Base de dados : LILACS
Pesquisa : D12.776.049.407.249 [Categoria DeCS]
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Id: lil-742561
Autor: Gallardo C, Natalia; Valenzuela L, Omar; Ibáñez V, Sebastián.
Título: Neumomediastino y necrosis cutánea en asociación a dermatomiositis: presentación de un caso clínico y revisión de la literatura / Pneumomediastinum and cutaneous necrosis in dermatomyositis: Report of one case
Fonte: Rev. méd. Chile;143(1):120-123, ene. 2015. ilus.
Idioma: es.
Resumo: We report a 37 years old male with a dermatomyositis treated with oral cyclophosphamide. He was admitted to the hospital due to a zone of skin necrosis with purulent exudate, located in the second left toe. A complete blood count showed a leukocyte count of 2,600 cells/mm³. A Chest CAT scan showed a pneumomediastinum with emphysema of adjacent soft tissue. Cyclophosphamide was discontinued and leukocyte count improved. The affected toe was amputated and a chest CAT scan showed a partial resolution of the pneumomediastinum. We discuss and review the pathogenesis, clinical presentation and management of pneumomediastinum and cutaneous necrosis in association with dermatomyositis.
Descritores: Benzoxazinas/uso terapêutico
Canabinoides/agonistas
Encefalomielite Autoimune Experimental/quimioterapia
Encefalomielite Autoimune Experimental/patologia
Morfolinas/uso terapêutico
Naftalenos/uso terapêutico
Neurônios/efeitos de drogas
Oligodendroglia/efeitos de drogas
-Precursor de Proteína beta-Amiloide/metabolismo
Análise de Variância
/metabolismo
CASPASE ABATTOIRS/metabolismo
Caspase 9/metabolismo
Contagem de Células/métodos
Sistema Nervoso Central/patologia
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/complicações
Macrófagos/efeitos de drogas
Degeneração Neural/etiologia
Degeneração Neural/prevenção & controle
Exame Neurológico
Poli(ADP-Ribose) Polimerases/metabolismo
Medula Espinal/efeitos de drogas
Medula Espinal/patologia
Linfócitos T/efeitos de drogas
Fatores de Tempo
Limites: Animais
Feminino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: lil-734386
Autor: Beauquis, Juan; Vinuesa, Ángeles; Pomilio, Carlos; Pavía, Patricio; Saravia, Flavia.
Título: Alteraciones hipocampales y cambios cognitivos preceden al deposito de placas amiloides en un modelo murino de la enfermedad de Alzheimer
Fonte: Medicina (B.Aires);74(4):282-286, ago. 2014. ilus, graf.
Idioma: es.
Resumo: Existen múltiples evidencias de alteraciones neuronales y gliales en etapas avanzadas de la enfemedad de Alzheimer con abundantes depósitos cerebrales de beta amiloide, aunque hay pocos datos de cambios tempranos que podrían contribuir al desarrollo de la enfermedad. Evaluamos alteraciones morfológicas neuronales y gliales, y cambios cognitivos y emocionales tempranos en ratones transgénicos PDAPP-J20 (Tg), portadores del gen humano de APP (amyloid precursor protein) mutado, a los 5 meses de edad, aún sin depósitos amiloides en el hipocampo y con niveles bajos de péptidos amiloides cerebrales. Mediante inmunohistoquímica para NeuN, los Tg presentaron menor número de neuronas piramidales y granulares en el hipocampo, junto con un menor volumen de la estructura, en comparación con los controles no transgénicos. La neurogénesis se encontró afectada, evidenciada por reducido número de neuronas DCX+ en el giro dentado. En la región CA3, hubo una menor densidad de sinaptofisina sugiriendo alteraciones sinápticas entre neuronas granulares y piramidales, sin cambios en la densidad de espinas dendríticas en CA1. Utilizando microscopía confocal, observamos una disminución del número de astrocitos GFAP+ con una reducción de la complejidad celular, sugiriendo atrofia glial. Se detectó un déficit cognitivo (reconocimiento de localización novedosa de un objeto) y un aumento de la ansiedad (campo abierto) en los Tg, con aumento en los núcleos c-Fos+ en amígdala, evidenciando el papel de la emocionalidad en los inicios de la enfermedad. El estudio de las alteraciones iniciales en la enfermedad amiloide podría contribuir al desarrollo de métodos de diagnóstico temprano y de terapéutica preventiva.

