Base de dados : LILACS
Pesquisa : D12.776.395.550.200.250 [Categoria DeCS]
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Texto completo SciELO Chile
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Id: biblio-950843
Autor: Negrón-Oyarzo, Ignacio; Lara-Vásquez, Ariel; Palacios-García, Ismael; Fuentealba, Pablo; Aboitiz, Francisco.
Título: Schizophrenia and reelin: a model based on prenatal stress to study epigenetics, brain development and behavior
Fonte: Biol. Res;49:1-10, 2016. ilus, graf.
Idioma: en.
Projeto: Millennium Center for the Neuroscience of Memory; . Ministry of Economy, Development and Tourism; . FONDECYT.
Resumo: Schizophrenia is a severe psychiatric disorder that results in a significant disability for the patient. The disorder is characterized by impairment of the adaptive orchestration of actions, a cognitive function that is mainly dependent on the prefrontal cortex. This behavioral deficit, together with cellular and neurophysiological alterations in the prefrontal cortex, as well as reduced density of GABAergic cells and aberrant oscillatory activity, all indicate structural and functional deficits of the prefrontal cortex in schizophrenia. Among the several risk factors for the development of schizophrenia, stress during the prenatal period has been identified as crucial. Thus, it is proposed that prenatal stress induces neurodevelopmental alterations in the prefrontal cortex that are expressed as cognitive impairment observed in schizophrenia. However, the precise mechanisms that link prenatal stress with the impairment of prefrontal cortex function is largely unknown. Reelin is an extracellular matrix protein involved in the development of cortical neural connectivity at embryonic stages, and in synaptic plasticity at postnatal stages. Interestingly, down-regulation of reelin expression has been associated with epigenetic changes in the reelin gene of the prefrontal cortex of schizophrenic patients. We recently showed that, similar to schizophrenic patients, prenatal stress induces down-expression of reelin associated with the methylation of its promoter in the rodent prefrontal cortex. These alterations were paralleled with altered prefrontal cortex functional connectivity and impairment in prefrontal cortex-dependent behavioral tasks. Therefore, considering molecular, cellular, physiological and behavioral evidence, we propose a unifying framework that links prenatal stress and prefrontal malfunction through epigenetic alterations of the reelin gene.
Descritores: Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Esquizofrenia/etiologia
Esquizofrenia/fisiopatologia
Estresse Fisiológico/fisiologia
Encéfalo/embriologia
Serina Endopeptidases/genética
Moléculas de Adesão Celular Neuronais/genética
Proteínas da Matriz Extracelular/genética
Epigênese Genética/fisiologia
Proteínas do Tecido Nervoso/genética
-Transtornos do Comportamento Social/fisiopatologia
Encéfalo/fisiopatologia
Expressão Gênica
Fatores de Risco
Transtornos Cognitivos/fisiopatologia
Metilação de DNA
Limites: Humanos
Feminino
Gravidez
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: CL1.1 - Biblioteca Central


  2 / 5 LILACS  
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Id: lil-421990
Autor: Jones, Marta.
Título: Ehi neonatal: Lem, o el premio a la superviviencia / Ehi newborn: Lem, or the prize to the survival
Fonte: Ludovica pediátr;7(2):38-50, ago. 2005. ilus.
Idioma: es.
Resumo: La hipoxia- isquemica es la principal causa de injuria del sistema nerviosos central en el feto y en el recién nacido, situación agravada, en algunas circunstancias, por infección intrauterina y respuesta inflamatoria fetal. La reducción en las cifras de mortalidad ha producido un incremento de morbilidad, la posibilidad de asistir a las secuelas de aquellas lesiones. En el niño pretérmino que sobrevive, el sustrato morfológico más frecuente de parálisis cerebral es la lucoencefalomalacia pereventricular, la cual forma parte de un expectro más amplio. Las secuelas son déficit en la mielinización, la pérdida de volúmen de sustancia blanca con consecuente ventriculomegalia, el compromiso de vías largas relacionado con el déficit motor del cuadro clínico de páralisis cerebral. En este artículo se sitúa a la leucoencefalomalacia periventricular en el expectro de lesiones hipóxico, isquémica del recién nacido, se detallan sus características clínicas y macra-microscópicas, y se comentan los recientes aportes de la fisiopatología celular. El rol principal del glutamato, la teoría de la excototoxicidad, las citoquinas, y la cascada inflamatoria operan a través de ventanas de vulnerabilidad, que exponen a la oligodendroglia como target esencial, y a la apoptosis como un mecanismo importante de lesión cerebral
Descritores: Apoptose
Hipóxia
Isquemia
Leucomalácia Periventricular
Moléculas de Adesão Celular Neuronais
Oligodendroglia
-Moléculas de Adesão Celular Neuronais/análise
Moléculas de Adesão Celular Neuronais/classificação
Necrose
Limites: Humanos
Gravidez
Responsável: AR481.1 - Biblioteca Hospital de Niños


