Some studies have shown numerous biological activities of Thiazolidine derivatives, including neuroprotection. The production of inflammatory markers and Reactive Oxygen Species (ROS) plays a major role in nerve damage that leads to memory impairment. Several studies have shown that alcohol consumption impairs memory in adults. However, the underlying mechanism is still unclear. Ethanol treatment also leads to memory impairment in mice. Exposure to ambient pollutants such as air pollutants also can be adversely impacted the Central Nervous System (CNS) by the activation of proinflammatory pathways and reactive oxygen species. Thus, targeting neuroinflammation and oxidative distress can be a useful strategy to eliminate the obvious symptoms of neurodegeneration. In addition, treatment with Thiazolidine-4-Carboxylic Acid derivatives reduces oxidative stress, neuroinflammation, and ethanol-induced memory impairment. In general, Thiazolidine derivatives may be useful in reducing neuroinflammation by acting on different stages of inflammation. In the current mini-review, we examined the neuroprotective potential of these compounds in a model of ethanol-induced neuritis.