Research Topic

Pathophysiology and molecular mechanisms of co-morbid depression

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The WHO estimates that 450 million people worldwide suffer from mental disorders (2010). The socioeconomic impact resulting from mental health related issues constitutes a burden greater than the combined devastation produced by cardiovascular disease and cancer. Thus, effective management and treatment of ...

The WHO estimates that 450 million people worldwide suffer from mental disorders (2010). The socioeconomic impact resulting from mental health related issues constitutes a burden greater than the combined devastation produced by cardiovascular disease and cancer. Thus, effective management and treatment of mental health concerns, is of critical importance not only to the sufferers, but to society more generally. However, the management of neuropsychiatric conditions presents significant challenges for healthcare professionals. Importantly, psychiatric disorders demonstrate significant comorbidity with a breadth of conditions. This complicates the clinical situation as the development of co-morbid psychiatric symptoms in addition to the primary diagnosis, mandates careful consideration of drug-drug interactions and contraindications. It is crucial that healthcare professionals recognise the importance of addressing any neuropsychiatric symptoms, as improved quality of life through effective treatment not only improves functional outcomes for patients but may also translate to tremendous health economic savings for society-at-large. (Goldston & Baillie, Clin Psych Rev 2007; Lichtman et al, Circulation 2008, Compare A, Front Psychol 2013).

Co-morbid depression is a common clinical observation. It has been reported to develop in association with a myriad of conditions including ischemic stroke, cardiovascular disease, hypertension, HIV, withdrawal from addictive substances, autoimmune diseases, schizophrenia, neurodegenerative diseases, and even childbirth. While the development of depression may be argued to be a psychological response to the primary condition in some instances, there is growing evidence that disease-related physiological and biochemical changes detected in patients are causative. Observations of primary clinical pathology may initiate further investigations of the biochemical events that a secondary disorder (depressive mood disorders), and how these events may inform future strategies for drug development and treatment of the conditions.

The goal of this research topic is to unify investigative efforts seeking to highlight diseases which are associated with a higher incidence of neuropsychiatric co-morbidity, and investigate the molecular pathology underlying this association. While the primary neuropsychiatric symptom of interest is depression, other symptoms such as anxiety and social withdrawal are also of interest. To generate broad interest in this topic, we propose a wide scope for submitted manuscripts which may range from epidemiological studies reporting altered rates of psychiatric symptoms in patient groups, and clinical studies linking the primary condition with higher incidence of neuropsychiatric symptoms (e.g. qualitative measurements linked with imaging studies or peripheral biomarkers), to investigative work in animal models, providing more causal evidence for the association. Animal model studies should, ideally, utilise models which were not originally developed to study major depressive disorder but have since been discovered to manifest a behavioural phenotype suggestive of depression-related behaviours (e.g. withdrawal from addictive substances). Such studies may probe the reported behavioural perturbations with behavioural and environmental interventions, pharmacological challenges or therapeutics, and proteomic or genomic profiling of molecular deficits associated with the phenotype.


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