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Texto completo SciELO Brasil
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Id: lil-421361
Autor: Porcionatto, M. A.
Título: The extracellular matrix provides directional cues for neuronal migration during cerebellar development
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;39(3):313-320, Mar. 2006.
Idioma: en.
Conferência: Apresentado em: Congresso Brasileiro de Biologia Celular, 11, Campinas, July 15-18, 2004.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo; . Conselho Nacional de Desenvolvimento Científico e Tecnológico.
Resumo: Normal central nervous system development relies on accurate intrinsic cellular programs as well as on extrinsic informative cues provided by extracellular molecules. Migration of neuronal progenitors from defined proliferative zones to their final location is a key event during embryonic and postnatal development. Extracellular matrix components play important roles in these processes, and interactions between neurons and extracellular matrix are fundamental for the normal development of the central nervous system. Guidance cues are provided by extracellular factors that orient neuronal migration. During cerebellar development, the extracellular matrix molecules laminin and fibronectin give support to neuronal precursor migration, while other molecules such as reelin, tenascin, and netrin orient their migration. Reelin and tenascin are extracellular matrix components that attract or repel neuronal precursors and axons during development through interaction with membrane receptors, and netrin associates with laminin and heparan sulfate proteoglycans, and binds to the extracellular matrix receptor integrins present on the neuronal surface. Altogether, the dynamic changes in the composition and distribution of extracellular matrix components provide external cues that direct neurons leaving their birthplaces to reach their correct final location. Understanding the molecular mechanisms that orient neurons to reach precisely their final location during development is fundamental to understand how neuronal misplacement leads to neurological diseases and eventually to find ways to treat them.
Descritores: Movimento Celular/fisiologia
Cerebelo/embriologia
Proteínas da Matriz Extracelular/fisiologia
Matriz Extracelular/fisiologia
Neurônios/fisiologia
-Moléculas de Adesão Celular Neuronais/fisiologia
Proteínas do Tecido Nervoso/fisiologia
Transdução de Sinais/fisiologia
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-330238
Autor: Todaro, L; Puricelli, L; Pallotta, M. G; Lastiri, J; Ciraolo, C; Lincuez, M. E; Bal de Kier Joffé, E; Sacerdote de Lustig, E; Varela, M. S.
Título: Alteración en los niveles de N-CAM soluble en pacientes con tumores cerebrales / Plasma levels of soluble N-CAM in patients with cerebral neoplasms
Fonte: Oncol. clín;7(4):787-791, nov. 2002. ilus.
Idioma: es.
Descritores: Neoplasias Encefálicas
Moléculas de Adesão Celular Neuronais/sangue
Biomarcadores Tumorais/sangue
-Neoplasias Encefálicas
Estudos de Casos e Controles
Ependimoma
Glioma
Neoplasias Pulmonares
Melanoma
Meningioma
Moléculas de Adesão Celular Neuronais
Biomarcadores Tumorais
Neoplasias Hipofisárias
Isoformas de Proteínas
Neoplasias do Colo do Útero
Limites: Humanos
Masculino
Adulto
Feminino
Pessoa de Meia-Idade
Responsável: AR144.1 - CIBCHACO - Centro de Información Biomedica del Chaco


  5 / 5 LILACS  
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Texto completo SciELO Brasil
Ramos, Ricardo Guelerman P
Texto completo
Id: lil-269389
Autor: Moda, Livia; Machado, Ricardo C; Ramos, Ricardo Guelerman P.
Título: Ubiquitous overexpression of a transgene encoding the extracellular portion of the Drosophila Roughest-Irregular Chiasm C protein induces early embryonic lethality
Fonte: An. acad. bras. ciênc;72(3):381-8, Sept. 2000. ilus, graf.
Idioma: en.
Resumo: The cell adhesion molecule Rst-irreC is a transmembrane glycoprotein of the immunoglobulin superfamily involved in several important developmental processes in Drosophila, including axonal pathfinding in the optic lobe and programmed cell death and pigment cell differentiation in the pupal retina. As an initial step towards the "in vivo" functional analysis of this protein we have generated transgenic fly stocks carrying a truncated cDNA construct encoding only the extracellular domain of Rst-IrreC under the transcriptional control of the heat shock inducible promoter hsp70. We show that heat-shocking embryos bearing the transgene during the first 8hs of development lead to a 3-4 fold reduction in their viability compared to wild type controls. The embryonic lethality can already be produced by applying the heat pulse in the first 3hs of embryonic development, does not seem to be suppressed in the absence of wildtype product and is progressively reduced as the heat treatment is applied later in embryogenesis. These results are compatible with the hypothesis of the lethal phenotype being primarily due to heterophilic interactions between Rst-IrreC extracellular domain and an yet unknown ligand.
Descritores: Moléculas de Adesão Celular Neuronais/genética
Drosophila melanogaster/genética
Embrião não Mamífero/fisiologia
Expressão Gênica
Genes Letais/fisiologia
Transgenes/fisiologia
-Moléculas de Adesão Celular Neuronais/fisiologia
Genes de Insetos/genética
Temperatura Alta
Fenótipo
Choque
Limites: Animais
Masculino
Feminino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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