Primary splenic angiosarcoma presenting with unexplained anemia in a young adult: a case report.

Depressive disorder is a predominant contributor to global disability-adjusted life years, manifesting as persistent affective disturbances (low mood, emotional dysregulation), cognitive dysfunction, and functional impairment-accounting for > 700,000 annual suicide deaths worldwide [, ]. Its rising prevalence among adolescents (10–24 years) is of particular concern, given this critical neurodevelopmental period involving dynamic brain maturation and heightened environmental stress sensitivity [, ]. This population shows marked clinical heterogeneity, ranging from classic MDD to subtypes with non-suicidal self-injury (NSSI) or recurrent suicide attempts []. However, current neurobiological frameworks insufficiently explain the multidimensional molecular pathways underlying these divergent phenotypes []. Although monoamine dysregulation hypotheses have been proposed, these models remain insufficient to explain the pronounced clinical heterogeneity observed in adolescent depression [, ]. Notably, emerging biomarker research increasingly supports the existence of distinct molecular pathways underlying depressive subtypes. For example, peripheral biomarkers exhibit subtype-specific associations: circulating endocannabinoid levels inversely correlate with depression severity [], while discrete immune signatures are linked to suicidality among adolescents with internalizing symptoms [], underscoring the importance of immunological differentiation in the biological stratification of depressive presentations. Consistent with these findings, growing evidence implicates -linked glycosylation as a key regulator of neuroimmune signaling, synaptic plasticity, and neuronal excitability [, ]. Glycans modulate the folding, trafficking, and function of essential synaptic proteins—including serotonin, glutamate, and GABA receptors—as well as ion channels and neurotransmitter transporters [, ]. Mechanistically, sialylated glycans have been shown to regulate voltage-gated ion channel activity and neurotransmitter uptake, thereby influencing neuronal communication and stress responsiveness. Generally, these molecular effects from preclinical and in vitro studies suggest that glycosylation dynamics may play a critical role in regulating mood, which supports the hypothesis that glycosylation may act as a potential mediator involved in the pathophysiology of depressive disorders. However, this potential mediating role has not been empirically verified in clinical samples of adolescent depression.