A comparative study of beta-amyloid peptides Abeta1-42 and Abeta25-35 toxicity in organotypic hippocampal slice cultures

Detalhes bibliográficos
Autor(a) principal: Frozza, Rudimar Luiz
Data de Publicação: 2009
Outros Autores: Horn, Ana Paula, Hoppe, Juliana Bender, Simão, Fabrício, Gerhardt, Daniéli, Comiran, Ricardo Argenta, Salbego, Christianne Gazzana
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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spelling 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
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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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