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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Neuroprotective Mechanism of Polygonatum sibiricum Polysaccharides in Alzheimer's Disease: Highlighting Role of

Xiang Zhang1, Sheng-Peng Zhang1, Chao Li1

  • 1Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui, School of Pharmacy, Wannan Medical College, Wuhu, Anhui Province, 241000, China.

Chinese Journal of Integrative Medicine
|January 5, 2026
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Summary

Polygonatum sibiricum polysaccharides (PSP) show promise in treating Alzheimer's disease (AD) by modulating the PI3K-AKT pathway. This natural compound improves cognitive function and reduces neuroinflammation and tau pathology in AD mice.

Keywords:
Polygonatum sibiricum polysaccharidesAlzheimer’s diseaseChinese medicinePI3K-AKTleptin receptornetwork pharmacology

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline.
  • Identifying effective therapeutic agents and their mechanisms of action is crucial for managing AD.
  • Polygonatum sibiricum polysaccharides (PSP) are natural compounds with potential therapeutic properties.

Purpose of the Study:

  • To elucidate the action mechanism of Polygonatum sibiricum polysaccharides (PSP) in Alzheimer's disease (AD).
  • To investigate the role of the PI3K-AKT signaling pathway and Leptin Receptor (LepR) in PSP's therapeutic effects on AD.
  • To evaluate the impact of PSP on cognitive function, neuroinflammation, and tau pathology in an AD mouse model.

Main Methods:

  • Network pharmacology and molecular docking were employed to predict key targets and pathways.
  • An Alzheimer's disease mouse model was established using D-galactose and AlCl3.
  • Behavioral tests (open field, elevated plus maze, Morris water maze, shuttle box) assessed cognitive and anxiety behaviors.
  • Western blot, immunofluorescence, immunohistochemistry, and ELISA were used to analyze signaling pathways, protein expression, and cytokine levels.
  • Leptin receptor knockdown (LepR-KD) was utilized to confirm the role of LepR in PSP's effects.

Main Results:

  • Network pharmacology identified the PI3K-AKT signaling pathway as a key target of PSP in AD.
  • PSP treatment significantly improved learning, memory, and anxiety behaviors in AD mice.
  • PSP upregulated the PI3K-AKT pathway, enhanced LepR and NeuN expression, and reduced Tau protein and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α).
  • LepR knockdown attenuated the neuroprotective effects of PSP, confirming LepR's essential role.

Conclusions:

  • PSP exerts neuroprotective effects in AD by modulating the PI3K-AKT signaling pathway in a LepR-dependent manner.
  • PSP treatment attenuates aberrant Tau protein deposition and neuroinflammation, potentially delaying AD pathogenesis.
  • These findings highlight PSP as a potential therapeutic agent for Alzheimer's disease.