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Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer's Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential
Kim, E.H.; Lee, W.S.; Kwon, D.R. Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer’s Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential. Int. J. Mol. Sci.2024, 25, 6088.
Kim, E.H.; Lee, W.S.; Kwon, D.R. Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer’s Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential. Int. J. Mol. Sci. 2024, 25, 6088.
Kim, E.H.; Lee, W.S.; Kwon, D.R. Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer’s Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential. Int. J. Mol. Sci.2024, 25, 6088.
Kim, E.H.; Lee, W.S.; Kwon, D.R. Microcurrent Therapy Mitigates Neuronal Damage and Cognitive Decline in an Alzheimer’s Disease Mouse Model: Insights into Mechanisms and Therapeutic Potential. Int. J. Mol. Sci. 2024, 25, 6088.
Abstract
Alzheimer's Disease (AD) presents a significant challenge in the wake of its multifaceted nature, characterized by cognitive decline, memory impairment, and neuroinflammation. Despite extensive research, effective pharmacological interventions remain elusive, prompting exploration into non-pharmacological approaches. Microcurrent therapy (MC), utilizing imperceptible currents, has emerged as a potent clinical protocol. While previous studies have focused on its therapeutic effects, this study investigates its impact 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 preservation of neuronal structure. Additionally, MC therapy significantly decreases amyloid-beta (Aβ) plaque deposition and inhibits apoptosis, indicating its potential to mitigate AD pathology. Our study discovered that MC therapy effectively reduces glial activation by inhibiting the TLR4-MyD88-NFκB pathway, consequently leading to decreased levels of inflammatory factors TNF-α, IL-1β, and IL-6, thus implicating TLR4 in neurodegenerative disease-related neuroinflammation. Furthermore, while our study did not observe significant adverse effects, further clinical trial into potential side effects and neuroinflammatory responses associated with MC therapy is warranted.
Medicine and Pharmacology, Neuroscience and Neurology
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