International Multiconference “Bioinformatics of Genome Regulation and Structure\Systems Biology”

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Cognitive Science and Genomics symposium

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Cognitive Science and Genomics symposiumInterplay between 5-HT and BDNF system in recombinant mouse strain upon chronic fluoxetine administration

Interplay between 5-HT and BDNF system in recombinant mouse strain upon chronic fluoxetine administration

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Poster (download)

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Rodnyy A.Ya.1, Kondaurova E.M2, Antonov Y.V.3, Ilchibaeva T.V.4, Tsybko A.S.5, Naumenko V.S.6
1Institute of Cytology and Genetics Novosibirsk, Russia, aleksandr1994rodny@gmail.com
2Institute of Cytology and Genetics Novosibirsk, Russia, kond_em@bionet.nsc.ru
3Institute of Cytology and Genetics Novosibirsk, Russia, yegor@bionet.nsc.ru
4Institute of Cytology and Genetics Novosibirsk, Russia, rbicehok@mail.ru
5Institute of Cytology and Genetics Novosibirsk, Russia, antontsybko@bionet.nsc.ru
6Institute of Cytology and Genetics Novosibirsk, Russia, naumenko2002@bionet.nsc.ru

BDNF plays a key role in the development, differentiation, synaptogenesis and survival of brain neurons and in the processes of their adaptation to external impacts. Serotonergic (5-HT) system is another basic player in brain development and neuroplasticity. The study presents a comparative analysis of chronic fluoxetine treatment in recombinant mice differing in distal chromosome 13 fragment containing Htr1A gene of CBA mice strain on C57Bl6 genetic background. The problem here to be studied is mechanism of BDNF and 5-HT systems` interactions in antidepressant insensitivity. We measured mRNA and protein levels of BDNF, p75NTR, TrkB, 5-HT1A and 5-HT7 receptors, levels of 5-HT and its primary metabolite 5-Hydroxyindoleacetic acid (5-HIAA) in the brain structures that could have play primary role in mechanism of depression – frontal cortex and hippocampus. At the heart of the discussion are the different changes in BDNF system as well as in 5-HT system which allows us to conclude that the chronic fluoxetine injection increased depressive-like behavior in recombinant mice carrying distal chromosome 13 fragment containing Htr1A gene of CBA mice.

Cognitive Science and Genomics symposiumPossibilities of enhancing the neuroprotective effect of autophagy activation in the brain by stimulation of an mTOR-independent pathway of its regulation in a transgenic mouse model of Parkinson’s disease

Possibilities of enhancing the neuroprotective effect of autophagy activation in the brain by stimulation of an mTOR-independent pathway of its regulation in a transgenic mouse model of Parkinson’s disease

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Akopyan A.A.1, Pupyshev A. B2, Tikhonova M.A.3
1Scientific Research Institute of Physiology and Basic Medicine Novosibirsk, Russia, annaaleksanovna@mail.ru
2Scientific Research Institute of Physiology and Basic Medicine Novosibirsk, Russia, apupyshev@mail.ru
3Scientific Research Institute of Physiology and Basic Medicine Novosibirsk, Russia, mar-a-tikh@mail.ru

Autophagy induction promotes cell survival that is especially important for neurons which have a limited proliferative resource. Autophagy is regulated by the classical mTOR-dependent mechanism activated by rapamycin, and also via mTOR-independent pathways triggered by trehalose, lithium, metformin, etc. The neuroprotective effect was shown upon combined activation of these pathways in vitro. However, the possibilities of enhancing the therapeutic effect of autophagy activation in vivo remain unclear.

