marina zanichelli barbosa (48 risultati)

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

PAP. Condizione: New. New Book. Shipped from UK. Established seller since 2000.

Taschenbuch. Condizione: Neu. "Microglial Modulation in Alzheimer's Disease" | How and when microglia change their profile from M2 to M1 | Marina Zanichelli Barbosa | Taschenbuch | Englisch | 2025 | Our Knowledge Publishing | EAN 9786200757296 | Verantwortliche Person für die EU: SIA OmniScriptum Publishing, Brivibas Gatve 197, 1039 RIGA, LETTLAND, customerservice[at]vdm-vsg[dot]de | Anbieter: preigu.

Taschenbuch. Condizione: Neu. 'Modulación microglial en la enfermedad de Alzheimer' | Cómo y cuándo la microglía cambia su perfil M2 a M1 | Marina Zanichelli Barbosa | Taschenbuch | Spanisch | 2025 | Ediciones Nuestro Conocimiento | EAN 9786200757272 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu.

Taschenbuch. Condizione: Neu. ' Modulation microgliale dans la maladie d'Alzheimer ' | Comment et quand la microglie passe du profil M2 au profil M1 | Marina Zanichelli Barbosa | Taschenbuch | Französisch | 2025 | Editions Notre Savoir | EAN 9786200757234 | Verantwortliche Person für die EU: SIA OmniScriptum Publishing, Brivibas Gatve 197, 1039 RIGA, LETTLAND, customerservice[at]vdm-vsg[dot]de | Anbieter: preigu.

Condizione: New.

Taschenbuch. Condizione: Neu. Neuware -Existem muitos mecanismos não esclarecidos sobre a patogênese da Doença de Alzheimer (DA) e nenhuma forma de prevenção ou cura. Sabe-se que no desenvolvimento da doença a microglia pode sofrer alteração de fenótipo e que isso pode influenciar diretamente o neurônio. A fim de entender mais sobre as interações neuroimunes existentes na Doença de Alzheimer, esse projeto apresenta como principal objetivo investigar em que momento e de que forma ocorre a alteração do padrão de microglia M2 para M1 no modelo triplo transgênico (3xTg-AD), o modelo murino que mais se assemelha a doença em humanos. Essa alteração de padrão reflete na neurodegeneração e está relacionada às placas beta-amiloides e emaranhados neurofibrilares. Sabemos que o aumento da produção de espécies reativas de oxigênio (EROs) acompanha a alteração do fenótipo M2 para M1, o qual é responsável pela liberação de citocinas pró-inflamatórias que podem ser diretamente tóxicas para os neurônios. Sendo assim, queremos saber em que momento ocorre e qual mecanismo está envolvido na mudança da via de ativação da microglia do fenótipo alternativo (M2) para o clássico (M1) em camundongos 3xTg-AD, triplo transgênico para DA.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 52 pp. Portugiesisch.

Taschenbuch. Condizione: Neu. "Modulazione microgliale nella malattia di Alzheimer" | Come e quando la microglia modifica il proprio profilo da M2 a M1 | Marina Zanichelli Barbosa | Taschenbuch | Italienisch | 2025 | Edizioni Sapienza | EAN 9786200757289 | Verantwortliche Person für die EU: SIA OmniScriptum Publishing, Brivibas Gatve 197, 1039 RIGA, LETTLAND, customerservice[at]vdm-vsg[dot]de | Anbieter: preigu.

Taschenbuch. Condizione: Neu. "Modulacja mikrogleju w chorobie Alzheimera" | Jak i kiedy mikroglej zmienia swój profil z M2 na M1 | Marina Zanichelli Barbosa | Taschenbuch | Polnisch | 2025 | Wydawnictwo Nasza Wiedza | EAN 9786200757159 | Verantwortliche Person für die EU: SIA OmniScriptum Publishing, Brivibas Gatve 197, 1039 RIGA, LETTLAND, customerservice[at]vdm-vsg[dot]de | Anbieter: preigu.

