Table 1 Pathophysiology of depression
From: Antidepressants and type 2 diabetes: highways to knowns and unknowns
Mechanisms | Findings | Ref. |
|---|---|---|
Monoamine theory | Reduction monoamines (dopamine, 5HT, and noradrenaline) in the limbic system. Deficiency of noradrenergic system in depression. Decrease of central serotonergic turnover in depression. Transport proteins of monoaminergic transmissions are increased in depression. Inflammation contributes in the pathogenesis of depression. | Fasipe et al. [65], Ogłodek et al. [66] Li et al. [69] Borroto-Escuela [70]., Wang et al. [71]. Kayabaşı et al. [74]. Dowlati et al. [80]. |
Inflammatory theory | Depression is increased after interferon alpha (IFN-α) treatment. Pro-inflammatory cytokine levels are increased in patients with depression. Type I INF induces depression. Prolonged stress reduces concentration of brain-derived neurotrophic factor (BDNF). | Chiu et al. [81]. Petralia et al. [82]. Blank et al. [84]. Horowitz et al. [88]. |
Neuroendocrine theory | The neuroendocrine dysregulation induces changes in monoaminergic systems. Hypothalamic-pituitary-adrenal (HPA) axis is activated in depression. | Keller et al. [96]. Yu et al. [103]. |