Transgenic mice of B6.Cg-Tg (Prnp-SNCA*A53T)23Mkle/J strain with overexpression of alpha-synuclein were used as a model of Parkinson’s disease (PD) in the study. In the striatum and substantia nigra, which are mainly affected in PD, trehalose caused an increase in autophagy, as measured by the expression of the autophagy marker LC3-II. Trehalose in combination with rapamycin increased LC3-II expression by two to three times in comparison with the action of rapamycin alone. In the frontal cortex no changes in LC3-II expression were observed neither under the action of trehalose nor with the combined treatment with trehalose and rapamycin. The most pronounced neuroprotective effect was observed upon the combined use of rapamycin and trehalose by the tyrosine hydroxylase expression in the nigrostriatal system marking the restoration of dopaminergic neurons. In the Rotarod test, the mice were tested for motor function. Animals treated with rapamycin, trehalose, or their combination stayed much longer on a rotating drum, compared to controls. Autophagy contribution to the therapeutic effects was confirmed by administration of autophagy inhibitor 3-methyladenine, which completely blocks the neuroprotective effects of the drugs.

Acknowledgments

This work was supportedВ  by a grant No. 16-04-01423 from
the Russian Foundation for Basic Research.

Cognitive Science and Genomics symposiumThe cross-talk molecular pathways of glutamate and leptin receptors

The cross-talk molecular pathways of glutamate and leptin receptors

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Anna L. Proskura1, Mariya Yu. Islamova2, Svetlana O. Vechkapova3
1The Institute of Computational Technologies of SB RAS, annleop@mail.ru
2The Institute of Computational Technologies of SB RAS, m.yu.islamova@gmail.com
3The Institute of Computational Technologies of SB RAS, svetavech@yandex.ru

The adipocyte-derived hormone leptin is an important regulator of body weight and metabolism through activation of brain leptin receptors expressed in different brain regions such as the hypothalamus. Moreover, it has pro-cognitive and anti-depressive effects in the central nervous system. Leptin receptor expressed in the different brain areas particularly hippocampus where are they had a modulating effect on the synaptic plasticity regulation, synaptogenesis and promotes hippocampal-dependent learning and memory. Leptin directly influences on the glutamate receptors recycling in the hippocampal CA1 field through PI3K-signalling pathway. To dissect the mechanisms by which leptin induced of synaptic PIP3 generation we analyzed proteins domains structure which to involve in the counter-regulation hippocampal excitatory synaptic network.

Cognitive Science and Genomics symposiumРЎognitive functions and polymorphism of the BDNF gene in patients with schizophrenia and healthy individuals

РЎognitive functions and polymorphism of the BDNF gene in patients with schizophrenia and healthy individuals

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Anastasiia Boiko1, Ekaterina Mikhalitskaya2, Elena Kornetova3, Svetlana Ivanova4
1Mental Health Research Institute Tomsk NRMC, anastasya-iv@yandex.ru
2Mental Health Research Institute Tomsk NRMC, uzen63@mail.ru
3Mental Health Research Institute Tomsk NRMC, kornetova@sibmail.com
4Mental Health Research Institute Tomsk NRMC, ivanovaniipz@gmail.com

In a number of schizophrenia concepts, the neurocognitive deficiency is distinguished to a separate domain along with positive and negative disorders and it is an important predictor of the unfavorable prognosis of the course of the disease and the development of persistent social dysfunction. The contribution of genetic mechanisms has been proven in the variability of attention instability and long-term memory impairment. Brain derived neurotrophic factor (BDNF) plays an important role in cell differentiation, survival, long-term potentiation, synaptic plasticity, learning and memory. The aim of the research is to study cognitive functions in patients with schizophrenia and healthy persons, and identify associations between cognitive function and polymorphism of BDNF gene. It was a complex clinical and biological examination of 550 patients with schizophrenia and 485 healthy persons. Significant differences in the distribution of genotypes of polymorphism rs6265 in patients with schizophrenia and healthy individuals were not found. Assessment of cognitive functions was carried out in 160 patients with schizophrenia and 106 healthy individuals using the BACS scale. The data obtained indicate that according to all BACS tests, the indicators of cognitive function in patients with schizophrenia are significantly worse than in healthy controls. Associations of genotypes of polymorphism rs6265 of the BDNF gene were detected by performing subtests of the BACS scale.

