Introduction to virtual special issue on glucagon-like peptide-1 agonists and the skin.

Traumatic brain injury (TBI), including non-severe TBI (nTBI), affects millions of people worldwide and often leaves a hidden legacy of emotional and cognitive challenges. While the immediate physical consequences of nTBI may be less apparent compared to more severe injuries, the disruption to the complex brain emotional circuitry can significantly alter an individual’s life. This impact can affect their relationships, overall well-being and ability to navigate daily life. A common and induced effect of TBI is emotional dysregulation, which may demonstrate increased emotional responses, mood swings, and impaired emotional regulation. One crucial aspect of this dysregulation is a significant impairment in the ability to recognize and interpret the emotions of others. Research involving TBI has shown that individuals with TBI often experience substantial difficulties in emotion recognition, particularly related to negative emotions such as fear and anger. A systematic review by of 17 studies found that the TBI group demonstrated moderate to large deficits (Hedges’ g = 0.79) in recognizing emotions compared to the healthy group, with the most pronounced impairments occurring for negative emotions. These impairments extend across various emotional categories and modalities, including across facial and vocal cues (). Moreover, TBI frequently affects cognitive functions essential for emotional well-being, including memory, executive functions, and self-awareness (; ; ). These cognitive deficits can directly lead to emotional challenges by impairing an individual’s capacity to recognize and manage emotions and engage effectively in social interactions. In addition to these direct effects, the cognitive and emotional consequences of nTBI can contribute to long-term psychological challenges. Conditions such as post-traumatic depression (PTD), characterized by persistent sadness, anxiety, and impaired concentration, are prevalent () and significantly reduce daily function and quality of life. Furthermore, 60% of participants with nTBI report reduced empathy (), further complicating social relationships and intensifying feelings of isolation. Advancements in neuroimaging technologies, particularly functional magnetic resonance imaging (fMRI) and dynamic causal modeling (DCM), have significantly enhanced our understanding of the neural mechanisms that underlie cognitive and emotional deficits following moderate TBI, revealing altered patterns of brain activity and connectivity (; ). These techniques enable researchers to visualize brain activity and the connectivity patterns involved in emotional processing, revealing notable disruptions in critical brain regions and networks (). fMRI studies have consistently shown altered neural activity in the amygdala, a key area responsible for processing emotions such as fear and pleasure, as well as in the prefrontal cortex, which plays a vital role in executive functions and emotional regulation. Additionally, DCM research has emphasized the significance of effective connectivity and how one brain region influences another when examining the effects of TBI on cognitive and emotional processing. Findings indicate changes in connectivity between the prefrontal cortex and limbic structures, which likely contribute to the emotional dysregulation commonly experienced by individuals suffering from moderate TBI ().