Although there is strong evidence about neuronal and glial disturbances at advanced stages of Alzheimer’s disease, less attention has been directed to early, pre-amyloid changes that could contribute to the progression of the disease. We evaluated neuronal and glial morphological changes and behavioral disturbances in PDAPP-J20 transgenic (Tg) mice, carrying mutated human APP gene (amyloid precursor protein), at 5 months of age, before brain amyloid deposition occurs. Using NeuN immunohistochemistry we found decreased numbers of pyramidal and granular neurons in the hippocampus associated with a reduction of hippocampal volume in Tg mice compared with controls. Neurogenesis was impaired, evidenced by means of DCX immunohistochemistry in the dentate gyrus. In the CA3 region we found a decreased density of synaptophysin, suggesting synaptic disturbance, but no changes were found in CA1 synaptic spine density. Using confocal microscopy we observed decreased number and cell complexity of GFAP+ astrocytes, indicating potential glial atrophy. Cognitive impairment (novel location recognition test) and increased anxiety (open field) were detected in Tg mice, associated with more c-Fos+ nuclei in the amygdala, possibly indicating a role for emotionality in early stages of the disease. The study of early alterations in the course of amyloid pathology could contribute to the development of diagnostic and preventive strategies.
Descritores: Doença de Alzheimer/patologia
Precursor de Proteína beta-Amiloide/genética
Modelos Animais de Doenças
Hipocampo/patologia
Comprometimento Cognitivo Leve/patologia
Placa Amiloide/patologia
-Precursor de Proteína beta-Amiloide/metabolismo
Transtornos de Ansiedade/patologia
Astrócitos/patologia
Giro Denteado/metabolismo
Progressão da Doença
MICE, INBRED CABDOMENABDOMINAL INJURIESBL
Camundongos Transgênicos
Comprometimento Cognitivo Leve/genética
Comprometimento Cognitivo Leve/metabolismo
Neurogênese/fisiologia
Neurônios/patologia
Sinaptofisina/isolamento & purificação
Limites: Animais
Humanos
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas


  3 / 17 LILACS  
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Id: lil-711982
Autor: Lobo, Francisco A.
Título: Anestesia, demencias y enfermedad de Alzheimer: ¿coincidencia o certeza? / Anesthesia, dementia and Alzheimer's disease: coincidence or certainty?
Fonte: Rev. argent. anestesiol;70(1):91-96, 2012.
Idioma: es.
Resumo: Existe creciente evidencia derivada de modelos experimentales in vitro, cultivos celulares y modelos animales que sugiere el efecto de la anestesia sobre la degeneración neuronal y una interacción entre la cirugía, la anestesia y la neuropatología denominada Alzheimer. También existe la firme creencia de que los ancianos corren el riesgo de sufrir deterioro cognitivo transitorio, aunque también puede ser persistente, después de haber sido sometidos a una cirugía mayor, y ese deterioro puede estar asociado a muerte o debilidad. En este trabajo revisamos brevemente los fundamentos básicos de la enfermedad de Alzheimer y su interacción con la anestesia general, y los pocos datos clínicos en humanos que han sido utilizados para proponer una posible asociación entre la anestesia general y las demencias.
Descritores: Anestesia Geral
Demência/complicações
Demência/etiologia
Doença de Alzheimer/complicações
-Doença de Alzheimer/metabolismo
Fatores Etários
Proteínas tau/fisiologia
Precursor de Proteína beta-Amiloide/fisiologia
Cérebro
Cérebro/metabolismo
Transtornos Cognitivos/complicações
Transtornos Cognitivos/etiologia
Complicações Pós-Operatórias
Limites: Humanos
Idoso
Responsável: AR1.1 - Biblioteca Rafael Herrera Vegas


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Id: lil-593148
Autor: Schaeffer, Evelin L; Figueiro, Micheli; Gattaz, Wagner F.
Título: Insights into Alzheimer disease pathogenesis from studies in transgenic animal models
Fonte: Clinics;66(supl.1):45-54, 2011. ilus, tab.
Idioma: en.
Resumo: Alzheimer disease is the most common cause of dementia among the elderly, accounting for ~60-70 percent of all cases of dementia. The neuropathological hallmarks of Alzheimer disease are senile plaques (mainly containing p-amyloid peptide derived from amyloid precursor protein) and neurofibrillary tangles (containing hyperphosphorylated Tau protein), along with neuronal loss. At present there is no effective treatment for Alzheimer disease. Given the prevalence and poor prognosis of the disease, the development of animal models has been a research priority to understand pathogenic mechanisms and to test therapeutic strategies. Most cases of Alzheimer disease occur sporadically in people over 65 years old, and are not genetically inherited. Roughly 5 percent of patients with Alzheimer disease have familial Alzheimer disease-that is, related to a genetic predisposition, including mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes. The discovery of genes for familial Alzheimer disease has allowed transgenic models to be generated through the overexpression of the amyloid precursor protein and/or presenilins harboring one or several mutations found in familial Alzheimer disease. Although none of these models fully replicates the human disease, they have provided valuable insights into disease mechanisms as well as opportunities to test therapeutic approaches. This review describes the main transgenic mouse models of Alzheimer disease which have been adopted in Alzheimer disease research, and discusses the insights into Alzheimer disease pathogenesis from studies in such models. In summary, the Alzheimer disease mouse models have been the key to understanding the roles of soluble b-amyloid oligomers in disease pathogenesis, as well as of the relationship between p-amyloid and Tau pathologies.
Descritores: Doença de Alzheimer/genética
Precursor de Proteína beta-Amiloide/genética
Modelos Animais de Doenças
Mutação/genética
-Precursor de Proteína beta-Amiloide/metabolismo
Camundongos Transgênicos
Limites: Animais
Humanos
Camundongos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Maluf, Sharbel Weidner
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Id: lil-512447
Autor: Lucatelli, Juliana Faggion; Barros, Alessandra Chiele; Maluf, Sharbel Weidner; Andrade, Fabiana Michelsen de.
Título: Influência genética sobre a doença de Alzheimer de início precoce / Genetic influence on early onset Alzeimer's disease
Fonte: Rev. psiquiatr. clín. (São Paulo) = Arch. clin. psychiatry (São Paulo, Impr.);36(1):25-30, 2009. tab.
Idioma: pt.
Resumo: CONTEXTO: A doença de Alzheimer de início precoce (DAIP) representa 5 por cento de todos os casos de doença de Alzheimer e está relacionada a mutações gênicas. OBJETIVO: Apresentar a influência de mutações gênicas na DAIP. MÉTODOS: Revisão da literatura, a partir de 1992, empregando o banco de dados PubMed. RESULTADOS: O alelo E*4 do gene da apolipoproteína E interfere na DAIP. No gene da proteína precursora da amiloide, foram descritas 20 mutações, que causam cerca de 10 por cento a 15 por cento dos casos de DAIP. Mutações no gene das presenilinas 1 e 2 causam 30 por cento a 70 por cento dos casos de DAIP. No gene da PSN1, há 30 mutações de troca de aminoácidos e três inserções/deleções. O gene da PSEN2 apresenta seis mutações de troca de aminácidos. No gene MAPT, apenas uma mutação se relaciona exclusivamente com a DA. CONCLUSÕES: O uso de informações genéticas para a detecção precoce de possíveis pacientes com DAIP ainda é bastante limitado. A heterogeneidade genética é ampla. Algumas mutações descritas nesta revisão foram responsáveis pela doença de Alzheimer em apenas algumas poucas famílias. A aplicação clínica desses métodos no rastreamento de indivíduos em risco para a DAIP ainda exige cautela.

BACKGROUND: Early onset Alzheimer's disease (EOAD) represents 5 percent of all cases of Alzheimer's disease, and it is connected to genic mutations. OBJECTIVES: To present the influence of genic mutations in EOAD. METHODS: Review of current literature, starting from 1992, utilizing the PubMed data bank. RESULTS: The E*4 allele of the apolipoprotein E gene interferes in EOAD. In the gene of the Amyloid Precursor Protein, 20 mutations were described, causing 10 percent to 15 percent of the cases of EOAD. Mutations in the gene of presenilins 1 and 2 cause 30 percent to 70 percent of the cases of EOAD. In PSN1 gene, 30 aminoacid change mutations and 3 insertions/deletions are known. In the PSEN2 gene, there are 6 aminoacid change mutations. Only one mutation in the MAPT gene is selectively associated with Alzheimer's disease. CONCLUSIONS: The use of genetic information for early detection of possible pacients of EOAD is still very limited. Genetic heterogeneity is broad. Some mutations described in this review were responsible for Alzheimer's disease only in a few families. The clinical utilization of these methods for screening individuals at risk for EOAD still asks for caution.
Descritores: Doença de Alzheimer/diagnóstico
Diagnóstico Precoce
Doença de Alzheimer/genética
-Proteínas tau
Apolipoproteínas E
Presenilinas
Precursor de Proteína beta-Amiloide
Responsável: BR66.1 - Divisão de Biblioteca e Documentação


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Texto completo SciELO Chile
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Id: lil-498184
Autor: Von Bernhardi M., Rommy.
Título: Mecanismos neurobiológicos de la enfermedad de Alzheimer / Neurobiological mechanisms of Alzheimer's disease
Fonte: Rev. chil. neuro-psiquiatr;43(2):123-132, abr.-jun. 2005. ilus.
Idioma: es.
Projeto: FONDECYT.
Resumo: En la medida que entendemos mejor la complejidad de la Enfermedad de Alzheimer, se revelan las bases biológicas subyacentes de su patogénesis, apareciendo nuevos blancos terapéuticos. Muchos agentes que son investigados en estos momentos apuntan a las etapas tempranas de la enfermedad. Su objetivo es prevenir o al menos retardar la progresión hacia la aparición del déficit clínico. Sin embargo, uno de los problemas que enfrenta la investigación en el área, es lograr distinguir entre los eventos primarios y secundarios. Los mecanismos patológicos involucrados consideran las diversas acciones del beta-amiloide, incluyendo la acumulación de agregados, la cascada inflamatoria, el daño oxidativo neuronal, alteraciones de la proteína tau y la formación de ovillos neurofibrilares, defectos sinápticos y depleción de neurotransmisores. Muchos de estos eventos son comunes para numerosos desórdenes neurodegenerativos de progresión lenta. Las formas familiares del Alzheimer, secundarias a mutaciones hereditarias, han ofrecido una aproximación para el análisis de los mecanismos moleculares implicados en la patogénesis de la enfermedad. Usando la Enfermedad de Alzheimer familiar como punto de partida, intentaremos avanzar en nuestra comprensión de los otros mecanismos biológicos envueltos en la neurodegeneración de la enfermedad.

As our understanding of the complexity of Alzheimer's disease improves, the biological bases underlying its pathogenesis are gradually being disclosed, and we can expect that new therapeutic targets will emerge. Many agents under investigation at this moment target the early stages of the disease process. Their aim is to prevent or at least slow down the progression towards clinica limpairment. However, one of the problems research face is the distinction between primary and secondary events. The pathological mechanisms involved include the actions of beta-amyloid, the accumulation of aggregates, the inflammatory cascade, oxidative neuronal damage, tau protein alterations and the formation of neurofibrillary tangles, synaptic failure and neurotransmitter depletion. Several of these events are common to many slowly progressive neurodegenerative disorder. The familial forms of Alzheimer's, secondary to inherited mutations have provide an insight into the molecular mechanisms implicated in disease pathogenesis. Using as an starting point familial Alzheimer's disease, we will work our way up to understand the other biological mechanisms involved in the neurodegeneration of the disease.
Descritores: Doença de Alzheimer/fisiopatologia
-Doença de Alzheimer/patologia
Precursor de Proteína beta-Amiloide
Estresse Oxidativo/fisiologia
Degeneração Neural/fisiopatologia
Placa Amiloide
Fatores de Risco
Envelhecimento
Morte Celular
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


  7 / 17 LILACS  
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Texto completo SciELO Chile
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Id: lil-495746
Autor: Paula-Lima, Andréia C; Arriagada, Christian; Toro, Rodrigo; Cárdenas, Ana María; Caviedes, Raúl; Ferreira, Sergio T; Caviedes, Pablo.
Título: Small-molecule aggregation inhibitors reduce excess amyloid in a trisomy 16 mouse cortical cell line
Fonte: Biol. Res;41(2):129-136, 2008. ilus, graf.
Idioma: en.
Projeto: Fondecyt; . Univ. of Chile; . Fondation Jéróme Lejeune, Paris, France (to PC); . Howard Hughes Medical Institute; . Conselho Nacional de Desenvolvimento Científico e Tecnológico; . Fundação de Amparo à Pesquisa do Estado do RJ; . FINEP/CT-Verde Amarelo (to STF).
Resumo: We have previously characterized a number of small molecule organic compounds that prevent the aggregation of the β-amyloid peptide and its neurotoxicity in hippocampal neuronal cultures. We have now evaluated the effects of such compounds on amyloid precursor protein (APP) accumulation in the CTb immortalized cell line derived from the cerebral cortex of a trisomy 16 mouse, an animal model of Down's syndrome. Compared to a non-trisomic cortical cell line (CNh), CTb cells overexpress APP and exhibit slightly elevated resting intracellular Ca2+ levéis ([Ca2+]¡). Here, we show that the compounds 2,4-dinitrophenol, 3-nitrophenol and 4-anisidine decreased intracellular accumulation of APP in CTb cells. Those compounds were non-toxic to the cells, and slightly increased the basal [Ca2+]¡. Results indícate that the compounds tested can be leads for the development of drugs to decrease intracellular vesicular accumulation of APP in trisomic cells.
Descritores: /farmacologia
TEMEFOS,ABBREVIATIONS AS TOPIC-DINITROPHENOL/farmacologia
Doença de Alzheimer/metabolismo
Precursor de Proteína beta-Amiloide/antagonistas & inibidores
Compostos de Anilina/farmacologia
Síndrome de Down/metabolismo
Nitrofenóis/farmacologia
-Precursor de Proteína beta-Amiloide/metabolismo
Linhagem Celular
Córtex Cerebral/citologia
Córtex Cerebral/efeitos de drogas
Córtex Cerebral/metabolismo
Modelos Animais de Doenças
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  8 / 17 LILACS  
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Id: lil-468202
Autor: Cartier R., Luis; Vergara R., Carmen; Valenzuela P., María Antonieta.
Título: Inmunohistoquímica de los cambios degenerativos del sistema nervioso central en paraparesias esp sticas asociadas al virus linfotrópico humanoTtipol(HTLV-l) / Immunohistochemistry of degenerative changes in the central nervous system in spastic paraparesis associated to human T lymphotropic virus type I (HTLV-I)
Fonte: Rev. méd. Chile;135(9):1139-1146, sept. 2007. ilus, tab.
Idioma: es.
Projeto: FONDECYT.
Resumo: Background: Human T lymphotropic virus type I is associated with tropical spastic paraparesis, that is a chronic and progressive disease which damages specially the cortiespinal tracts. The pathogenesis of this degenerative process remains unknown. Aim: To identify histopathological aspects that could suggest a pathogenic hypothesis we studied immunohistochemical features in spinal cords obtained from patients that died due to progressive spastic paraparesis. Patients and Methods: Five males and five females, who died between 1990 and 2000, with a mean age of 52 years and mean disease duration of 8.6, were studied. All had a complete clinical and virological diagnosis. Samples were obtained from the frontal motor cortex and spinal cord (cervical, dorsal and lumbar segments), were fixed in formol (10 percent), included in paraffin, and stained with Haematoxylin and Luxol-fast-blue. Immunohistochemical study was made with anti-neurofilament antibodies 1:100 (M0762, DAKO), anti-APP 1:20 (Rabbit Pre Amyloid protein 51-2700 ZYMED), anti-tau 1:100 (A0024DAKO) and anti-ubiquitine 1:50 (NCL UBIQm Novocastra). Results: All cases had demyelinization and axonal loss in the cortico-spinal tracts; distal and segmental demyelinization of Goll tract; axonal thickening, amyloid precursor protein deposits in the white matter; tau protein aggregation in the spinal cord oligodendrocytes; axonal ubiquitination of sensitive and motor tracts, and subcortical white matter. Neurona! injury was absent. Conclusions: The systematic damage of motor and sensitive tracts of the spinal-cord and the absence of neurona! damage, defines a degenerative process limited to axons. This central axonopathie could be caused by a disturbance of axoplasmic transport.
Descritores: Vírus 1 Linfotrópico T Humano
Degeneração Neural/patologia
Paraparesia Espástica Tropical/patologia
Medula Espinal/patologia
-Precursor de Proteína beta-Amiloide/metabolismo
Transporte Axonal/fisiologia
Axônios/patologia
Axônios/virologia
Imuno-Histoquímica
Degeneração Neural/virologia
Paraparesia Espástica Tropical/virologia
Reação em Cadeia da Polimerase
Medula Espinal/virologia
Coloração e Rotulagem
Ubiquitina/metabolismo
Proteínas tau/metabolismo
Limites: Adulto
Idoso
Feminino
Humanos
Masculino
Meia-Idade
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  9 / 17 LILACS  
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Id: lil-443670
Autor: Opazo, C; Ruiz, F. H; Inestrosa, N. C.
Título: Amyloid-beta-peptide reduces copper(II) to copper(I) independent of its aggregation state
Fonte: Biol. Res;33(2):125-131, 2000. tab, graf, ilus.
Idioma: en.
Resumo: Alzheimer's disease (AD) is characterized by the deposition of amyloid beta-peptide (A beta) and neuronal degeneration in brain regions involved in learning and memory. One of the leading etiologic hypotheses regarding AD is the involvement of free radical-mediated oxidative stress in neuronal degeneration. Recent evidence suggests that metals concentrated in amyloid deposits may contribute to the oxidative insults observed in AD-affected brains. We hypothesized that A beta peptide in the presence of copper enhances its neurotoxicity generating free radicals via copper reduction. In the present study, we have examined the effect of the aggregation state of amyloid-beta-peptide on copper reduction. In independent experiments we measured the copper-reducing ability of soluble and fibrillar A beta(1-40) forms by bathocuproine assays. As it was previously observed for the amyloid precursor protein (APP), the A beta peptide showed copper-reducing ability. The capacity of A beta to reduce copper was independent of the aggregation state. Finally, the A beta peptide derived from the human sequence has a greater effect than the A beta peptide derived from the rat sequence, suggesting that histidine 13 may play a role in copper reduction. In agreement with this possibility, the A beta peptide reduces less copper in the presence of exogenous histidine.
Descritores: Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/metabolismo
Cobre/metabolismo
-Doença de Alzheimer/etiologia
Precursor de Proteína beta-Amiloide/metabolismo
Peroxidação de Lipídeos/fisiologia
Oxirredução
Estresse Oxidativo/fisiologia
Limites: Humanos
Responsável: BR1.1 - BIREME


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Id: lil-406188
Autor: Villegas Lanau, Carlos A; Bedoya Berrio, Gabriel; Toro Castaño, Maria F; Lopera Restrepo, Francisco; Madrigal, Lucía.
Título: Evaluación de la expresión de la proteína precursora de amiloide en células sanguíneas de pacientes con la mutación E280A en el gen de la presenilina 1 / Expression of amyloid precursor protein in peripheral blood cells of patients with the E280A mutation in the presenilin-1 gene
Fonte: Iatreia;18(1):27-39, mar. 2005. tab, graf.
Idioma: es.
Resumo: LA enfermedad de Alzheimer es un problema mundial de salud pública. El estudio de los mecanismos moleculares responsables de su aparición permitirá avances terapéuticos y en las técnicas para la evaluación de las personas afectadas y de las que están en riesgo de desarrollar la enfermedad. La mutación E280A en el gen de la Presenilina 1 (PS1) es responsable de una forma grave de la enfermedad de Alzheimer familiar. Con el fin de conocer su efecto sobre la Proteína Precursora de Amiloide (PPA), se cuantificó la producción de esta por células de sangre periférica (mononucleares y linfocitos B) de individuos portadores de dicha mutación. Se analizaron cultivos celulares (HeLa y CHO) como controles positivos, y sangre periférica procedente de portadores sanos de la mutación, de portadores afectados y de un grupo control sano, no portador. Todas las células (HeLa, CHO, mononucleares y linfocitos B) se analizaron por citometría de flujo para detectar la PPA en la membrana citoplasmática y en el espacio intracelular. Se halló un nivel mayor de expresión de esta proteína en el interior de las células que en la membrana celular. En células HeLa y CHO los niveles de expresión intracelular fueron muy variables mientras que en los mononucleares fueron uniformemente bajos. Otros trabajos han detectado niveles mayores de la proteína en los enfermos, pero nuestros resultados indican que no hay diferencia entre los controles sanos, los portadores sanos y los portadores enfermos, lo cual indica que la mutación E280A de la PS1 no ejerce un papel directo en la expresión de la PPA en células mononucleares de sangre periférica. AUT
Descritores: Citometria de Fluxo
Doença de Alzheimer
Precursor de Proteína beta-Amiloide
Responsável: CO56.1 - Biblioteca



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