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Introduction Depression in women is supported by specific psychoendocrine factors. Neuroprotection is reduced in conditions of exposure to psychostress by increase of endogenous cortisol due to excessive HPA activity associated with somatic risks. Decrease of neuroprotection after hypercortisolemia due to excessive HPA activity is associated with somatic obvious risks that may cause an increase in social malfunction of women with depression. Material and methods Retrospective-prospective study on a sample of 206 female patients, with positive history for depressive disorder, hospitalized in the Mental Health Center (MHC) of Craiova, monitored between January, 1st 2012 and June, 31st 2012. At these patients we evaluated depression evolution, somatic comorbidities, cognitive impairment and psychosocial stress. Results Somatic comorbidities (obesity and cardiovascular disease, 41 patients - 19.9%, obesity and diabetes and metabolic syndrome, 36 patients - 17.5%, hysterectomy, 35 patients - 17.5%) occurred during maintenance therapy emphasizes evolutionary risk of depressive disorder in women and cognitive impairment, especially in peri- and postmenopausal period (68.6%). Appeared in a large number of cases of the syndrome MCI (Mild Cognitive Impairment) (29 patients - 14.1%) and 4 cases of Alzheimer's disease also increase the predictive value of perimenopausal depression and psychostress conditions (13.1%). Conclusions Vulnerability to depression is correlated with peri- and postmenopausal ovarian steroid imbalance favoring the disruption of brain neurotransmission. Excess of serotonin activating substance therapy may promote the emergence of hypodopaminergy with risk of increased somatic and cognitive deficiency. Hypodopaminergy conduced to an increased glutamatergic activity, with significant decreases in neuroprotection and neurodegenerative risk. |
