Anti-Alzheimer’s Potential of Flaxseed (Linum usitatissumum) in Aluminium Chloride Induced Alzheimer’s Disease in Zebrafish Model

Abstract

Objectives: Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder predominantly affecting the elderly population and is characterized by memory loss, cognitive impairment, and behavioural disturbances. Despite extensive research, currently approved therapies for AD are largely limited to symptomatic management and fail to modify the underlying disease pathology. Therefore, the identification of safe and effective disease-modifying agents remains a major therapeutic challenge. The present study aimed to establish an Alzheimer’s-like cognitive impairment model in zebrafish using Aluminium Chloride (AlCl₃) and to evaluate the neuroprotective potential of Flax Seed Extract (FSE). Materials and Methods: AlCl₃ is a well-known neurotoxic agent that induces oxidative stress, cholinergic dysfunction, and neuronal damage, thereby replicating key pathological features of AD. Exposure to AlCl₃ resulted in significant deficits in cognitive performance, increased anxiety-like behaviour, and reduced locomotor activity in zebrafish, confirming the successful induction of Alzheimer’s-like pathology. Results: Treatment with flaxseed extract significantly ameliorated the behavioural impairments in a dose-dependent manner, with higher doses showing superior protective effects. The improvement in memory and motor functions suggests a strong neuroprotective role of flaxseed against AlCl₃-induced neurotoxicity. These beneficial effects are likely attributed to the presence of bioactive phytochemicals such as flavonoids, phenols, tannins, and alkaloids, which are known to exhibit antioxidant, anti-inflammatory, and antiapoptotic activities. Conclusion: Overall, the findings validate the zebrafish AlCl₃-induced model as a reliable platform for preclinical evaluation of anti-Alzheimer’s agents and highlight flaxseed as a promising, natural, and cost-effective therapeutic candidate for AD. Further studies focusing on molecular mechanisms, biomarker analysis, and clinical translation are warranted to substantiate these findings.