Arbutin attenuates aluminium chloride-induced neurotoxicity and cognitive deficits in a zebrafish model of Alzheimer's disease.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised by amyloid-beta plaques, tau tangles, and oxidative stress, ultimately leading to neuronal death and cognitive decline. Current treatments primarily target symptoms rather than underlying pathology, highlighting the need for novel therapeutic strategies. Arbutin, a glycoside with anti-inflammatory and antioxidant properties, remains largely unexplored in AD research. This study evaluates its neuroprotective potential in a zebrafish model of AD. Zebrafish larvae were exposed to arbutin for toxicity assessment, followed by aluminium chloride-induced cognitive impairment. Behavioural analysis (ToxTrac software), oxidative stress markers (ROS, apoptosis, lipid peroxidation, AO, 2' - 7'-DCFH-DA, and DPPP staining), and gene expression (RT-qPCR) were evaluated. Arbutin (50 µM) showed no significant morphological toxicity but improved cognitive function and reduced oxidative stress markers in AlCl-exposed larvae. Additionally, it restored antioxidant activity and mitigated neuroinflammation, highlighting its neuroprotective effects. These findings suggest that arbutin is a potential candidate for AD therapy, warranting further preclinical investigation.