G
Gigliola Ramírez
Researcher at Pontifical Catholic University of Chile
Publications - 18
Citations - 630
Gigliola Ramírez is an academic researcher from Pontifical Catholic University of Chile. The author has contributed to research in topics: Microglia & Neuroinflammation. The author has an hindex of 12, co-authored 18 publications receiving 542 citations. Previous affiliations of Gigliola Ramírez include University of the Andes, Chile & University of Los Andes.
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Oligodendrocytes damage in Alzheimer's disease: Beta amyloid toxicity and inflammation
TL;DR: Reports on oligodendrocytes' compromise in AD are analyzed and experimental data indicative of Abeta toxicity in culture are discussed, showing an astrocyte-mediated protective effect over Abeta-induced damage on hippocampal cells and modulation of the activation of microglial cells in culture.
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Microglia astrocyte interaction in Alzheimer's disease: friends or foes for the nervous system?
TL;DR: Brain glial cells secrete several molecules that can modulate the survival of neurons after various types of damage to the CNS, and the events occurring in response to injury may lead to changes in the nature and relative concentration of the various factors involved.
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Age-dependent changes on TGFβ1 Smad3 pathway modify the pattern of microglial cell activation
Juan E. Tichauer,Betsi Flores,Bernardita Soler,Laura Eugenín-von Bernhardi,Gigliola Ramírez,Rommy von Bernhardi +5 more
TL;DR: Age-related impairment of TGFβ1-Smad3 can reduce protective activation while facilitating cytotoxic activation of microglia, potentiating microglIA-mediated neurodegeneration.
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Protection of rat primary hippocampal cultures from Aβ cytotoxicity by pro-inflammatory molecules is mediated by astrocytes
TL;DR: LPS + IFN-gamma, traditionally considered as pro-apoptotic, reduced apoptosis induced by A beta through the activation of neuroprotective mechanisms mediated by astrocytes, suggesting that astroCytes are pivotal in the modulation of inflammation of the CNS.
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Pro-inflammatory conditions promote neuronal damage mediated by Amyloid Precursor Protein and decrease its phagocytosis and degradation by microglial cells in culture.
TL;DR: The hypothesis that, in neuroinflammation, microglial scavenger function is impaired and reactivity against APP enhanced as an initial step for neurodegeneration is supported.