Neuroinflammation and aging: focus on experimental Alzheimer´s disease

Autores
Saravia, Flavia Eugenia
Año de publicación
2019
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
The incidence of metabolic disorders including obesity, diabetes and metabolic syndrome have seriously increased in the last decades. These diseases - with growing impact in modern societies - constitute major risk factors for neurodegenerative disorders such as Alzheimer´s disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. The dentate gyrus of the hippocampus- a neurogenic area associated with memory and learning processes- is a recognized target for diabetic alterations and neurodegeneration. We explored the hippocampal neurogenesis and its microenvironment (microglia, astrocytes, vascularisation and glucocorticoid influence) in different dysmetabolic scenarios provided by spontaneous or induced experimental models. We found astrogliosis, reactive microglia, and reduced vascular arborization in association with cognitive impairment and lower or disturbed neurogenic ability, even in young animals. These phenomena were accompanied by a insulin-resistant state in the hippocampus, an impaired response to insulin. In the context of Alzheimer´s disease (AD), hippocampal alterations have been well described in advanced stages of the pathology, when amyloid deposition, inflammation and glial activation occur, but less attention has been directed to studying early stages. The neurogenic capability, measured as DCX+ cells, was strongly diminished and associated to alterations in cell maturity in a transgenic mouse model of AD, at early stages, when no amyloid deposits are present. Microglia already exhibited mostly intermediate and ameboid morphology-suggestive of activated state-and less corresponding to the ramified phenotype. Microglia, is able to sense pathogens and but also react against metabolic insults through phagocytosis and the release of cytokines. A chronic microglia stimulation may contribute to a persistent inflammation that can precede the neurodegenerative process.
Fil: Saravia, Flavia Eugenia.
Pan American Neuroendocrine Society: laissez la bonne science rouler
New Orleans
Estados Unidos
Pan American Neuroendocrine Society
Materia
BRAIN AGING
ALZHEIMER'S DISEASE
MICROGLIA
AUTOPHAGY
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/133720

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spelling Neuroinflammation and aging: focus on experimental Alzheimer´s diseaseSaravia, Flavia EugeniaBRAIN AGINGALZHEIMER'S DISEASEMICROGLIAAUTOPHAGYhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The incidence of metabolic disorders including obesity, diabetes and metabolic syndrome have seriously increased in the last decades. These diseases - with growing impact in modern societies - constitute major risk factors for neurodegenerative disorders such as Alzheimer´s disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. The dentate gyrus of the hippocampus- a neurogenic area associated with memory and learning processes- is a recognized target for diabetic alterations and neurodegeneration. We explored the hippocampal neurogenesis and its microenvironment (microglia, astrocytes, vascularisation and glucocorticoid influence) in different dysmetabolic scenarios provided by spontaneous or induced experimental models. We found astrogliosis, reactive microglia, and reduced vascular arborization in association with cognitive impairment and lower or disturbed neurogenic ability, even in young animals. These phenomena were accompanied by a insulin-resistant state in the hippocampus, an impaired response to insulin. In the context of Alzheimer´s disease (AD), hippocampal alterations have been well described in advanced stages of the pathology, when amyloid deposition, inflammation and glial activation occur, but less attention has been directed to studying early stages. The neurogenic capability, measured as DCX+ cells, was strongly diminished and associated to alterations in cell maturity in a transgenic mouse model of AD, at early stages, when no amyloid deposits are present. Microglia already exhibited mostly intermediate and ameboid morphology-suggestive of activated state-and less corresponding to the ramified phenotype. Microglia, is able to sense pathogens and but also react against metabolic insults through phagocytosis and the release of cytokines. A chronic microglia stimulation may contribute to a persistent inflammation that can precede the neurodegenerative process.Fil: Saravia, Flavia Eugenia.Pan American Neuroendocrine Society: laissez la bonne science roulerNew OrleansEstados UnidosPan American Neuroendocrine SocietyPan American Neuroendocrine Society2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/133720Neuroinflammation and aging: focus on experimental Alzheimer´s disease; Pan American Neuroendocrine Society: laissez la bonne science rouler; New Orleans; Estados Unidos; 2019; 33-33CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://paneuroendo.org/pans2019-archived/Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:38:25Zoai:ri.conicet.gov.ar:11336/133720instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:38:26.113CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Neuroinflammation and aging: focus on experimental Alzheimer´s disease
title Neuroinflammation and aging: focus on experimental Alzheimer´s disease
spellingShingle Neuroinflammation and aging: focus on experimental Alzheimer´s disease
Saravia, Flavia Eugenia
BRAIN AGING
ALZHEIMER'S DISEASE
MICROGLIA
AUTOPHAGY
