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  • 1
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    Data_Sheet_1.xlsx
    Frontiers Media SA ; 2022
    In:  Frontiers in Molecular Neuroscience Vol. 15 ( 2022-10-24)
    Details
    In: Frontiers in Molecular Neuroscience, Frontiers Media SA, Vol. 15 ( 2022-10-24)
    Abstract: Background: The amygdala is crucial for emotional cognitive processing. Affective or emotional states can bias cognitive processes, including attention, memory, and decision-making. This can result in optimistic or pessimistic behaviors that are partially driven by the activation of the amygdala. The resulting emotional cognitive bias is a common feature of anxiety and mood disorders, both of which are interactively influenced by genetic and environmental factors. It is also known that emotional cognitive biases can be influenced by environmental factors. However, little is known about the effects of genetics and/or gene-environment interactions on emotional cognitive biases. We investigated the effects of the genetic background and environmental enrichment on the transcriptional profiles of the mouse amygdala following a well-established cognitive bias test. Methods: Twenty-four female C57BL/6J and B6D2F1N mice were housed either in standard (control) conditions or in an enriched environment. After appropriate training, the cognitive bias test was performed on 19 mice that satisfactorily completed the training scheme to assess their responses to ambiguous cues. This allowed us to calculate an “optimism score” for each mouse. Subsequently, we dissected the anterior and posterior portions of the amygdala to perform RNA-sequencing for differential expression and other statistical analyses. Results: In general, we found only minor changes in the amygdala’s transcriptome associated with the levels of optimism in our mice. In contrast, we observed wide molecular effects of the genetic background in both housing environments. The C57BL/6J animals showed more transcriptional changes in response to enriched environments than the B6D2F1N mice. We also generally found more dysregulated genes in the posterior than in the anterior portion of the amygdala. Gene set overrepresentation analyses consistently implicated cellular metabolic responses and immune processes in the differences observed between mouse strains, while processes favoring neurogenesis and neurotransmission were implicated in the responses to environmental enrichment. In a correlation analysis, lipid metabolism in the anterior amygdala was suggested to influence the levels of optimism. Conclusions: Our observations underscore the importance of selecting appropriate animal models when performing molecular studies of affective conditions or emotional states, and suggest an important role of immune and stress responses in the genetic component of emotion regulation.
    Type of Medium: Online Resource
    ISSN: 1662-5099
    URL: Article
    URL: Article
    DOI: 10.3389/fnmol.2022.1025389
    DOI: 10.3389/fnmol.2022.1025389.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2452967-9
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  • 2
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    Isolation of Vibrio cholera El Tor Inaba from Lemna minor and Eichhornia crassipens Roots in Veracruz, Mexico
    Briefland ; 2014
    In:  Jundishapur Journal of Microbiology Vol. 7, No. 3 ( 2014-03-01)
    Details
    In: Jundishapur Journal of Microbiology, Briefland, Vol. 7, No. 3 ( 2014-03-01)
    Type of Medium: Online Resource
    ISSN: 2008-3645 , 2008-4161
    URL: Journal
    URL: Article
    DOI: 10.5812/jjm
    DOI: 10.5812/jjm.6855
    Language: Unknown
    Publisher: Briefland
    Publication Date: 2014
    detail.hit.zdb_id: 2815501-4
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  • 3
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    Table_1.XLSX
    Frontiers Media SA ; 2022
    In:  Frontiers in Nutrition Vol. 9 ( 2022-7-1)
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    In: Frontiers in Nutrition, Frontiers Media SA, Vol. 9 ( 2022-7-1)
