery systems. Transforming adiponectin-based treatments into practical applications is still difficult despite encouraging preclinical data because of things like blood-brain barrier permeability, ideal dosage, and possible systemic effects. Future studies should concentrate on creating pharmacological treatments, gene therapies, or adiponectin analogues that improve adiponectin signalling in the central nervous system. Novel insights into the pathophysiology of PD and potential treatment approaches may arise from an understanding of the interaction between metabolic control and neuroinflammation. The therapeutic promise of adiponectin is highlighted in this study, along with the necessity of additional research to fully utilise its neuroprotective properties in the treatment of Parkinson’s disease.</p> Graphical abstract <p></p>

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Adiponectin in neuroinflammation and parkinson’s disease: A macromolecular and therapeutic perspective

  • Kanupriya Chauhan,
  • Mayur Porwal,
  • Shamsher Singh

摘要

Parkinson’s Disease (PD) is a neurodegenerative disorder that exacerbates over time and is the result of long-term neuroinflammation and the degeneration of dopaminergic neurons. New research shows that adiponectin, an adipokine with strong anti-inflammatory and neuroprotective effects, could be a useful treatment for PD. This review explores molecular processes by which adiponectin changes important signaling pathways like AMPK, PPAR-γ, and NF-κB to lower oxidative stress, stop microglial activation, and improve neuronal survival. The article additionally addresses adiponectin-based treatments for PD, including as receptor agonists, bioengineered versions, and improved delivery systems. Transforming adiponectin-based treatments into practical applications is still difficult despite encouraging preclinical data because of things like blood-brain barrier permeability, ideal dosage, and possible systemic effects. Future studies should concentrate on creating pharmacological treatments, gene therapies, or adiponectin analogues that improve adiponectin signalling in the central nervous system. Novel insights into the pathophysiology of PD and potential treatment approaches may arise from an understanding of the interaction between metabolic control and neuroinflammation. The therapeutic promise of adiponectin is highlighted in this study, along with the necessity of additional research to fully utilise its neuroprotective properties in the treatment of Parkinson’s disease.

Graphical abstract