title_short Neuroinflammation and aging: focus on experimental Alzheimer´s disease
title_full Neuroinflammation and aging: focus on experimental Alzheimer´s disease
title_fullStr Neuroinflammation and aging: focus on experimental Alzheimer´s disease
title_full_unstemmed Neuroinflammation and aging: focus on experimental Alzheimer´s disease
title_sort Neuroinflammation and aging: focus on experimental Alzheimer´s disease
dc.creator.none.fl_str_mv Saravia, Flavia Eugenia
author Saravia, Flavia Eugenia
author_facet Saravia, Flavia Eugenia
author_role author
dc.subject.none.fl_str_mv BRAIN AGING
ALZHEIMER'S DISEASE
MICROGLIA
AUTOPHAGY
topic BRAIN AGING
ALZHEIMER'S DISEASE
MICROGLIA
AUTOPHAGY
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The incidence of metabolic disorders including obesity, diabetes and metabolic syndrome have seriously increased in the last decades. These diseases - with growing impact in modern societies - constitute major risk factors for neurodegenerative disorders such as Alzheimer´s disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. The dentate gyrus of the hippocampus- a neurogenic area associated with memory and learning processes- is a recognized target for diabetic alterations and neurodegeneration. We explored the hippocampal neurogenesis and its microenvironment (microglia, astrocytes, vascularisation and glucocorticoid influence) in different dysmetabolic scenarios provided by spontaneous or induced experimental models. We found astrogliosis, reactive microglia, and reduced vascular arborization in association with cognitive impairment and lower or disturbed neurogenic ability, even in young animals. These phenomena were accompanied by a insulin-resistant state in the hippocampus, an impaired response to insulin. In the context of Alzheimer´s disease (AD), hippocampal alterations have been well described in advanced stages of the pathology, when amyloid deposition, inflammation and glial activation occur, but less attention has been directed to studying early stages. The neurogenic capability, measured as DCX+ cells, was strongly diminished and associated to alterations in cell maturity in a transgenic mouse model of AD, at early stages, when no amyloid deposits are present. Microglia already exhibited mostly intermediate and ameboid morphology-suggestive of activated state-and less corresponding to the ramified phenotype. Microglia, is able to sense pathogens and but also react against metabolic insults through phagocytosis and the release of cytokines. A chronic microglia stimulation may contribute to a persistent inflammation that can precede the neurodegenerative process.
Fil: Saravia, Flavia Eugenia.
Pan American Neuroendocrine Society: laissez la bonne science rouler
New Orleans
Estados Unidos
Pan American Neuroendocrine Society
description The incidence of metabolic disorders including obesity, diabetes and metabolic syndrome have seriously increased in the last decades. These diseases - with growing impact in modern societies - constitute major risk factors for neurodegenerative disorders such as Alzheimer´s disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. The dentate gyrus of the hippocampus- a neurogenic area associated with memory and learning processes- is a recognized target for diabetic alterations and neurodegeneration. We explored the hippocampal neurogenesis and its microenvironment (microglia, astrocytes, vascularisation and glucocorticoid influence) in different dysmetabolic scenarios provided by spontaneous or induced experimental models. We found astrogliosis, reactive microglia, and reduced vascular arborization in association with cognitive impairment and lower or disturbed neurogenic ability, even in young animals. These phenomena were accompanied by a insulin-resistant state in the hippocampus, an impaired response to insulin. In the context of Alzheimer´s disease (AD), hippocampal alterations have been well described in advanced stages of the pathology, when amyloid deposition, inflammation and glial activation occur, but less attention has been directed to studying early stages. The neurogenic capability, measured as DCX+ cells, was strongly diminished and associated to alterations in cell maturity in a transgenic mouse model of AD, at early stages, when no amyloid deposits are present. Microglia already exhibited mostly intermediate and ameboid morphology-suggestive of activated state-and less corresponding to the ramified phenotype. Microglia, is able to sense pathogens and but also react against metabolic insults through phagocytosis and the release of cytokines. A chronic microglia stimulation may contribute to a persistent inflammation that can precede the neurodegenerative process.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/133720
Neuroinflammation and aging: focus on experimental Alzheimer´s disease; Pan American Neuroendocrine Society: laissez la bonne science rouler; New Orleans; Estados Unidos; 2019; 33-33
CONICET Digital
CONICET
url http://hdl.handle.net/11336/133720
identifier_str_mv Neuroinflammation and aging: focus on experimental Alzheimer´s disease; Pan American Neuroendocrine Society: laissez la bonne science rouler; New Orleans; Estados Unidos; 2019; 33-33
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://paneuroendo.org/pans2019-archived/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv Pan American Neuroendocrine Society
publisher.none.fl_str_mv Pan American Neuroendocrine Society
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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