    Abstract: During early phases of life, such as prenatal or early postnatal development and adolescence, an organism's phenotype can be shaped by the environmental conditions it experiences. According to the Match-Mismatch hypothesis (MMH), changes to this environment during later life stages can result in a mismatch between the individual's adaptations and the prevailing environmental conditions. Thus, negative consequences in welfare and health can occur. We aimed to test the MMH in the context of food availability, assuming adolescence as a sensitive period of adaptation. Methods We have previously reported a study of the physiological and behavioral effects of match and mismatch conditions of high ( ad libitum ) and low (90% of ad libitum intake) food availability from adolescence to early adulthood in female C57BL/6J mice ( n = 62). Here, we performed RNA-sequencing of the livers of a subset of these animals ( n = 16) to test the effects of match and mismatch feeding conditions on the liver transcriptome. Results In general, we found no effect of the match-mismatch situations. Contrarily, the amount of food available during early adulthood (low vs. high) drove the differences we observed in final body weight and gene expression in the liver, regardless of the amount of food available to the animals during adolescence. Many of the differentially expressed genes and the corresponding biological processes found to be overrepresented overlapped, implicating common changes in various domains. These included metabolism, homeostasis, cellular responses to diverse stimuli, transport of bile acids and other molecules, cell differentiation, major urinary proteins, and immunity and inflammation. Conclusions Our previous and present observations found no support for the MMH in the context of low vs high food availability from adolescence to early adulthood in female C57BL/6J mice. However, even small differences of approximately 10% in food availability during early adulthood resulted in physiological and molecular changes with potential beneficial implications for metabolic diseases.
    Type of Medium: Online Resource
    ISSN: 2296-861X
    URL: Article
    URL: Article
    DOI: 10.3389/fnut.2022.910762
    DOI: 10.3389/fnut.2022.910762.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2776676-7
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  • 4
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    Tau, APP, NCT and BACE1 in lymphocytes through cognitively normal ageing and neuropathology
    FapUNIFESP (SciELO) ; 2013
    In:  Anais da Academia Brasileira de Ciências Vol. 85, No. 4 ( 2013), p. 1489-1496
    Details
    In: Anais da Academia Brasileira de Ciências, FapUNIFESP (SciELO), Vol. 85, No. 4 ( 2013), p. 1489-1496
    Abstract: Embora a doença de Alzheimer seja um distúrbio do cérebro, uma série de alterações periféricas têm sido encontradas nesses pacientes; no entanto, pouco se sabe sobre como os genes envolvidos na fisiopatologia se expressam nas células periféricas, tais como em linfócitos durante o envelhecimento normal em comparação com o neuropatológico. Analisamos por RT-PCR a expressão dos genes de tau, da proteína precursora do amilóide, de nicastrin e da enzima de clivagem do sítio β da APP, em linfócitos de um pequeno grupo de pacientes com início tardio da Doença de Alzheimer, de um grupo de pacientes idosos que sofrem de doenças neuropsicológicas diferentes de Alzheimer, e de um grupo de indivíduos cognitivamente saudáveis, divididos em quatro grupos por idade. Também foram investigadas as correlações entre a expressão dos genes e os níveis de pressão arterial, glicose, colesterol total e triglicérides, como fatores de risco para doença de Alzheimer. Os resultados mostram a ausência de expressão de tau em linfócitos, a ausência de detecção da expressão do gene de nicastrina em pacientes com Alzheimer, e a correlação entre as condições médicas estudadas e a expressão gênica nos linfócitos. Acreditamos que a expressão de nicastrin em linfócitos deve ser considerada de interesse para análises em uma população mais ampla, para investigar se ela pode representar um potencial biomarcador para diferenciar a doença de Alzheimer de outros distúrbios neuropsicológicos.
