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Astrocytes protect neurons from Aβ1-42 peptide-induced neurotoxicity increasing TFAM and PGC-1 and decreasing PPAR-γ and SIRT-1.

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Astrocytes protect neurons from Aβ1-42 peptide-induced neurotoxicity increasing TFAM and PGC-1 and decreasing PPAR-γ and SIRT-1.

dc.contributor.author	Aguirre Rueda, Diana
dc.contributor.author	Guerra Ojeda, Sol
dc.contributor.author	Aldasoro Celaya, Martín
dc.contributor.author	Iradi Casal, Antonio
dc.contributor.author	Obrador, Elena
dc.contributor.author	Ortega Valero, Ángel L.
dc.contributor.author	Mauricio Aviñó, María Dolores
dc.contributor.author	Vila Salinas, José María
dc.contributor.author	Vallés Martí, Lilián Soraya
dc.date.accessioned	2016-01-08T12:22:37Z
dc.date.available	2016-01-08T12:22:37Z
dc.date.issued	2015
dc.identifier.citation	Aguirre Rueda, Diana; Guerra Ojeda, Sol; Aldasoro Celaya, Martín; Iradi, Antonio; Obrador, Elena; Ortega, Angel; Mauricio, María Dolores; Vila, José María; Valles, Soraya L. (2015) Astrocytes protect neurons from Aβ1-42 peptide-induced neurotoxicity increasing TFAM and PGC-1 and decreasing PPAR-γ and SIRT-1. International Journal Of Medical Sciences jan 1 12 (1) 48 56
dc.identifier.uri	http://hdl.handle.net/10550/49869
dc.description.abstract	One of the earliest neuropathological events in Alzheimer¿s disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) and mitochondrial transcription factor A (TFAM), protecting mitochondria against Aβ1-42-induced damage and promoting mitochondrial biogenesis. In summary our data suggest that astrocytes may have a key role in protecting neurons, increasing neural viability and mitochondrial biogenesis, acquiring better oxidative stress protection and perhaps modulating inflammatory processes against Aβ1-42 toxic peptide. This might be a sign of a complex epigenetic process in Alzheimer¿s disease development.
dc.language.iso	eng
dc.relation.ispartof	International Journal Of Medical Sciences, 2015, vol. jan 1, num. 12 (1), p. 48-56
dc.subject	Neurologia
dc.subject	Fisiologia humana
dc.title	Astrocytes protect neurons from Aβ1-42 peptide-induced neurotoxicity increasing TFAM and PGC-1 and decreasing PPAR-γ and SIRT-1.
dc.type	journal article	es_ES
dc.date.updated	2016-01-08T12:22:38Z
dc.identifier.doi	10.7150/ijms.10035
dc.identifier.idgrec	106093
dc.rights.accessRights	open access	es_ES