Taschenbuch. Condizione: Neu. "Mikrogliale Modulation bei Alzheimer" | Wie und wann Mikroglia ihr Profil von M2 zu M1 ändern | Marina Zanichelli Barbosa | Taschenbuch | 56 S. | Deutsch | 2025 | Verlag Unser Wissen | EAN 9786200757197 | Verantwortliche Person für die EU: SIA OmniScriptum Publishing, Brivibas Gatve 197, 1039 RIGA, LETTLAND, customerservice[at]vdm-vsg[dot]de | Anbieter: preigu.

Paperback. Condizione: new. Paperback. There are many unclear mechanisms regarding the pathogenesis of Alzheimer's disease (AD) and no form of prevention or cure. It is known that in the development of the disease, microglia can undergo phenotypic changes and that this can directly influence neurons. In order to understand more about the neuroimmune interactions that exist in Alzheimer's disease, this project's main objective is to investigate when and how the change from M2 to M1 microglia occurs in the triple transgenic model (3xTg-AD), the murine model that most closely resembles the disease in humans. This pattern change reflects neurodegeneration and is related to beta-amyloid plaques and neurofibrillary tangles. We know that increased production of reactive oxygen species (ROS) accompanies the change from the M2 to M1 phenotype, which is responsible for the release of pro-inflammatory cytokines that can be directly toxic to neurons. Therefore, we want to know when this occurs and what mechanism is involved in the change in the activation pathway of microglia from the alternative phenotype (M2) to the classic phenotype (M1) in 3xTg-AD mice, triple transgenic for AD. This item is printed on demand. Shipping may be from multiple locations in the US or from the UK, depending on stock availability.

Paperback. Condizione: new. Paperback. De nombreux mecanismes de la pathogenese de la maladie d'Alzheimer (MA) restent inexpliques et il n'existe aucun moyen de prevention ou de guerison. On sait que, au cours du developpement de la maladie, la microglie peut subir une modification phenotypique qui peut influencer directement les neurones. Afin de mieux comprendre les interactions neuro-immunes existant dans la maladie d'Alzheimer, ce projet a pour objectif principal d'etudier a quel moment et de quelle maniere se produit le changement de profil des microglies M2 vers M1 dans le modele transgenique triple (3xTg-AD), le modele murin qui ressemble le plus a la maladie chez l'homme. Ce changement de profil se reflete dans la neurodegenerescence et est lie aux plaques beta-amyloides et aux enchevetrements neurofibrillaires. Nous savons que l'augmentation de la production d'especes reactives de l'oxygene (ERO) accompagne le changement de phenotype M2 vers M1, qui est responsable de la liberation de cytokines pro-inflammatoires pouvant etre directement toxiques pour les neurones. Nous souhaitons donc savoir a quel moment cela se produit et quel mecanisme est implique dans le changement de voie d'activation de la microglie du phenotype alternatif (M2) au phenotype classique (M1) chez les souris 3xTg-AD, triple transgeniques pour la MA. This item is printed on demand. Shipping may be from multiple locations in the US or from the UK, depending on stock availability.

Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware 52 pp. Englisch.

Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware 52 pp. Spanisch.

