Protective Role of Mansonone G Against Alzheimer-Like Memory Impairment in Danio rerio

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuronal dysfunction, representing a major global health challenge. Current pharmacological treatments provide only symptomatic relief and are often limited by side effects, prompting the search for natural compounds with neuroprotective potential. Mansonone G, a bioactive quinone isolated from Mansonia gagei, exhibits antioxidant and anti-inflammatory properties, which may contribute to the preservation of neuronal function. This study aimed to investigate the effects of Mansonone G on cognitive performance in zebrafish (Danio rerio) exposed to an AD-like experimental model. Zebrafish were assigned to six experimental groups: control (DMSO), galantamine, okadaic acid, and OKA combined with Mansonone G at concentrations of 1, 3, or 6 μg/L. Cognitive function was evaluated using the Y-maze test for spatial memory and locomotor activity and the Novel Object Recognition (NOR) test for recognition memory. Group differences were analyzed statistically, with pairwise comparisons conducted to determine significant effects. Exposure to OKA significantly impaired both spatial and recognition memory, whereas galantamine restored cognitive performance. Treatment with Mansonone G at 3 and 6 μg/L significantly improved cognitive outcomes, increasing exploration of the novel arm, enhancing preference for new objects, and stimulating locomotor activity. The 1 μg/L dose did not produce significant effects.
These findings indicate that Mansonone G mitigates OKA-induced cognitive deficits in zebrafish and highlight its potential as a natural neuroprotective agent for AD, supporting further preclinical investigations.