ArticleMetabolic brain disease2026
Neuroprotective effects of trans-anethole on AlCl₃-induced memory impairment: targeting AChE, oxidative stress, and NLRP3 inflammasome: a promising approach for neurodegeneration prevention.
Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aluminum, a widely occurring environmental metal, has been implicated as a neurotoxic agent and is associated with the development of several neurodegenerative conditions, including Alzheimer's disease (AD). Its neurotoxicity is largerly attributed to the induction of oxidative stress , which exacerbates neuroinflammation, leading to cognitive deficits and progressive neuronal dysfunction. Trans-anethole (TA) possesses diverse pharmacological activities, including anti-inflammatory, antioxidant, antifungal, and anticancer effects. However, its neuroprotective potential against AlCl₃-induced neurodegeneration, particularly in the context of memory impairment mediated by inflammation and oxidative stress, remains unknown. Therefore, this study was conducted to evaluate the potential role of TA in mitigating neurodegeneration. To establish an aluminum-induced neuroinflammation-associated neurodegenerative model, rats received oral administration of 150 mg/kg AlCl₃ for 90 days. TA was administered at three different dosages between days 31 and 90: 40, 80, and 160 mg/kg between days 31 and 90. Cognitive performance was assessed using the Morris water maze (MWM) and passive avoidance test (PAT). Neuroprotective effects were evaluated by analyzing acetylcholinesterase (AChE) activity, oxidative stress markers (catalase, glutathione, and malondialdehyde levels), and neuroinflammatory mediators (NLRP3 inflammasome, Interleukin-1β, and TNF-α) in AlCl₃-exposed rats. TA significantly mitigated aluminum-induced neuronal damage by restoring antioxidant defence, inhibiting AChE activity, and downregulating inflammatory proteins, including NLRP3, TNF-α, and IL-1β. Histopathological analysis further confirmed its neuroprotective role. The findings of this study suggests that TA holds therapeutic potential for neurodegenerative disorders by mitigating memory deficits, neuroinflammation, and oxidative stress.
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