    Type of Medium: Online Resource
    ISSN: 0001-3765
    URL: Article
    DOI: 10.1590/0001-376520130013
    Language: Unknown
    Publisher: FapUNIFESP (SciELO)
    Publication Date: 2013
    detail.hit.zdb_id: 2046885-4
    SSG: 11
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  • 5
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    Abeta(1-42) induces abnormal alternative splicing of tau exons 2/3 in NGF-induced PC12 cells
    FapUNIFESP (SciELO) ; 2014
    In:  Anais da Academia Brasileira de Ciências Vol. 86, No. 4 ( 2014-12), p. 1927-1934
    Details
    In: Anais da Academia Brasileira de Ciências, FapUNIFESP (SciELO), Vol. 86, No. 4 ( 2014-12), p. 1927-1934
    Abstract: Proteína Tau desempenha um papel crucial na fisiopatologia da doença de Alzheimer, onde sua hiper-fosforilação promove agregação e desestabilização de microtúbulo. Tau submete-se a splicing alternativo que gera seis isoformas no cérebro humano, devido a inclusão/exclusão dos exons 2, 3 e 10. A desregulação do processo de splicing do exon tau 10 é suficiente para causar Taupatia e mostrou-se ser influenciado por peptídeos beta-amilóides, entretanto o splicing de outros exons é menos estudado. Nós estudamos os efeitos da beta-amiloide(42) no splicing alternativo de exons tau 2/3 e 6, usando células PC12 não tratadas ou estimuladas pelo fator de crescimento do nervo. A exposição de beta-amilóide levou processos celulares formados a retrair em células diferenciadas e alterou a expressão de exons 2/3 tanto em células indiferenciadas como diferenciadas. A expressão do exon 6 foi reprimida apenas em células indiferenciadas. Nossos resultados sugerem que beta-amilóide interfere com o processo de splicing de exons 2/3, favorecendo a sua exclusão e, portanto, a expressão de isoformas imaturas de tau que são menos eficientes em estabilizar microtúbulos e também podem ser mais propensas a hiper-fosforilação. O mecanismo molecular para essa interação amilóide-tau permanece a ser determinado, mas pode ter implicações potenciais para a compreensão dos processos neuropatológicos fundamentais na doença de Alzheimer.
    Type of Medium: Online Resource
    ISSN: 0001-3765
    URL: Article
    DOI: 10.1590/0001-3765201420130333
    Language: Unknown
    Publisher: FapUNIFESP (SciELO)
    Publication Date: 2014
    detail.hit.zdb_id: 2046885-4
    SSG: 11
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  • 6
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    Table_1.XLSX
    Frontiers Media SA ; 2023
    In:  Frontiers in Neurology Vol. 14 ( 2023-3-8)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 14 ( 2023-3-8)
    Abstract: The measurement of neurofilament light chain (NfL) in blood is a promising biomarker of neurological injury and disease. We investigated the genetic factors that underlie serum NfL levels (sNfL) of individuals without neurological conditions. Methods We performed a discovery genome-wide association study (GWAS) of sNfL in participants of the German BiDirect Study ( N = 1,899). A secondary GWAS for meta-analysis was performed in a small Austrian cohort ( N = 287). Results from the meta-analysis were investigated in relation with several clinical variables in BiDirect. Results Our discovery GWAS identified 12 genomic loci at the suggestive threshold (( p & lt; 1 × 10 −5 ). After meta-analysis, 7 loci were suggestive of an association with sNfL. Genotype-specific differences in sNfL were observed for the lead variants of meta-analysis loci (rs34523114, rs114956339, rs529938, rs73198093, rs34372929, rs10982883, and rs1842909) in BiDirect participants. We identified potential associations in meta-analysis loci with markers of inflammation and renal function. At least 6 protein-coding genes ( ACTG2, TPRKB, DMXL1, COL23A1, NAT1 , and RIMS2 ) were suggested as genetic factors contributing to baseline sNfL levels. Discussion Our findings suggest that polygenic regulation of neuronal processes, inflammation, metabolism and clearance modulate the variability of NfL in the circulation. These could aid in the interpretation of sNfL measurements in a personalized manner.
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fneur.2023.1145737
    DOI: 10.3389/fneur.2023.1145737.s001
    DOI: 10.3389/fneur.2023.1145737.s002
    DOI: 10.3389/fneur.2023.1145737.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2564214-5
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