关键词: Alzheimer’s disease microcurrent therapy neuronal damage β-amyloid

Mesh : Animals Alzheimer Disease / therapy metabolism pathology Disease Models, Animal Mice Mice, Transgenic Cognitive Dysfunction / therapy etiology metabolism Neurons / metabolism pathology Myeloid Differentiation Factor 88 / metabolism genetics Toll-Like Receptor 4 / metabolism Amyloid beta-Peptides / metabolism Neuroinflammatory Diseases / metabolism etiology pathology Plaque, Amyloid / pathology metabolism NF-kappa B / metabolism Apoptosis

来  源:   DOI:10.3390/ijms25116088   PDF(Pubmed)

Abstract:
Alzheimer\'s disease (AD) presents a significant challenge due to its multifaceted nature, characterized by cognitive decline, memory loss, and neuroinflammation. Though AD is an extensively researched topic, effective pharmacological interventions remain elusive, prompting explorations into non-pharmacological approaches. Microcurrent (MC) therapy, which utilizes imperceptible currents, has emerged as a potent clinical protocol. While previous studies have focused on its therapeutic effects, this study investigates the impact of MC on neuronal damage and neuroinflammation in an AD mouse model, specifically addressing potential side effects. Utilizing 5xFAD transgenic mice, we examined the effects of MC therapy on neuronal integrity and inflammation. Our findings suggest that MC therapy attenuates memory impairment and reduces neurodegeneration, as evidenced by improved performance in memory tests and the preservation of the neuronal structure. Additionally, MC therapy significantly decreases amyloid-beta (Aβ) plaque deposition and inhibits apoptosis, indicating its potential to mitigate AD pathology. This study determined that glial activation is effectively reduced by using MC therapy to suppress the TLR4-MyD88-NFκB pathway, which consequently causes the levels of inflammatory factors TNF-α, IL-1β, and IL-6 to decrease, thus implicating TLR4 in neurodegenerative disease-related neuroinflammation. Furthermore, while our study did not observe significant adverse effects, a further clinical trial into potential side effects and neuroinflammatory responses associated with MC therapy is warranted.
摘要:
阿尔茨海默病(AD)由于其多面性而提出了重大挑战,以认知能力下降为特征,记忆丧失,和神经炎症。虽然AD是一个广泛研究的话题,有效的药理干预仍然难以捉摸,促使探索非药理学方法。微电流(MC)治疗,利用不易察觉的电流,已经成为一种有效的临床方案。虽然以前的研究集中在其治疗效果上,这项研究调查了MC对AD小鼠模型中神经元损伤和神经炎症的影响,专门解决潜在的副作用。利用5xFAD转基因小鼠,我们研究了MC治疗对神经元完整性和炎症的影响.我们的研究结果表明,MC治疗减轻记忆障碍和减少神经变性,记忆测试中的表现和神经元结构的保存证明了这一点。此外,MC治疗显著减少淀粉样β(Aβ)斑块沉积并抑制细胞凋亡,表明其减轻AD病理的潜力。这项研究确定,通过使用MC疗法抑制TLR4-MyD88-NFκB通路,可以有效降低胶质细胞的活化,从而导致炎症因子TNF-α的水平,IL-1β,和IL-6减少,因此,TLR4与神经退行性疾病相关的神经炎症有关。此外,虽然我们的研究没有观察到明显的不良反应,有必要对MC治疗相关的潜在副作用和神经炎症反应进行进一步的临床试验.
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