scholarly journals New insights into the role of the GABAA–benzodiazepine receptor in psychiatric disorder

2001 ◽  
Vol 179 (5) ◽  
pp. 390-396 ◽  
Author(s):  
David J. Nutt ◽  
Andrea L. Malizia
Keyword(s):  
Molecular Biology ◽  
Molecular Basis ◽  
Current Knowledge ◽  
Molecular Genetic ◽  
Benzodiazepine Receptor ◽  
Receptor Complex ◽  
Genetic Studies ◽  
Substantial Growth ◽  
Disease States

BackgroundIn the 40 years since the first benzodiazepine was brought into clinical use there has been a substantial growth in understanding the molecular basis of action of these drugs and the role of their receptors in disease states.AimsTo present current knowledge about the role of the GABAA–benzodiazepine receptor in anxiety disorders, new insights into the molecular biology of the receptor complex and neuroimaging studies suggesting involvement of these receptors in disease states.MethodAn overview of published literature, including some recent data.ResultsThe molecular biology of this receptor is detailed. Molecular genetic studies suggesting involvement of the GABAA–benzodiazepine receptor in animal behaviour and learning are outlined; possible parallels with human psychopathology are discussed.ConclusionsCurrent insights into the role of the GABAA–benzodiazepine receptor in the action of benzodiazepines and as a factor in disease states, in both animals and humans, may lead to new, more sophisticated interventions at this receptor complex and potentially significant therapeutic gains.

scholarly journals MOLECULAR GENETIC STUDIES OF COMORBIDITY

2015 ◽  
Vol 14 (6) ◽  
pp. 94-102
Author(s):  
Ye. Yu. Bragina ◽  
M. B. Freidin
Keyword(s):  
Molecular Biology ◽  
Genetic Basis ◽  
Molecular Genetic ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Genetic Studies ◽  
Gene Environment ◽  
Genome Variations ◽  
Genetic Specificity

This review focuses at the problem of the genetic basis of comorbidity. We discuss the concepts and terms relating to combinations of diseases. The guidelines of the study of comorbidity using modern high throughput methods and approaches of genetics, molecular biology and bioinformatics are designated. In this review we present results of studies showing genetic specificity for the combined phenotypes dif-ferent from the isolated disease, we considergene-gene and gene-environment interactions in comorbidity. We also discuss the role of single nucleotide polymorphisms and structural genome variations in the development of comorbidity. Own results of researching shared genes of inversely comorbid diseases like as bronchial asthma and tuberculosis are presented.

scholarly journals Prospects for the Personalized Multimodal Therapy Approach to Pain Management via Action on NO and NOS

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2431
Author(s):  
Natalia A. Shnayder ◽  
Marina M. Petrova ◽  
Tatiana E. Popova ◽  
Tatiana K. Davidova ◽  
Olga P. Bobrova ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Molecular Genetic ◽  
Pain Syndrome ◽  
Medical Problem ◽  
Single Nucleotide Variants ◽  
Genetic Studies ◽  
Pain Syndromes ◽  
Nos Inhibitors ◽  
Peripheral Pain

Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Back pain, neuropathic pain, and posttraumatic pain are the most important pathological processes associated with chronic pain in adults. Standard approaches to the treatment of them do not solve the problem of pain chronicity. This is the reason for the search for new personalized strategies for the prevention and treatment of chronic pain. The nitric oxide (NO) system can play one of the key roles in the development of peripheral pain and its chronicity. The purpose of the study is to review publications devoted to changes in the NO system in patients with peripheral chronical pain syndromes. We have carried out a search for the articles published in e-Library, PubMed, Oxford Press, Clinical Case, Springer, Elsevier, and Google Scholar databases. The search was carried out using keywords and their combinations. The role of NO and NO synthases (NOS) isoforms in peripheral pain development and chronicity was demonstrated primarily from animal models to humans. The most studied is the neuronal NOS (nNOS). The role of inducible NOS (iNOS) and endothelial NOS (eNOS) is still under investigation. Associative genetic studies have shown that single nucleotide variants (SNVs) of NOS1, NOS2, and NOS3 genes encoding nNOS, iNOS, and eNOS may be associated with acute and chronic peripheral pain. Prospects for the use of NOS inhibitors to modulate the effect of drugs used to treat peripheral pain syndrome are discussed. Associative genetic studies of SNVs NOS1, NOS2, and NOS3 genes are important for understanding genetic predictors of peripheral pain chronicity and development of new personalized pharmacotherapy strategies.

