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Angélica Castaño

Researcher at University of Seville

Publications -  34
Citations -  2146

Angélica Castaño is an academic researcher from University of Seville. The author has contributed to research in topics: Microglia & Dopaminergic. The author has an hindex of 21, co-authored 34 publications receiving 1984 citations. Previous affiliations of Angélica Castaño include Mansfield University of Pennsylvania & University of Oxford.

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Lipopolysaccharide intranigral injection induces inflammatory reaction and damage in nigrostriatal dopaminergic system.

TL;DR: The results suggest that the nigrostriatal dopaminergic system is susceptible to damage by inflammatory events and that these may be implicated in neurodegeneration processes such as Parkinson's disease.
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The Single Intranigral Injection of LPS as a New Model for Studying the Selective Effects of Inflammatory Reactions on Dopaminergic System

TL;DR: It is suggested that the injection of a single dose of LPS within the SN is an interesting model for studying the selective effects of inflammatory reaction on dopaminergic system and also potentially useful for studying PD.
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The degenerative effect of a single intranigral injection of LPS on the dopaminergic system is prevented by dexamethasone, and not mimicked by rh‐TNF‐α, IL‐1β and IFN‐γ

TL;DR: Results suggest that inflammatory response is implicated in LPS‐induced neurodegeneration, and may be due, at least in part, to a cascade of events independent of that described for TNF‐α/IL‐1β/IFN‐γ.
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Cellular environment facilitates protein accumulation in aged rat hippocampus

TL;DR: It is demonstrated that unfolding protein response (UPR) is not correctly activated in aged rat hippocampus, and the up-regulation of apoptotic pathway mediators is increased in aged rats, suggesting the existence of age-related deficits in the systems involved in the defense against unfolded proteins.
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Anti-inflammatory Activity of a Honey Flavonoid Extract on Lipopolysaccharide-Activated N13 Microglial Cells

TL;DR: It is demonstrated that HFE is a potent inhibitor of microglial activation and thus a potential preventive-therapeutic agent for neurodegenerative diseases involving neuroinflammation.