A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures
Autor(a) principal: | |
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Data de Publicação: | 2009 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/218251 |
Resumo: | Accumulation of the neurotoxic amyloid b-peptide (Ab) in the brain is a hallmark of Alzheimer’s disease (AD). Several synthetic Ab peptides have been used to study the mechanisms of toxicity. Here, we sought to establish comparability between two commonly used Ab peptides Ab1-42 and Ab25-35 on an in vitro model of Ab toxicity. For this purpose we used organotypic slice cultures of rat hippocampus and observed that both Ab peptides caused similar toxic effects regarding to propidium iodide uptake and caspase-3 activation. In addition, we also did not observe any effect of both peptides on Akt and PTEN phosphorylation; otherwise the phosphorylation of GSK-3b was increased. Although further studies are necessary for understanding mechanisms underlying Ab peptide toxicity, our results provide strong evidence that Ab1-42 and the Ab25-35 peptides induce neural injury in a similar pattern and that Ab25-35 is a convenient tool for the investigation of neurotoxic mechanisms involved in AD. |
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Frozza, Rudimar LuizHorn, Ana PaulaHoppe, Juliana BenderSimão, FabrícioGerhardt, DaniéliComiran, Ricardo ArgentaSalbego, Christianne Gazzana2021-02-26T04:12:45Z20090364-3190http://hdl.handle.net/10183/218251001061825Accumulation of the neurotoxic amyloid b-peptide (Ab) in the brain is a hallmark of Alzheimer’s disease (AD). Several synthetic Ab peptides have been used to study the mechanisms of toxicity. Here, we sought to establish comparability between two commonly used Ab peptides Ab1-42 and Ab25-35 on an in vitro model of Ab toxicity. For this purpose we used organotypic slice cultures of rat hippocampus and observed that both Ab peptides caused similar toxic effects regarding to propidium iodide uptake and caspase-3 activation. In addition, we also did not observe any effect of both peptides on Akt and PTEN phosphorylation; otherwise the phosphorylation of GSK-3b was increased. Although further studies are necessary for understanding mechanisms underlying Ab peptide toxicity, our results provide strong evidence that Ab1-42 and the Ab25-35 peptides induce neural injury in a similar pattern and that Ab25-35 is a convenient tool for the investigation of neurotoxic mechanisms involved in AD.application/pdfengNeurochemical research. New York, NY. Vol. 34, no. 2 (Feb. 2009), p. 295-303Peptídeos beta-amilóidesCaspase 3Doença de AlzheimerAlzheimer’s diseaseAmyloid b-peptideOrganotypic cultureCaspase-3A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice culturesEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001061825.pdf.txt001061825.pdf.txtExtracted Texttext/plain0http://www.lume.ufrgs.br/bitstream/10183/218251/2/001061825.pdf.txtd41d8cd98f00b204e9800998ecf8427eMD52ORIGINAL001061825.pdfTexto completo (inglês)application/pdf3376896http://www.lume.ufrgs.br/bitstream/10183/218251/1/001061825.pdfac938ed1c06a5dfa320cb2dc6249928eMD5110183/2182512021-04-12 08:32:34.519122oai:www.lume.ufrgs.br:10183/218251Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2021-04-12T11:32:34Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
title |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
spellingShingle |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures Frozza, Rudimar Luiz Peptídeos beta-amilóides Caspase 3 Doença de Alzheimer Alzheimer’s disease Amyloid b-peptide Organotypic culture Caspase-3 |
title_short |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
title_full |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
title_fullStr |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
title_full_unstemmed |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
title_sort |
A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures |
author |
Frozza, Rudimar Luiz |
author_facet |
Frozza, Rudimar Luiz Horn, Ana Paula Hoppe, Juliana Bender Simão, Fabrício Gerhardt, Daniéli Comiran, Ricardo Argenta Salbego, Christianne Gazzana |
author_role |
author |
author2 |
Horn, Ana Paula Hoppe, Juliana Bender Simão, Fabrício Gerhardt, Daniéli Comiran, Ricardo Argenta Salbego, Christianne Gazzana |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Frozza, Rudimar Luiz Horn, Ana Paula Hoppe, Juliana Bender Simão, Fabrício Gerhardt, Daniéli Comiran, Ricardo Argenta Salbego, Christianne Gazzana |
dc.subject.por.fl_str_mv |
Peptídeos beta-amilóides Caspase 3 Doença de Alzheimer |
topic |
Peptídeos beta-amilóides Caspase 3 Doença de Alzheimer Alzheimer’s disease Amyloid b-peptide Organotypic culture Caspase-3 |
dc.subject.eng.fl_str_mv |
Alzheimer’s disease Amyloid b-peptide Organotypic culture Caspase-3 |
description |
Accumulation of the neurotoxic amyloid b-peptide (Ab) in the brain is a hallmark of Alzheimer’s disease (AD). Several synthetic Ab peptides have been used to study the mechanisms of toxicity. Here, we sought to establish comparability between two commonly used Ab peptides Ab1-42 and Ab25-35 on an in vitro model of Ab toxicity. For this purpose we used organotypic slice cultures of rat hippocampus and observed that both Ab peptides caused similar toxic effects regarding to propidium iodide uptake and caspase-3 activation. In addition, we also did not observe any effect of both peptides on Akt and PTEN phosphorylation; otherwise the phosphorylation of GSK-3b was increased. Although further studies are necessary for understanding mechanisms underlying Ab peptide toxicity, our results provide strong evidence that Ab1-42 and the Ab25-35 peptides induce neural injury in a similar pattern and that Ab25-35 is a convenient tool for the investigation of neurotoxic mechanisms involved in AD. |
publishDate |
2009 |
dc.date.issued.fl_str_mv |
2009 |
dc.date.accessioned.fl_str_mv |
2021-02-26T04:12:45Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10183/218251 |
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0364-3190 |
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001061825 |
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0364-3190 001061825 |
url |
http://hdl.handle.net/10183/218251 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Neurochemical research. New York, NY. Vol. 34, no. 2 (Feb. 2009), p. 295-303 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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