Glyphosate (GYP) is a phosphonate type of herbicide and potentially causes neurodegenerations. Astaxanthin (AST) is a red pigment and is a group of carotenoids. It possesses potential antioxidants and neuroprotective actions. However, the ameliorative role of AST in GYP-induced neurocognitive dysfunction has not been studied yet. Hence, the present study is designed to investigate the ameliorative potential of AST in GYPinduced cognitive dysfunction via regulations of acid phosphatase (AP) and annexin A2 (AXA2) actions in the zebrafish model. The cognitive dysfunction was induced by exposure to GYP (0.5 mg/L for 30 minutes/ day) for 14 consecutive days. The AST (50, 75, and 100 mg/L for 30 minutes/day) and reference drug i.e., donepezil (DP; 1 µg/mL for 30 minutes/day) were exposed for 14 consecutive days before GYP exposure. On the 14th day, cognitive changes i.e., three horizontal compartment test, optokinetic motor response (OMR), startle response (SR), and T-maze tests were assessed. The changes of biomarkers i.e., acetylcholinesterase (AChE) activity, thio barbituric acid reactive substances (TBARS), reduced glutathione (GSH), AP, and AXA2 levels were estimated in brain tissue. The administration of AST ameliorates the GYP-induced neurocognitive dysfunctions via the antioxidant, regulation of AP and AXA2 actions. Hence, it can be used for neurocognitive disorders against the phosphonate type of herbicide (GYP) toxicity.