Cell degeneration induced by amyloid-ß peptides
Autor(a) principal: | |
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Data de Publicação: | 2004 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/8503 https://doi.org/10.1385/JMN:23:1-2:097 |
Resumo: | Abstract Extracellular accumulation of amyloid-ß (Aß) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer’s disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Aß might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Aß triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Aß-induced toxicity and for the role of mitochondria in apoptotsis triggered by Aß. In addition, the endoplasmic reticulum (ER) seems to play a role in Aß-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Aß induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD. |
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Cell degeneration induced by amyloid-ß peptidesAbstract Extracellular accumulation of amyloid-ß (Aß) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer’s disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Aß might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Aß triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Aß-induced toxicity and for the role of mitochondria in apoptotsis triggered by Aß. In addition, the endoplasmic reticulum (ER) seems to play a role in Aß-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Aß induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD.2004info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/8503http://hdl.handle.net/10316/8503https://doi.org/10.1385/JMN:23:1-2:097engJournal of Molecular Neuroscience. 23:1 (2004) 97-104Pereira, CláudiaFerreiro, ElisabeteCardoso, SandraOliveira, Catarina deinfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2021-12-01T17:20:58Zoai:estudogeral.uc.pt:10316/8503Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:43:34.747464Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Cell degeneration induced by amyloid-ß peptides |
title |
Cell degeneration induced by amyloid-ß peptides |
spellingShingle |
Cell degeneration induced by amyloid-ß peptides Pereira, Cláudia |
title_short |
Cell degeneration induced by amyloid-ß peptides |
title_full |
Cell degeneration induced by amyloid-ß peptides |
title_fullStr |
Cell degeneration induced by amyloid-ß peptides |
title_full_unstemmed |
Cell degeneration induced by amyloid-ß peptides |
title_sort |
Cell degeneration induced by amyloid-ß peptides |
author |
Pereira, Cláudia |
author_facet |
Pereira, Cláudia Ferreiro, Elisabete Cardoso, Sandra Oliveira, Catarina de |
author_role |
author |
author2 |
Ferreiro, Elisabete Cardoso, Sandra Oliveira, Catarina de |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Pereira, Cláudia Ferreiro, Elisabete Cardoso, Sandra Oliveira, Catarina de |
description |
Abstract Extracellular accumulation of amyloid-ß (Aß) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer’s disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Aß might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Aß triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Aß-induced toxicity and for the role of mitochondria in apoptotsis triggered by Aß. In addition, the endoplasmic reticulum (ER) seems to play a role in Aß-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Aß induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD. |
publishDate |
2004 |
dc.date.none.fl_str_mv |
2004 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10316/8503 http://hdl.handle.net/10316/8503 https://doi.org/10.1385/JMN:23:1-2:097 |
url |
http://hdl.handle.net/10316/8503 https://doi.org/10.1385/JMN:23:1-2:097 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Journal of Molecular Neuroscience. 23:1 (2004) 97-104 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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1799133707830820864 |