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Purpose of Review <p>Neurodegenerative disorders, including Alzheimer’s disease and Parkinson’s disease, are characterized by progressive neuronal loss, synaptic dysfunction, and cognitive and motor impairments, for which disease-modifying therapies remain limited. Anatabine, a minor alkaloid derived from <i>Solanaceae</i> plants, has recently gained attention due to its antioxidant, anti-inflammatory, and neuromodulatory properties. Although extensively studied in inflammatory and metabolic conditions, its therapeutic relevance in neurodegeneration has not been comprehensively evaluated. This review systematically examines the neuroprotective potential of anatabine in NDs by integrating evidence <i>from </i>in vitro, in vivo, and computational studies to elucidate its mechanistic and translational significance.</p> Recent Findings <p>In vitro studies demonstrate that anatabine reduces reactive oxygen species production, activates Nrf-2/ARE signaling, and suppresses NF-κB and STAT3-mediated neuroinflammation. Anatabine dose-dependently downregulates BACE1 expression and reduces Aβ₁–₄₀/₄₂ accumulation, thereby attenuating Aβ-induced synaptic and mitochondrial dysfunction. Whereas, in vivo studies demonstrate that anatabine decreases cerebral Aβ burden, microglial activation (Iba-1, CD45), and pro-inflammatory mediators including iNOS, COX-2, TNF-α, IL-1β, IL-6, IL-17, and IFN-γ. These molecular effects preserve dopaminergic neuron integrity, stabilize striatal dopamine signaling, and improve behavioral outcomes such as locomotor activity, sociability, working memory, and attention. Molecular docking analyses further reveal high-affinity interactions of anatabine with key neurodegenerative targets, including Aβ (-22.6&#xa0;kcal/mol), dopamine D2 receptor (-7.2&#xa0;kcal/mol), TNF-α (-5.9&#xa0;kcal/mol), NF-κB (-5.2&#xa0;kcal/mol), and STAT3 (-5.8&#xa0;kcal/mol), corroborating its multi-target mode of action.</p> Summary <p>By integrating mechanistic insights, molecular docking data, and behavioral outcomes, this review underscores the potential of anatabine as a disease-modifying therapeutic candidate for neurodegenerative disorders. Nonetheless, further preclinical validation and well-designed clinical studies are required to establish its safety, efficacy, and translational applicability in human populations.</p>

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From Bench to Bedside: Unveiling the Effects of Anatabine as a Promising Neuroprotective Agent in the Battle Against Neurodegenerative Disorders

  • 期刊论文

  • 发表日期：

    2026年4月25日

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  • Anish Singh,
  • Lovedeep Singh,
  • Diksha Dalal

摘要

Purpose of Review

Neurodegenerative disorders, including Alzheimer’s disease and Parkinson’s disease, are characterized by progressive neuronal loss, synaptic dysfunction, and cognitive and motor impairments, for which disease-modifying therapies remain limited. Anatabine, a minor alkaloid derived from Solanaceae plants, has recently gained attention due to its antioxidant, anti-inflammatory, and neuromodulatory properties. Although extensively studied in inflammatory and metabolic conditions, its therapeutic relevance in neurodegeneration has not been comprehensively evaluated. This review systematically examines the neuroprotective potential of anatabine in NDs by integrating evidence from in vitro, in vivo, and computational studies to elucidate its mechanistic and translational significance.

Recent Findings

In vitro studies demonstrate that anatabine reduces reactive oxygen species production, activates Nrf-2/ARE signaling, and suppresses NF-κB and STAT3-mediated neuroinflammation. Anatabine dose-dependently downregulates BACE1 expression and reduces Aβ₁–₄₀/₄₂ accumulation, thereby attenuating Aβ-induced synaptic and mitochondrial dysfunction. Whereas, in vivo studies demonstrate that anatabine decreases cerebral Aβ burden, microglial activation (Iba-1, CD45), and pro-inflammatory mediators including iNOS, COX-2, TNF-α, IL-1β, IL-6, IL-17, and IFN-γ. These molecular effects preserve dopaminergic neuron integrity, stabilize striatal dopamine signaling, and improve behavioral outcomes such as locomotor activity, sociability, working memory, and attention. Molecular docking analyses further reveal high-affinity interactions of anatabine with key neurodegenerative targets, including Aβ (-22.6 kcal/mol), dopamine D2 receptor (-7.2 kcal/mol), TNF-α (-5.9 kcal/mol), NF-κB (-5.2 kcal/mol), and STAT3 (-5.8 kcal/mol), corroborating its multi-target mode of action.

Summary

By integrating mechanistic insights, molecular docking data, and behavioral outcomes, this review underscores the potential of anatabine as a disease-modifying therapeutic candidate for neurodegenerative disorders. Nonetheless, further preclinical validation and well-designed clinical studies are required to establish its safety, efficacy, and translational applicability in human populations.