Cognitive Science and Genomics symposiumAltered expression of genes Npas4 and Nr1d1 in adult female mice with history of early-life stress

Altered expression of genes Npas4 and Nr1d1 in adult female mice with history of early-life stress

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[pdf-embedder url=”https://bgrssb.icgbio.ru/wp-content/uploads/2020/07/302.pdf”]
Yuliya Ryabushkina1, Vasiliy Reshetnikov2, Natalya Bondar3
1ICG SB RAS, Novosibirsk, Russia, ryabushkina@bionet.nsc.ru
2ICG SB RAS, Novosibirsk, Russia, vasiliyreshetnikov@bionet.nsc.ru
3ICG SB RAS, Novosibirsk, Russia, nbondar@bionet.nsc.ru

Stressful events early in life alter neuronal plasticity of the brain regions that regulate social behavior. Previous works have shown that brief and prolonged separation of pups from their mothers leads to enhanced social behavior in adult female mice. In this study, we performed Egr1, Npas4, Arc, and Homer1 gene expression level analysis in the prefrontal cortex and dorsal hippocampus of adult female mice after exposure to early life stress. Also was evaluated expression level of stress-related genes glucocorticoid and mineralocorticoid receptors (Nr3c1 and Nr3c2) as well as Nr1d1, which encodes a transcription factor REVERBО±, which regulates sociability and anxiety-related behavior. C57Bl/6 mice were exposed to maternal separation (MS, 3 h once a day) or handling (HD, 15 min once a day) on postnatal days 2 through 14. As adults, female mice behavior was analyzed by behavioral tests, on the day after last testing gene expression level analysis was performed. We found evaluation of Npas4 expression in prefrontal cortex and Nr1d1 both in prefrontal cortex and dorsal hippocampus of adult female mice of MS group, not in HD group. The expression of stress-related genes Nr3c1 and Nr3c2 was unchanged in both groups. This upregulation of Npas4 and Nr1d1 genes in female mice with stressful events early in life and enhanced social behavior may be an adaptation mechanism reversing possible aberrations caused by early-life stress.

Cognitive Science and Genomics symposiumAssociations of polymorphic variants of the genes of neurotrophic factors BDNF, NGF, NRG1 with remission in patients with depressive disorders

Associations of polymorphic variants of the genes of neurotrophic factors BDNF, NGF, NRG1 with remission in patients with depressive disorders

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Natalia Vyalova1, German Simutkin2, Nikolay Bokhan3, Svetlana Ivanova4
1Mental Health Research Institute of the Federal State Budget Scientific Institution \”Tomsk National Research Medical Center of the Russian Academy of Sciences\”, Natarakitina@yandex.ru
2Mental Health Research Institute of the Federal State Budget Scientific Institution \”Tomsk National Research Medical Center of the Russian Academy of Sciences\”, ggsimutkin@gmail.com
3Mental Health Research Institute of the Federal State Budget Scientific Institution \”Tomsk National Research Medical Center of the Russian Academy of Sciences\”, bna909@gmail.com
4Mental Health Research Institute of the Federal State Budget Scientific Institution \”Tomsk National Research Medical Center of the Russian Academy of Sciences\”, ivanovaniipz@gmail.com

The investigation the relationship between BDNF, NGF and NRG1 genotypes with remission in patients with MDD was made in a group of 208 patients. The study showed that rs3924999 of the NRG1 gene was associated with clinical remission, rated on the HDRS-17 scale on day 28 of antidepressant therapy.

