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Purpose of Review <p>Parkinson’s disease (PD) is a progressive neurodegenerative disorder driven by multifactorial pathogenic mechanisms, including early oxidative stress and mitochondrial dysfunction, followed by α-synuclein aggregation, neuroinflammation, and impaired neurotrophic support. Given that current therapies are largely symptomatic and non-disease-modifying, there is a need for multitarget therapeutic strategies. Therefore, the present study aims to evaluate the antiparkinsonian potential of apigenin, a naturally occurring flavone, in modulating key pathogenic targets of PD.</p> Methodology <p>A comprehensive literature-based mechanistic analysis was conducted to elucidate the molecular pathways underlying apigenin-mediated neuroprotection in PD. Relevant studies were systematically retrieved from PubMed, ScienceDirect, Scopus, Embase, and Google Scholar. In addition, in-silico molecular docking studies were performed to evaluate the binding interactions of apigenin with key pathological targets, including α-synuclein and dopamine receptors (D2, D3, and D4). Furthermore, ADMET analysis was carried out to assess the drug-likeness, pharmacokinetic properties, and safety profile of apigenin.</p> Key Findings <p>The findings indicate that apigenin exerts robust anti-Parkinson potential through modulation of multiple signaling pathways, including inhibition of NF-κB-mediated pro-inflammatory cytokine production, suppression of pro-apoptotic mediators, and attenuation of MAPK-driven neuroinflammatory responses. Furthermore, apigenin influences critical PD-related mediators such as α-synuclein aggregation, TGF-β, acetylcholinesterase activity, dopaminergic signaling, and ROS. Molecular docking revealed favorable interactions of apigenin with α-synuclein and dopamine receptors, while ADMET profiling suggested acceptable pharmacokinetic and safety characteristics.</p> Summary <p>This study highlights that apigenin possesses significant multitargeted activity against key pathogenic mechanisms of PD, underscoring its potential as a promising candidate for further preclinical and translational research toward disease-modifying therapies.</p>

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Mechanistic insights into the Therapeutic Potential of Apigenin in Parkinson’s Disease: An In Silico Docking and ADMET Study

  • 期刊论文

  • 发表日期：

    2026年2月7日

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  • Anish Singh,
  • Lovedeep Singh,
  • Diksha Dalal

摘要

Purpose of Review

Parkinson’s disease (PD) is a progressive neurodegenerative disorder driven by multifactorial pathogenic mechanisms, including early oxidative stress and mitochondrial dysfunction, followed by α-synuclein aggregation, neuroinflammation, and impaired neurotrophic support. Given that current therapies are largely symptomatic and non-disease-modifying, there is a need for multitarget therapeutic strategies. Therefore, the present study aims to evaluate the antiparkinsonian potential of apigenin, a naturally occurring flavone, in modulating key pathogenic targets of PD.

Methodology

A comprehensive literature-based mechanistic analysis was conducted to elucidate the molecular pathways underlying apigenin-mediated neuroprotection in PD. Relevant studies were systematically retrieved from PubMed, ScienceDirect, Scopus, Embase, and Google Scholar. In addition, in-silico molecular docking studies were performed to evaluate the binding interactions of apigenin with key pathological targets, including α-synuclein and dopamine receptors (D2, D3, and D4). Furthermore, ADMET analysis was carried out to assess the drug-likeness, pharmacokinetic properties, and safety profile of apigenin.

Key Findings

The findings indicate that apigenin exerts robust anti-Parkinson potential through modulation of multiple signaling pathways, including inhibition of NF-κB-mediated pro-inflammatory cytokine production, suppression of pro-apoptotic mediators, and attenuation of MAPK-driven neuroinflammatory responses. Furthermore, apigenin influences critical PD-related mediators such as α-synuclein aggregation, TGF-β, acetylcholinesterase activity, dopaminergic signaling, and ROS. Molecular docking revealed favorable interactions of apigenin with α-synuclein and dopamine receptors, while ADMET profiling suggested acceptable pharmacokinetic and safety characteristics.

Summary

This study highlights that apigenin possesses significant multitargeted activity against key pathogenic mechanisms of PD, underscoring its potential as a promising candidate for further preclinical and translational research toward disease-modifying therapies.