Protection of rat primary hippocampal cultures from A beta cytotoxicity by pro-inflammatory molecules is mediated by astrocytes

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dc.contributor.authorRamirez, G
dc.contributor.authorToro, R
dc.contributor.authorDobeli, H
dc.contributor.authorvon Bernhardi, R
dc.date.accessioned2024-01-10T14:21:29Z
dc.date.available2024-01-10T14:21:29Z
dc.date.issued2005
dc.description.abstractThe brain of Alzheimer's disease patients shows abundant dystrophic neurites in close proximity to fibrillar beta-amyloid (A beta) plaques, and activated glial cells. We evaluated the influence of pro-inflammatory molecules (LPS + IFN-gamma) on A beta(1-42) neurotoxicity. 2 mu M A beta(1-42) induced apoptosis of hippocampal cells and LPS + IFN-gamma reduced the apoptosis induced by A beta. However, LPS + IFN-gamma prevented apoptosis only in hippocampal cultures containing astrocytes. Also, LPS + IFN-gamma induced the secretion of TGF beta, a cytokine having neuroprotective effects, only in hippocampal cultures that contained astrocytes. Astrocytes had a regulatory effect over microglial and neuronal responses to A. The results suggest that LPS + IFN-gamma, traditionally considered as pro-apoptotic, reduced apoptosis induced by A beta through the activation of neuroprotective mechanisms mediated by astrocytes. We propose that astrocytes are pivotal in the modulation of inflammation of the CNS. The impairment of the regulatory functions performed by activated astrocytes could represent an important pathogenic mechanism for neurodegenerative diseases. (c) 2005 Elsevier Inc. All rights reserved.
dc.fechaingreso.objetodigital03-04-2024
dc.format.extent12 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.nbd.2005.01.007
dc.identifier.eissn1095-953X
dc.identifier.issn0969-9961
dc.identifier.pubmedidMEDLINE:15837580
dc.identifier.urihttps://doi.org/10.1016/j.nbd.2005.01.007
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79680
dc.identifier.wosidWOS:000228672900026
dc.information.autorucMedicina;Von Bernhardi R;S/I;62523
dc.issue.numero1-2
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final254
dc.pagina.inicio243
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.revistaNEUROBIOLOGY OF DISEASE
dc.rightsacceso restringido
dc.subjectAlzheimer's disease
dc.subjectamyloid peptide
dc.subjectcytotoxicity
dc.subjectneuroprotection
dc.subjectastrocytes
dc.subjectGROWTH-FACTOR-BETA
dc.subjectGAMMA GENE-EXPRESSION
dc.subjectNEURONAL CELL-DEATH
dc.subjectTOLL-LIKE RECEPTORS
dc.subjectAMYLOID-BETA
dc.subjectALZHEIMERS-DISEASE
dc.subjectINTERFERON-GAMMA
dc.subjectIN-VITRO
dc.subjectNITRIC-OXIDE
dc.subjectSENSORY NEURONS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleProtection of rat primary hippocampal cultures from A beta cytotoxicity by pro-inflammatory molecules is mediated by astrocytes
dc.typeartículo
dc.volumen19
sipa.codpersvinculados62523
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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