Paperback. Condizione: new. Paperback. Istnieje wiele niewyjasnionych mechanizmow dotyczacych patogenezy choroby Alzheimera (AD) i nie ma zadnej formy zapobiegania ani leczenia. Wiadomo, ze w trakcie rozwoju choroby mikroglej moze ulegac zmianom fenotypowym, co moze miec bezposredni wplyw na neurony. Aby lepiej zrozumiec interakcje neuroimmunologiczne wystepujace w chorobie Alzheimera, glownym celem tego projektu jest zbadanie, w ktorym momencie i w jaki sposob nastepuje zmiana wzorca mikroglia M2 na M1 w potrojnym modelu transgenicznym (3xTg-AD), modelu mysim najbardziej zblizonym do choroby u ludzi. Ta zmiana wzorca odzwierciedla neurodegeneracje i jest zwiazana z plytkami beta-amyloidowymi i splatkami neurofibrylarnymi. Wiemy, ze wzrost produkcji reaktywnych form tlenu (ERO) towarzyszy zmianie fenotypu z M2 na M1, ktory jest odpowiedzialny za uwalnianie prozapalnych cytokin, ktore moga byc bezposrednio toksyczne dla neuronow. W zwiazku z tym chcemy wiedziec, w ktorym momencie nastepuje zmiana sciezki aktywacji mikrogleju z fenotypu alternatywnego (M2) na klasyczny (M1) u myszy 3xTg-AD, potrojnych transgenicznych myszy z DA. This item is printed on demand. Shipping may be from multiple locations in the US or from the UK, depending on stock availability.

Paperback. Condizione: new. Paperback. Es gibt viele ungeklaerte Mechanismen hinsichtlich der Pathogenese der Alzheimer-Krankheit (AD) und keine Moeglichkeit zur Praevention oder Heilung. Es ist bekannt, dass Mikroglia im Verlauf der Krankheit eine Phaenotypaenderung erfahren koennen und dass dies einen direkten Einfluss auf die Neuronen haben kann. Um mehr ueber die neuroimmunen Wechselwirkungen bei der Alzheimer-Krankheit zu erfahren, hat dieses Projekt das Hauptziel, zu untersuchen, wann und wie die Veraenderung des Mikroglia-Musters von M2 zu M1 im dreifach transgenen Modell (3xTg-AD) erfolgt, dem Mausmodell, das der Krankheit beim Menschen am aehnlichsten ist. Diese Musterveraenderung spiegelt sich in der Neurodegeneration wider und steht im Zusammenhang mit Beta-Amyloid-Plaques und neurofibrillaeren Verwicklungen. Wir wissen, dass die erhoehte Produktion reaktiver Sauerstoffspezies (ROS) mit der Veraenderung des Phaenotyps von M2 zu M1 einhergeht, der fuer die Freisetzung proinflammatorischer Zytokine verantwortlich ist, die fuer Neuronen direkt toxisch sein koennen. Daher moechten wir wissen, wann dies geschieht und welcher Mechanismus an der Veraenderung des Aktivierungswegs der Mikroglia vom alternativen Phaenotyp (M2) zum klassischen Phaenotyp (M1) bei 3xTg-AD-Maeusen, einem dreifachen Transgen fuer AD, beteiligt ist. This item is printed on demand. Shipping may be from multiple locations in the US or from the UK, depending on stock availability.

Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware 52 pp. Französisch.

Paperback. Condizione: new. Paperback. There are many unclear mechanisms regarding the pathogenesis of Alzheimer's disease (AD) and no form of prevention or cure. It is known that in the development of the disease, microglia can undergo phenotypic changes and that this can directly influence neurons. In order to understand more about the neuroimmune interactions that exist in Alzheimer's disease, this project's main objective is to investigate when and how the change from M2 to M1 microglia occurs in the triple transgenic model (3xTg-AD), the murine model that most closely resembles the disease in humans. This pattern change reflects neurodegeneration and is related to beta-amyloid plaques and neurofibrillary tangles. We know that increased production of reactive oxygen species (ROS) accompanies the change from the M2 to M1 phenotype, which is responsible for the release of pro-inflammatory cytokines that can be directly toxic to neurons. Therefore, we want to know when this occurs and what mechanism is involved in the change in the activation pathway of microglia from the alternative phenotype (M2) to the classic phenotype (M1) in 3xTg-AD mice, triple transgenic for AD. This item is printed on demand. Shipping may be from our UK warehouse or from our Australian or US warehouses, depending on stock availability.

Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 52 pp. Englisch.

Taschenbuch. Condizione: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering.

Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 52 pp. Spanisch.

Taschenbuch. Condizione: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering.