The present study aimed at establishing a new pharmacologically-induced Alzheimer’s (AD) model in zebrafish by administering okadaic acid (OKA). This model involves most of the pathophysiological conditions predominant in AD while also cutting down time constraints and cost which hinder previously established AD models. Zebrafish were divided into 5 groups containing 5-6 fish per group. Each group was exposed to a respective concentration of OKA of 10nM, 100nM, 500nM, and 1μM along with a control group. Each exposure lasted for 9 days with a learning and memory test performed at the end. Fish were tested individually in a spatial alternation task in order to assess learning and memory capabilities. Fish were placed in a 10 L aquarium that was divided into two equal sections by a white divider that allowed for adequate room for the fish to swim from one side of the aquarium to the other. Each trial was initiated with a light tap at the center of each aquarium. After the light tap, there is a 5 second delay followed by food presentation on one side of the tank. In 20 minutes intervals, food presentation continued on alternating sides for a total of 28 trials (14 on each side). A response was considered correct if the fish was present on the side of food presentation during or shortly after food presentation. Each trial ended 5 seconds after the food was presented. Zebrafish are deemed to have learned the task when 75% or more of the responses are correct. After completing the learning and memory tests, fish were euthanized and their brains were further analyzed by conducting immunohistochemistry analysis for phospho-glycogen synthase-3 α/β (p-GSK-3 α/β), GSK-3 α/β, Aβ, p-tau, and tau. All parameters of expression of p-GSK-3α/β, GSK-3α/β, Aβ, p-tau, and tau were analyzed using a student’s t-test. A value of p<0.05 was considered to be significant. It was observed that brain hemorrhages and higher mortality rates were caused in fish with increasing concentration of OKA. The 500nM and 1μM exposure groups observed the highest mortality rates of 60%-70%. The control group demonstrated rapid learning with maximal learning shown to be between 75%-80%. The exposed groups never demonstrated learning with their probabilities of correctness continuously staying around 50%. OKA exposure resulted in the increased phosphorylation of GSK-3 α/β, increased phosphorylation of tau, Aβ deposition, and the formation of Aβ plaques. These experiments were able to establish an AD model that incorporates most of the hallmarks of AD pathophysiology. This model can now be used to study drug discovery for AD and the molecular mechanisms involved in AD without the time and cost constraints that other AD models entail.