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In vitro and in vivo activation of astrocytes by amyloid-beta is potentiated by pro-oxidant agents

AutorGarcía-Matas, Silvia ; Vera, Núria de ; Aznar, A. O.; Marimon, J. M.; Adell, Albert ; Planas, Anna M. ; Cristòfol, Rosa ; Sanfeliu, Coral
Palabras claveInflammation
Iron
Oxidative stress
Rat model of Alzheimer's disease
Human astrocyte cultures
Amyloid-β peptide
Fecha de publicación2010
EditorIOS Press
CitaciónJournal of Alzheimer's Disease 20(1): 229 (2010)
ResumenAlzheimer's disease (AD) is a devastating age-related neurodegenerative disease. Age is the main risk factor for sporadic AD, which is the most prevalent type. Amyloid-β peptide (Aβ) neurotoxicity is the proposed first step in a cascade of deleterious events leading to AD pathology and dementia. Glial cells play an important role in these changes. Astrocytes provide vital support to neurons and modulate functional synapses. Therefore, the toxic effects of Aβ on astrocytes might promote neurodegenerative changes that lead to AD. Aging reduces astrocyte antioxidant defenses and induces oxidative stress. We studied the effects of Aβ {42} on cultures of human astrocytes in the presence or absence of the following pro-oxidant agents: buthionine sulfoximine (BSO), a glutathione synthesis inhibitor, and FeSO{4}, which liberates redox active iron. Pro-oxidant conditions potentiated Aβ toxicity, as shown by the generation of free radicals, inflammatory changes, and apoptosis. Similar treatments were assessed in rats in vivo. A combination of Aβ {40} and Aβ {42} or Aβ {42} alone was infused intracerebroventricularly for 4 weeks. Other animal groups were also infused with BSO and FeSO{4}. A long-term analysis that ended 4 months later showed greater cognitive impairment in the Morris water maze task, which was induced by Aβ plus pro-oxidant agent treatments. Pro-oxidant agents also potentiated brain tissue pathology. This was demonstrated in histological studies that showed highly increased astrocyte reactivity in AD-vulnerable areas, Aβ deposits, and oxidative damage of AD-sensitive hippocampal neurons. To increase our understanding of AD, experimental models should be used that mimic age-related brain changes, in which age-related oxidative stress potentiates the effects of Aβ.
Versión del editorhttps://doi.org/10.3233/JAD-2010-1365
URIhttp://hdl.handle.net/10261/147753
DOI10.3233/JAD-2010-1365
Identificadoresissn: 1387-2877
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