The essential feature of gambling disorder is persistent and recurrent maladaptive gambling behavior that has recently gained much attention because of its increasing prevalence and devastating personal, familial, and social consequences. Based on similarities between gambling and substance-use disorders in neurocognitive and other domains, gambling disorder has recently been classified into “substance-related and addictive disorders” in the DSM-5, as “Non-Substance-Related Disorders”. For a better understanding of the causes of gambling disorder and its underlying neural mechanisms, we provide an integrative review of cognitive dysfunction of gambling disorders studies implicated in cognitive distortions, reward and punishment sensitivity, attention bias, and decision making. The future research needs to study more on the mechanism and development process of gambling disorders from the perspective of cognitive neuroscience, pay attention to the brain structural alterations and functional brain networks in gambling disorders, and integrate them into clinical neurobiological mechanisms to find more effective interventions and clinical treatments. we summarize the research on the cognitive dysfunction and neural mechanisms involved in gambling disorder. (1) it investigated brain regions underpinning gambling-related cognitive distortions. ‘Near-miss’ events, where unsuccessful outcomes are proximal to a win, recruit overlapping neural circuitry with actual monetary wins. Illusion of control over a gamble is also known to increase confidence in one’s chances of winning, showed an increased neural activity within a cortico-striatal network. ‘Loss-chasing’, or continued gambling in an attempt to recover losses, is implicated a complex of executive-control and impulsivity-related systems involved in loss-processing. (2) Differences in sensitivity to punishments and rewards can influence an individual's behavior and may be pertinent to the development of gambling disorder. The deficit in rewards and losses processing typically observed a reduction of ventral striatal activation in individuals with gambling disorder. We intend to add evidence on relevant brain structures in this functional brain system. Functional neuroimaging studies on gambling disorder found changes in the mesolimbic reward system (i.e., ventral striatum) and in the prefrontal cortex during reward processing and executive functions. In accordance with the observations, there are evidences that higher grey matter volumes in ventral striatum and anterior prefrontal cortex in gambling disorder as compared with controls. (3) Gambling-related cues can enhance the activities in the cognitive-controlled brain circuits (prefrontal cortex, anterior cingulate gyrus, etc.) as well as emotional processing brain circuits (amygdala, insula, nucleus accumbens, etc.), which may be a potential neural basis for attentional bias toward gambling disorders, resulting in increased attention to the gambling-related stimuli. In addition, the findings of relatively diminished hippocampal and amygdalar volumes in gambling disorder individuals. (4) These individuals’ poor decision making may be a product of an imbalance between the emotion and motivation-related brain regions (amygdala, insula, etc.) and the prefrontal cortex. Finally, we propose that future studies should (1) More concerned about the relationship between functional and structural alterations to add evidence on relevant brain structures in this functional brain system. (2) analyze the cognition, pathological state and working mechanism of the gambling disorders in a dynamic functional connectivity networks, explore the relationship between gambling disorders and brain function connectivity, and reveal the neural mechanism of gambling disorders. (3) Integrate neuroimaging measures into pathophysiological offers the opportunity to understand the mechanisms underlying effective treatments, and translating neurobiological advances into more effective prevention and treatment strategies.