Alzheimer's disease is a multifactorial neurodegenerative condition manifested through acute cognitive decline, amyloid plaque deposits and neurofibrillary tangles. Complete cure for this disease remains elusive as the conventional drugs address only a single molecular target while Alzheimer's disease involves a complex interplay of different sets of molecular targets and signaling networks. In this context, the possibility of employing multi-drug combinations to rescue neurons from the dysregulated metabolic changes is being actively investigated. The present work investigates a poly-herbal formulation, Brahmi Nei that has been traditionally used for anxiolytic disorders and immunomodulatory effects, for its efficiency in ameliorating cognitive decline through a combination of behavioral, biochemical, histopathological, gene and protein expression analyses. Our results reveal that the formulation shows excellent neuroregenerative properties, rescues neurons from inflammatory damage, reduces neuritic plaque deposits and improves working memory in rodent models with scopolamine-induced dementia. The microarray analysis shows that the formulation induces the expression of pro-survival pathways and positively modulates genes involved in memory consolidation, axonal growth and proliferation in a concentration-dependent manner with therapeutic concentrations restoring the normal conditions in the brain of the diseased animals. The neuritic spine morphology confirms the long-term memory potentiation through improved mushroom spine density, increased dendritic length and connectivity. Taken together, our study provides mechanistic evidence to prove that the traditional formulation can be a superior therapeutic strategy to treat cognitive decline when compared to the conventional mono-drug treatment.

阿尔茨海默病是一种多因素神经退行性疾病，表现为急性认知能力下降、淀粉样斑块沉积和神经原纤维缠结。这种疾病的完全治愈仍然难以捉摸，因为传统药物仅针对单个分子靶标，而阿尔茨海默病涉及不同分子靶标和信号网络的复杂相互作用。在这种情况下，正在积极研究采用多药组合从失调的代谢变化中拯救神经元的可能性。目前的工作研究了一种多草药配方，Brahmi Nei传统上用于抗焦虑症和免疫调节作用，因为它通过行为、生化、组织病理学、基因和蛋白质表达分析的组合有效改善认知能力下降。我们的研究结果表明，该配方显示出优异的神经再生特性，可以挽救神经元免受炎症损伤，减少神经炎斑块沉积，并改善东莨菪碱诱导的痴呆啮齿动物模型的工作记忆。微阵列分析表明，该制剂诱导促存活通路的表达，并以浓度依赖性方式正向调节参与记忆巩固、轴突生长和增殖的基因，治疗浓度可恢复患病动物大脑的正常状态。神经炎棘形态通过改善蘑菇棘密度、增加树突长度和连接性证实了长期记忆增强。总之，我们的研究提供了机械证据，证明与传统的单一药物治疗相比，传统配方可以成为治疗认知能力下降的优越治疗策略。