Post-traumatic stress disorder (PTSD) is a well-known psychiatric disorder that affects millions of people worldwide. Pharmacodynamic and cognitive-behavioral therapies (CBT) have been used to treat patients with PTSD. However, it remains unclear whether there are concurrent changes in psychopathological and neurophysiological factors associated with PTSD patients. Past reports described those PTSD patients with efficient fatty acid metabolism, neurogenesis, mitochondrial energy balance could improve ability to cope against the conditioned fear responses and traumatic memories. Furthermore, cognitive, behavioral, cellular, and molecular evidence can be combined to create personalized therapies for PTSD sufferers either with or without comorbidities such as depression or memory impairment. Unfortunately, there is still evidence lacking to establish a full understanding of the underlying neurophysiological and psychopathological aspects associated with PTSD. This review has extensively discussed the single nucleotide polymorphism (SNPs) of genetic factors to cause PTSD, the implications of inflammation, neurotransmitter genomics, metabolic alterations, neuroendocrine disturbance (hypothalamus-pituitary-adrenal (HPA) axis), mitochondrial dynamics, neurogenesis, and premature aging related to PTSD-induced psychopathology and neurophysiology. In addition, the review delineated the importance of CBT and several pharmacodynamic therapies to mitigate symptomatology of PTSD.
Addictive behavioral disorders are multifactorial diseases with clinical, neurophysiological, and genetic heterogeneity, a high comorbidity with other disorders, and a low curability. The etiopathogenetic mechanisms of non-chemical forms of addictive behavior have not been sufficiently studied, which makes it difficult to search for effective therapeutic procedures.Objective: to study the psychological and genetic components of a non-chemical addictive disorder as the phenomenon of codependency.Patients and methods. The investigation enrolled 256 women who were divided into three comparison groups: 1) those with the phenomenon of codependency, 2) phenotypically healthy women; 3) a population sample. Psychometric testing was carried out using the «Hand Test» by E. Wagner (adapted by A.I. Gerasimov and S.N. Enikolopov) and the clinical and genealogical characteristics of women with the phenomenon of codependency were studied. Results and discussion. There was a statistically significant predominance of the level of aggressiveness as autoaggression in the structure of the personality profile of women with the phenomenon of codependency (t=2.924–3.015; p=0.004–0.005). The clinical and genealogical characteristics of persons with addictive behavioral disorder as the phenomenon of codependency suggest that there is a statistically significantly high frequency of secondary alcoholism among first-degree and second-degree relatives or both and first-degree male relatives (p<0.001).Conclusion. The phenomenon of codependency as a non-chemical addiction includes psychological and genetic components. Women with codependency had autoaggressive destructive behavior patterns and a family history of alcoholism. The identified psychogenic characteristics can be considered as a risk for an addictive disease and somatoform disorders.
Background: pathogen heterogeneity and complexity are the main obstacles for schizophrenia and autism spectrum disorders (ASD) differential diagnosis in children. The role of oxidative stress in the molecular mechanisms of schizophrenia and autism pathogenesis is beyond doubt. Free radicals that accumulate during stress can cause oxidative modifications and the formation of breaks in the сell-free DNA (cfDNA) and nuclear DNA of blood cells. To date, it has been proven that 8-hydroxy-2’- deoxyguanosine (8-OHdG) can be considered as an oxidative stress biomarker. However, it is still unclear how pronounced the genotoxic consequences of oxidative stress are in ASD of varying severity and in childhood onset schizophrenia (COS). Objective: to study the relationship between the oxidative DNA damage level in peripheral blood cells and the circulating cell-free DNA characteristics with the severity of COS and the course of ASD in children. Patients and methods: blood samples of 96 patients with childhood autism (CA — F84.0 according to ICD-10), atypical autism (AA — F84.1 according to ICD-10) and with childhood onset schizophrenia (COS — F20.8 according to ICD-10) were obtained from the Child Psychiatry Department of the Mental health research center. Blood samples of the control group (34 people) — from the collection of samples of the Research Centre for medical Genetics. The selection of patients was carried out using the clinical and psychopathological method. Cell-free DNA was isolated by extraction with organic solvents. The concentration of cfDNA was determined fluorimetrically. The level of 8-OHdG in cell-free DNA was determined by binding of the corresponding antibodies on membrane filters, endonuclease activity was determined by radial diffusion in a gel. G0-peripheral blood lymphocytes were isolated by gradient centrifugation. The level of 8-OHdG and the level of the phosphorylated form of histone H2AX (yH2AX) in G0-peripheral blood lymphocytes were analyzed in fixed cells by flow cytofluorometry using appropriate antibodies. Statistical processing was carried out using Microsoft Office Excel, Statistica 6.0, StatGraph. Results and conclusions: oxidative stress has different severity in ASD, occurring in severe form (AA) and mild/moderate form (CA). In CA, the level of oxidative damage to the DNA of lymphocytes tends to increase, but does not reach statistically significant level; the level of oxidative damage to cfDNA does not differ from the control. In AA and, to an even stronger extent, in COS, the level of oxidative damage to the DNA of cells and cfDNA is significantly increased, which indicates the development of systemic oxidative stress, which is not compensated by the body’s antioxidant system. The level of 8-OHdG in the composition of the cfDNA and DNA of the nuclei of peripheral blood cells can be a marker of oxidative stress, which is important not only for diagnosing the severity of the pathological process, but also for treatment regimens development for COS and ASD in children.
Мутации в гене GRIN2A встречаются у пациентов с детской идиопатической эпилепсией. Основными симптомами заболевания являются приобретённая афазия, слуховая агнозия, дизартрия, диспраксия как у гомо-, так и у гетерозигот. В данной работе был проведён поиск вариантов гена GRIN2A у пациента с детской эпилепсией, сопровождающейся задержкой развития, в результате чего была обнаружена мутация, приводящая к развитию патологического фенотипа. A mutation in the GRIN2A gene occurs in patients with pediatric idiopathic epilepsy. The main symptoms of the disease are acquired aphasia, auditory agnosia, dysarthria, dyspraxia with both homo- and heterozygotes. In this work a search for a variants of the GRIN2A gene was made by a patient with child epilepsy, accompanied by a developmental delay, as a result of which a mutation was detected, that led to the development of a pathological phenotype.
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