The integration of artificial intelligence (AI) in mental healthcare holds promise for enhancing diagnostic precision, treatment efficacy, and personalized care. Despite AI’s potential to analyze vast datasets and identify subtle patterns, its clinical adoption in psychiatry remains limited. This review critically examines the emerging role of AI in psychiatry, elucidating its utility, challenges, and implications for clinical practice. Through an extensive analysis of the existing literature and empirical evidence, we seek to inform psychiatric stakeholders about both opportunities and obstacles that are presented by AI. We evaluate AI’s potential to improve diagnostic accuracy, prognostic performance, and therapeutic interventions. Our pragmatic approach bridges the gap between theoretical advancements and practical implementation, providing valuable insights and actionable recommendations for psychiatric professionals. This article highlights the supportive role of AI, advocating for its judicious integration to enhance patient outcomes while maintaining the human-centric essence of psychiatric practice. By addressing these challenges and fostering collaboration, AI can significantly advance mental healthcare, reduce clinical burdens, and improve patient outcomes.

Diabetes-associated cognitive dysfunction (DACD) is increasingly recognized as a critical complication of diabetes. The complex pathology of DACD remains unknown. Here, we performed single-nucleus RNA sequencing (snRNA-seq) to demonstrate unique cellular and molecular patterns of the hippocampus from a mouse model of diabetes. More in-depth analysis of oligodendrocytes (OLs) distinguished five subclusters, indicating different functional states of OLs and transcriptional changes in each subcluster. Based on the results of snRNA-seq and experiments in vivo, we observed demyelination and disharmony of oligodendroglial lineage cell composition in male diabetic mice. Serum/glucocorticoid regulated kinase 1 (SGK1) expression was significantly increased in the hippocampus OLs of male diabetic mice, and SGK1 knockdown in hippocampus reversed demyelination and DACD via N-myc downstream-regulated gene 1 (NDRG1)-mediated pathway. The findings illustrated a transcriptional landscape of hippocampal OLs and substantiated impaired myelination in DACD. Our results provided direct evidence that inhibition of SGK1 or the promotion of myelination might be a potential therapeutic strategy for DACD.

Addiction, particularly in relation to psychostimulants and opioids, persists as a global health crisis with profound social and economic ramifications. Traditional interventions, including medications and behavioral therapies, often encounter limited success due to the chronic and relapsing nature of addictive disorders. Consequently, there is significant interest in the development of innovative therapeutics to counteract the effects of abused substances. In recent years, vaccines have emerged as a novel and promising strategy to tackle addiction. Anti-drug vaccines are designed to stimulate the immune system to produce antibodies that bind to addictive compounds, such as nicotine, cocaine, morphine, methamphetamine, and heroin. These antibodies effectively neutralize the target molecules, preventing them from reaching the brain and eliciting their rewarding effects. By obstructing the rewarding sensations associated with substance use, vaccines aim to reduce cravings and the motivation to engage in drug use. Although anti-drug vaccines hold significant potential, challenges remain in their development and implementation. The reversibility of vaccination and the potential for combining vaccines with other addiction treatments offer promise for improving addiction outcomes. This review provides an overview of anti-drug vaccines, their mechanisms of action, and their potential impact on treatment for substance use disorders. Furthermore, this review summarizes recent advancements in vaccine development for each specific drug, offering insights for the development of more effective and personalized treatments capable of addressing the distinct challenges posed by various abused substances.

In substance use disorder (SUD)/drug addiction, individuals often seek drug rewards at a large cost. Recent findings demonstrate that natural rewards may offer significant therapeutic potential against SUD. However, the mechanism by which natural rewards counteract SUD remains unclear. While incentive sensitization theory provides valuable insights, a comprehensive understanding is still lacking. In this review, we first summarize the evidence and potential neurobiological mechanisms that support the protective effect of natural rewards against SUD, such as palatable food, social interaction, physical exercise, and environmental enrichment. Then, we propose an updated incentive sensitization framework to explain how natural rewards resist SUD by modulating wanting and liking. This review contributes to our understanding of the interaction between natural rewards and drug rewards, potentially facilitating the development of novel therapeutic strategies for SUD.