Neuropharmacology of Depression: a Review
نویسنده
چکیده
The selected theories are based on studies investigating the possible role of stress hormones and cytokine; gammaaminobutyric acid (GABA); glutamate; monoaminergic transmitters such as serotonin, norepinephrine, dopamine; omega-3 fatty acid; Tcell; β-endorphine; synaptic plasticity; endocrine system and endocannabinoids in the pathophysiology of depression. Because all theories of depression apply to only some types of depressed patients but not others, and because depressive pathophysiology may vary considerably across the course of illness, the current extant knowledge argues against a unified hypothesis of depression. As a consequence, antidepressant treatments, including psychological and biological approaches, should be tailored for individual patients and disease states. Individual depression hypotheses based on neurobiological knowledge are discussed in terms of their interest to both clinicians in daily practice and clinical researchers developing novel therapies. INTRODUCTION: Major depressive disorder (MDD) is a common and costly disorder which is usually associated with severe and persistent symptoms leading to important social role impairment and increased mortality 1, 2 . It is one of the most important causes of disability worldwide 3 . The high rate of inadequate treatment of the disorder remains a serious concern 1 . The World Health Organization (WHO) defines depression as a common mental disorder characterized by sadness, loss of interest or pleasure, feelings of guilt or low self-worth, disturbed sleep or appetite, feelings of tiredness, and poor concentration 4 .
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