Cognitive Science and Genomics symposiumCompulsive-like behaviors in DISC1-mice

Compulsive-like behaviors in DISC1-mice

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[pdf-embedder url=”https://bgrssb.icgbio.ru/wp-content/uploads/2020/07/355.pdf”]
Nadezhda Chizhova1, Kristina Smirnova2
1ICG SB RAS, chnadezhda1995@gmail.com
2NSU, PhBMRI, vedelina@mail.ru

The DISC1 gene is associated with the development of mental disorders in humans. Currently a number of genetic models of psychopathologies withВ  mutations in the gene have been created, including genetic lines of mice with point mutations DISC1-Q31L-/- (model of depression) and DISC1-L100P-/- (model of schizophrenia), which are available at the unique scientific installation “Biological collection – genetic biomodels of neuropsychiatric diseases” (State Scientific-Research Institute of Physiology and Basic Medicine, Novosibirsk). In additional mice DISC1-Q31L-/- showed compulsive-like behavior, and in this connection was proposed to study this type of behavior in heterozygotes and diheterozygotes for these mutations. The work performed allows us to conclude that the presence of only one mutant allele (both DISC1-Q31L and DISC1-L100P) is not sufficient for the expression of compulsive-like behavior in mice. However, mice that combine both mutations are predisposed to this behavior and exhibit it depending on their sex and mother’s genotype: this behaviour characterise males whose mothers were homozygous for DISC1-Q31L mutation, and females whose mothers were homozygous for DISC1-L100P mutation. The conclusion about the influence of homozygosity and, accordingly, the behavior of mothers on the compulsive-like behavior of females and males can be verified in further experiments.

Cognitive Science and Genomics symposiumReconstruction of Dementia Gene Network Using Online Bioinformatics Tools

Reconstruction of Dementia Gene Network Using Online Bioinformatics Tools

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Oleg Fateev1, Sergey S. Kovalev2, Yuriy L. Orlov3
1I.M.Sechenov First Moscow State Medical University, Moscow, Russia, fodmr1997@gmail.com
2Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia, kovalev@bionet.nsc.ru
3Institute of Digital Medicine I.M.Sechenov First Moscow State Medical University), Moscow, Russia, orlov@bionet.nsc.ru

In this work, the set of genes associated with mental diseases such as dementia was examined and analyzed using previously developed gene ontology annotation tools and databases. The aim of the study is to describe the molecular mechanisms of dementia based on the analysis of the gene set as a whole, using available bioinformatics databases, annotation and recent publications. Dementia is a chronic, general, usually irreversible decrease in cognitive function that affects all aspects of cognitive activity. The enriched gene ontology categories for dementia genes are regulation of neuronal death, regulation of cell death, organization of cellular components, and cognition. The study of the structure of the gene network shows a high connectivity of genes and their products.

Cognitive Science and Genomics symposiumStudy of personal qualities and EEG activity in a stop signal paradigm in residents of northern regions

Study of personal qualities and EEG activity in a stop signal paradigm in residents of northern regions

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Tatiana Asakhova1, Alexander Saprigyn2, Sergey Tamozhnikov3, Alexandra Karpova4, Natalya Borisova5, Elena Afanaseva6, Alexander Savostyanov7
1NSU, Novosibirsk, Russia, t.astakhova@g.nsu.ru
2State Scientific-Research Institute of Physiology & Basic Medicine, Novosibirsk, Russia, saprigyn@mail.ru
3State Scientific-Research Institute of Physiology & Basic Medicine, Novosibirsk, Russia, stam@physiol.ru
4North-Eastern Federal University, Yakutsk, Russia, karpova74@list.ru
5North-Eastern Federal University, Yakutsk, Russia, borinat@yandex.ru
6North-Eastern Federal University, Yakutsk, Russia, eb.afanaseva@mail.ru
7State Scientific-Research Institute of Physiology & Basic Medicine, Novosibirsk, Russia ICG SB RAS, Novosibirsk, Russia NSU, Novosibirsk, Russia, alexander.savostyanov@gmail.com

It is known that the adaptation to new conditions depends on personality traits. The results obtained showed that the lower level of anxiety and neurotism, the better behavioural control and adaptation. Also, the adaptation level is the lowest right after the move to another place, and it grows by the time along with the growth of behavioral control.