scholarly journals The role of genetic research with family design in the study of affective disorders

2019 ◽  
pp. 106-108
Author(s):  
E. D. Kasyanov ◽  
G. E. Maso ◽  
A. O. Kibitov
Keyword(s):  
Affective Disorders ◽  
Bipolar Affective Disorder ◽  
Molecular Genetic ◽  
Genetic Research ◽  
Important Criterion ◽  
Genetic Studies ◽  
The Family ◽  
Polygenic Diseases ◽  
Potential Biomarkers

Affective disorders (recurrent depressive disorder and bipolar affective disorder) are multifactorial and polygenic diseases, which suggests the involvement of multiple neurobiological mechanisms. The phenotype of affective disorders is a heterogeneous group of clinically similar psychopathological symptoms, which also makes it difficult to detect potential biomarkers and new therapeutic targets. To study families at high risk of developing affective disorders using both clinical and molecular genetic approaches can help to study the neurobiological basis of depressive conditions, as well as to identify endophenotypes of affective disorders. The most important criterion for an endophenotype is its heritability, which can be proved only within the framework of the family design of the study. Comprehensive clinical and molecular genetic studies based on family design have the best prospects.

The human cortical autonomic network and volitional exercise in health and disease

2018 ◽  
Vol 43 (11) ◽  
pp. 1122-1130 ◽  
Author(s):  
Baraa K. Al-Khazraji ◽  
J. Kevin Shoemaker
Keyword(s):  
Current Knowledge ◽  
Insular Cortex ◽  
Cardiovascular Control ◽  
Anterior Cingulate ◽  
Disease States ◽  
Autonomic Activation ◽  
Imaging Research ◽  
Health And Disease ◽  
Cortical Regions

The autonomic nervous system elicits continuous beat-by-beat homeostatic adjustments to cardiovascular control. These modifications are mediated by sensory inputs (e.g., baroreceptors, metaboreceptors, pulmonary, thermoreceptors, and chemoreceptors afferents), integration at the brainstem control centres (i.e., medulla), and efferent autonomic neural outputs (e.g., spinal, preganglionic, and postganglionic pathways). However, extensive electrical stimulation and functional imaging research show that the brain’s higher cortical regions (e.g., insular cortex, medial prefrontal cortex, anterior cingulate cortex) partake in homeostatic regulation of the cardiovascular system at rest and during exercise. We now appreciate that these cortical areas form a network, namely the “cortical autonomic network” (CAN), which operate as part of a larger central autonomic network comprising 2-way communication of cortical and subcortical areas to exert autonomic influence. Interestingly, differential patterns of CAN activity and ensuing cardiovascular control are present in disease states, thereby highlighting the importance of considering the role of CAN as an integral aspect of cardiovascular regulation in health and disease. This review discusses current knowledge on human cortical autonomic activation during volitional exercise, and the role of exercise training on this activation in both health and disease.

Molecular breeding for improving heat stress tolerance in wheat.

2021 ◽  
pp. 82-89
Author(s):  
Kuo-hai Yu ◽  
Hui-ru Peng ◽  
Zhong-fu Ni ◽  
Ying-yin Yao ◽  
Zhao-rong Hu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Tolerance ◽  
Molecular Basis ◽  
Molecular Genetic ◽  
Wheat Breeding ◽  
Heat Response ◽  
Breeding Programmes ◽  
Resource Exploration ◽  
Heat Stress Tolerance

Abstract This paper discusses wheat responses to heat stress (including morphological and growth, cellular structure and physiological responses) and the molecular-genetic bases of heat response in wheat (including topics on mapping quantitative trait loci related to heat tolerance and the role of functional genes in response to heat stress). The improvement of heat tolerance of wheat by comprehensive strategies is also described. It is believed that with the emphasis on genetic resource exploration and with better understanding of the molecular basis, heat tolerance will be improved during wheat breeding programmes in the future.

