Recent advances in the study of the comorbidity of depressive and anxiety disorders

Abstract

Depressive and anxiety disorders often comorbid, which causes more severe impairments. The high comorbidity and shared genetic and psychological factors between the 2 disorders have brought arguments about whether they represent a common construct, and whether the current classification is meaningful. In this editorial, a state-of-the-art overview of recent studies on the underlying mechanism of such comorbidity, and the association between and differentiation of the 2 disorders is provided. Recent studies employing datadriven approaches such as latent class analysis (LCA) and network analysis to investigate the symptomatology of depression and anxiety have indicated unique characteristics and bridging symptoms of their comorbidity. Whereas previous neurobiological and neuroendocrinological studies reported common alterations in prefrontal-limbic pathways, serotonergic projections and the hypothalamic-pituitary-adrenal (HPA) axis, recent research suggests that distinct neural circuits and heterogeneous changes in HPA activity may exist in depression when compared to anxiety. Lastly, both depression and anxiety have been long associated with decision-making deficits; however, emerging evidence from computational psychiatry demonstrate that there may be unique neurocognitive and computational alterations in each disorder. By investigating the common and unique symptomatic characteristics and underlying neurobiological and neurocomputational mechanisms of the 2 disorders as well as their comorbidity, it can be concluded that recent studies have greatly advanced our understanding of the etiology and neuropathophysiology of these disorders.

Antidepressant Effect of Intermittent Long-Term Systemic Administration of Irisin in Mice

“…To shed light on the complex depression pathophysiology, a recent computational psychiatry approach was used to create mathematical models that mimicked the specific neural and/or cognitive functions of depressive behaviors and distinguished them from the anxiety ones [ 18 ].…”

The Relationship between Stress, Inflammation, and Depression

“…Thus, our findings support the notion that inflammation is the main pathway for stress-related diseases, such as depression, and that it contributes to disease progression by affecting the early course of the disease. The altered activity of the hypothalamic–pituitary–adrenal (HPA) axis, the weakened blood–brain barrier (BBB), and the facilitated passage of pro-inflammatory cytokines may be related to the serotonergic, noradrenergic, and dopaminergic dysfunction of major depression [ 176 , 177 , 178 ]. In addition, the tryptophan–kynurenine metabolic pathway is involved in the process of chronic neuroinflammation, which is associated with major depression, in the context of pro-inflammatory cytokines and the immune response [ 179 , 180 ].…”

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan–Kynurenine Metabolic System

“…The lifetime prevalence of MDD ranged from 2 to 21% [ 281 ]. The pathogenesis of depression has been linked to air pollution and depressive symptom frequently presents with cormobid conditions including anxiety, cognitive impairment, and chronic pain [ 282 , 283 , 284 , 285 ]. The monoamine hypothesis has prevailed for the pathogenesis of depression.…”