Depression stress-related

Titus GAL3 antagonists may represent an alternate class of therapeutic agents for the treatment of depression, anxiety, and stress-related disorders. 

Together, the anatomical data and the results from genetically modified animals support the idea that SP and other tael-derived neuropeptides, play a major role in stress responses, anxiety, and depression. Therefore, modulation of the SP-NKl system may have therapeutic value in the treatment of stress-related neuropsychiatric disorders. 

To summarize, there is now strong evidence that sleep disturbances encountered in major depression are associated with an increase of wake-promoting mechanisms linked to a stress-related hyperarousal reaction implicating the CRH and the LC-AN systems. 

Evidence suggesting an abnormality in immune function in those subject to severe stress or suffering from depression largely relates to an abnormality in function. Such abnormalities do not appear to occur in schizophrenia. Possibly because of its well-established genetic component, many aspects of the immune system would appear to be deranged in schizophrenic patients. Thus abnormalities in the concentration of serum immunoglobulins and deficiencies in immune responsiveness have been reported to occur in such patients. 

Jacobs N, Kenis G, Peeters F, Deron C, Vlietinck R, van Os J. Stress-related negative affectivity and genetically altered serotonin transporter function evidence of synergism in shaping risk of depression. Arch Gen Psychiatry 2006 63 989-96. 

Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry. 2006 59 1116-1127. Schmidt HD, Duman RS. The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-hke behavior. Behav. Pharmacol. 2007 18 391-418. 

Cumulatively, these data suggest that the development of therapeutic agents that are selective toward the c a-AR subtype, although devoid of effects at the a2C-AR subtype, would be valuable therapeutic agents in reducing stress-related depressive events in human beings. 

It is interesting to note the parallels observed when assessing the behavioral despair seen in a2A-AR / mice with the findings in the male tree shrew subordinate stress model these collective data suggest that chronic stress may (via an unknown mechanism) reduce beneficial effects of the a2A-AR in depression and stress, leading to behavioral despair, as witnessed in animals deficient for the oc2A-AR. Moreover, a2A-AR activation (or protection from downregulation) could offer a protective mechanism to combat stressful or stress-related events. 

I Adverse early experience— physical, emotional, or sexual abuse—may alter HPA axis function in a lasting way, conferring vulnerability to depression and stress-related disorders in adulthood. 

In addition, feelings of depression can often be overstated or understated because they reflect the definition and standards of normalcy within an individual s unique social and environmental context. As a first step toward acquiring effective treatment, a clear, concise, psychosocial-criteria-based diagnostic standard must be applied. All diagnostic interpretations must be sensitive to the influence of cultural and stress-related environmental and social factors. 

Benzodiazepine anxiolytics have been prescribed to almost anyone with stress-related symptoms, unhappiness or minor physical trauma. This kind of use is now considered unsuitable. Neither are they considered appropriate for treating depression, phobic or obsessional states or chronic psychosis. 

Aromatherapy is mostly applied to procure alleviation of chronic pain, depression, cognitive disorders, anxiety, insomnia, and stress-related disorders [48]. In this context, the influence of essential oils on the nervous system is studied [49]. Linalool-containing essences are traditionally used as sedatives, analgesics, and anxiolytics [50]. 

There is ample support for the hypothesis of noradrenergic system dysfunction in depression however, the inconsistencies in findings rule out any simple model of increased or decreased noradrenergic activity. It is important to determine which noradrenergic system abnormalities relate specifically to the pathogenesis of mood disorders, and which are related to nonspecific effects of stress, homeostatic mechanisms, or comorbid psychopathology. More work is needed on the mood-state-depen-dence of noradrenergic function. 

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