Abstract
This study aimed to evaluate the cognitive-enhancing and neuroprotective effects of cardamonin in the 5XFAD transgenic mouse model of Alzheimer's disease (AD). We treated six-month-old female 5XFAD mice with cardamonin at 5mg/kg, 10mg/kg, and 20mg/kg. Cognitive function was assessed using the Morris Water Maze (MWM) and Novel Object Recognition (NOR) tests. ELISA, western blot, and PCR analyses evaluated amyloid-beta (Aβ) levels, neuroinflammation markers, and apoptosis-related factor expression. All animals survived without toxicity. Cardamonin treatment significantly improved spatial learning and memory retention in MWM and NOR tests, with the 20mg/kg dose showing the most pronounced effects. Additionally, cardamonin reduced soluble and insoluble Aβ levels in the frontal cortex and hippocampus. The treatment also significantly decreased neuroinflammatory markers, with IL-1β, IL-6, and TNF-α levels dropping substantially at higher doses. Cardamom treatment also normalizes cleaved caspase 3, GFAP, Iba-1, PSD-95, and synaptophysin, which aids in restoring synaptic integrity. Furthermore, cardamonin led to a marked reduction in apoptosis-related gene expression, indicating its potential to mitigate neurodegeneration. Cardamonin demonstrates significant cognitive-enhancing and neuroprotective properties in the 5XFAD mouse model, suggesting its potential as a therapeutic agent for AD. These findings support further investigation into cardamonin's mechanisms and applicability in treating neurodegenerative disorders.
Published Version
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