Mechanism of action of β2-glycoprotein I-dependent lupus anticoagulants

Lupus ◽  
1998 ◽  
Vol 7 (2_suppl) ◽  
pp. 23-28 ◽  
Author(s):  
J Amout ◽  
J Vermylen
Keyword(s):  
Mechanism Of Action ◽  
Molecular Basis ◽  
Current Knowledge ◽  
Indirect Evidence ◽  
Integrated Model ◽  
Anticardiolipin Antibodies ◽  
Pathogenic Role ◽  
Lupus Anticoagulants ◽  
Glycoprotein I

There is accumulating evidence showing that lupus anticoagulants (LA) are more strongly associated with thrombosis than anticardiolipin antibodies. In addition, indirect evidence has been presented indicating that β2GPI-dependent LA are more strongly associated with thrombosis than prothrombin-dependent LA. From this, one may assume that anti-β2GPl antibodies with LA activity are more pathogenic than anti-β2GPI antibodies without LA activity. Therefore, it is of the utmost importance to understand the molecular basis on which some anti-β2GPI antibodies behave as LA. In this presentation, the current knowledge on the interaction of β2GPI with phospholipids and with anti-β2GPI antibodies is reviewed and an integrated model for the anti-β2GPI - dependent LA activity is proposed with implications for a pathogenic role of these particular antibodies.

scholarly journals The Role Of rs1799883 Polymorphism Of The FABP2 Gene In The Pathogenesis Of Nosological Syntropy Of Gallstone Disease And Metabolic Syndrome

2021 ◽  
Vol 03 (06) ◽  
pp. 46-51
Author(s):  
Raximov Anvar Pulatboevich ◽  
◽  
Ismailov O’ktam Safaevich ◽  
Batirov Davronbek Yusupovich ◽  
◽  
...  
Keyword(s):  
Gallstone Disease ◽  
Molecular Genetic ◽  
Case Control ◽  
Control Model ◽  
Molecular Medicine ◽  
Genetic Studies ◽  
Homozygous Genotype ◽  
Risk Of Disease ◽  
Fabp2 Gene

Objective: to study the role of the rs1799883 polymorphism of the FABP2 gene in the pathogenesis of gallstone disease in combination with MS. Material and methods. Molecular genetic studies were carried out in the Department of Molecular Medicine and Cell Technologies of the RSNPMC Hematology. The analysis of the associations of the rs1799883 polymorphisms of the FABP2 gene was carried out using a case-control model. The main group consisted of 118 patients with cholelithiasis in combination with MS living in the Khorezm region. Results: As a result of our research, we identified a significant association of the homozygous genotype for the Thr allele with the development of gallstone disease in combination with MS. The indicator of the ratio of the chances of developing gallstone disease in combination with MS in carriers of this genotype was OR = 2.9 at 95% CI: 1.122- 7.424. The relative risk of disease was RR = 2.5 with 95% CI: 1.11-5.76. Conclusion: Our results allow us to conclude that the homozygous Thr/Thr genotype plays an important role in the formation of gallstone disease and obesity in people of Uzbek nationality.

scholarly journals The Role of Brain-Derived Neurotrophic Factor in Mediating the Action of Antidepressants in the Treatment of Depression

2019 ◽  
Vol 74 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Tamara I. Vazagaeva ◽  
Roman V. Akhapkin ◽  
Yuri A. Alexandrovsky
Keyword(s):  
Neurotrophic Factor ◽  
Depressive Disorders ◽  
Therapeutic Response ◽  
Molecular Genetic ◽  
Genetic Studies ◽  
Trkb Receptor ◽  
Treatment Of Depression ◽  
Antidepressant Efficacy ◽  
Chronic Course

According to the neurotrophic hypothesis of depression proposed two decades ago, the most important role in the pathogenesis of depressive disorders is played by abnormalities in the maintenance of neuronal plasticity regulated by brain neurotrophic factor (BDNF). Although the decline in BDNF activity in depression is now widely documented, it remains unclear whether it is a factor contributing to the onset of depression, or a consequence of the chronic course of the disease. In preclinical studies, it was found that exogenous BDNF infusions causes antidepressant-like effects, prevents the depressogenic effects of chronic stress and increases cell survival in the hippocampus and the prefrontal cortex, but the mechanisms mediating these effects have not been fully studied. The results of molecular genetic studies confirmed that BDNF is essential in mediating the therapeutic effect of antidepressants, while the role of genetic polymorphisms in predicting antidepressant efficacy in depression remains uncertain. The mechanisms of action of monoaminergic antidepressants are related to their effect on the expression of BDNF and its TrkB receptor, however, apparently, the effect size varies for different drugs. Peripheral BDNF levels increase during treatment with antidepressants, and this increase is clearly observed only during the acute phase treatment of depression, but not during the period of maintenance therapy. The serum level of BDNF is a potentially useful marker for diagnosing depression and prediction of a therapeutic response.

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