BackgroundCoping with stress is defined as all activities undertaken by a human in a stressful situation. The effect of stress on depression, its role in triggering the subsequent phases of the disease, and the factors that mediate the stress-depression relationship become more and more often subjects of research in psychiatry and psychology. Factors important for the formation of depressive symptoms and disease progression are significantly associated with coping strategies used in the face of stress.The main aim of the study was to evaluate the most popular strategies of coping with stress in people with depression in comparison to healthy subjects.Material/MethodsInitial research was carried on 80 patients aged from 20 to 66 years with a diagnosis of depression. The control group consisted of 30 healthy subjects aged 22 to 57 years. Analysis of the most popular strategies of coping with stress was performed with the Multiphasic Inventory for Measuring Coping (COPE) by Carver, Scheier, and Weintraub.ResultsIn contrast with healthy people, patients with depression in stressful situations more often use strategies based on avoidance and denial and have more difficulties in finding positive aspects of stressful events.ConclusionsDepression may be an important factor in the negative assessment of one’s own ability to cope with difficult situations and can aggravate a tendency to perceive stressful events as overwhelming.
Data show that up to 38.2% of the European population have a mental disorder and that recurrent depressive disorder (rDD) is among the most commonly diagnosed disabling diseases. Over the last few years, neurocognitive impairments in rDD have become a new research front focusing on the role of cognitive decline during the course of rDD and in relation to its clinical presentation and prognosis. Both immune-inflammatory and oxidative and nitrosative stress (O&NS) processes potentially play a role in development of cognitive dysfunction in rDD. New evidence shows that chronic inflammatory and O&NS reactions occur in the brains of patients with neurodegenerative disorders and those with rDD. This narrative review presents the current state of knowledge on the possible impact of selected inflammatory and O&NS enzymes on cognitive functioning in patients with rDD. We focus on manganese superoxide dismutase (MnSOD), inducible nitric oxide synthase (iNOS), and myeloperoxidase (MPO).
BackgroundRecurrent depressive disorder is a multifactorial disease; one of the typical features is cognitive impairment. The purpose of this study was analysis of ASMT gene expression both on mRNA and protein levels in patients with recurrent depressive disorder (rDD) and assessment of the relationship between plasma level of ASMT protein, gene expression on mRNA level, and cognitive performance.Material/MethodsThe study included 236 subjects: patients with rDD (n=131) and healthy subjects (n=105, CG). Cognitive function assessment was based on: Trail Making Test, The Stroop Test, Verbal Fluency Test (VFT), and Auditory Verbal Learning Test (AVLT).ResultsBoth mRNA and protein expression levels of ASMT gene were significantly higher in healthy subjects when compared to rDD. The average ASMT mRNA expression level measured for the entire group was M=0.21 (SD=0.09), and the protein level was M=12.84 (SD=3.29). In patients with rDD, statistically significant correlations occurred between both mRNA and protein expression levels and part A of the TMT (negative correlation) and verbal fluency test (positive correlation). In the group CG, there was no statistically significant association between the analyzed variables. In the entire group there was a statistically significant correlation between both ASMT mRNA and protein expression levels and all the neuropsychological tests used in the survey.Conclusions1. Our study confirms previous results showing decreased mRNA and protein expression levels of ASMT gene in depression. 2. Our data suggest a relationship between decreased mRNA and protein expression levels of ASMT gene and cognitive impairment.
Cel pracyCelem tej pracy było zbadanie roli genu Dvl3 w etiologii zaburzeń depresyjnych poprzez porównanie ekspresji genu Dvl3 na poziomie mRNA i białka jak i polimorfizmu w locus rs 1969253 w obrębie intronu genu Dvl3 u pacjentów z depresją w odniesieniu do osób zdrowych oraz poszukiwanie zmiennych klinicznych mających związek z polimorfizmem lub ekspresją badanego genu.MetodaBadaniami objęto grupę 181 osób z rozpoznaniem zaburzeń depresyjnych nawracających lub epizodu depresyjnego. Grupę kontrolną stanowiły 102 zdrowe osoby. Od wszystkich uczestników pobrano próbki krwi obwodowej celem pomiaru poziomu ekspresji genu Dvl3 na poziomie mRNA i białka jak i polimorfizmu w locus rs 1969253. Od pacjentów zebrano przy włączeniu do badania dane dotyczące płci, wieku, przebiegu choroby a także zbadano natężenie objawów depresyjnych za pomocą Skali Depresji Hamiltona. Uzyskane dane opracowano statystycznie.WynikiU pacjentów z depresją stwierdzono istotne statystycznie obniżenie ekspresji Dvl3 na poziomie mRNA i białka względem zdrowych uczestników. Na ekspresję genu Dvl3 u pacjentów z depresją nie miały wpływu płeć, wiek, liczba epizodów, nasilenie objawów, czas trwania choroby lczy wiek wystąpienia pierwszego epizodu. Ocena polimorfizmu w locus rs 1969253 wykazała, że osoby z genotypem CA i CC miały ponad trzykrotnie wyższe ryzyko zachorowania na depresję w porównaniu z osobami o genotypie AA (OR = 3,3 ,% CI = 1,56-6,99). Nie obserwowano natomiast zależności między badanym polimorfizmem a analizowanymi zmiennymi klinicznymiWnioskiZmiany ekspresji i polimorfizm genu Dvl3 mogą mieć istotny związek z mechanizmami patogenetycznymi występującymi w przebiegu zaburzeń depresyjnych.
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