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Título : Increased tau phosphorylation and receptor for advanced glycation endproducts (RAGE) in the brain of mice infected with Leishmania amazonensis
Autor: Gasparotto, Juciano
Senger, Mario Roberto
Kunzler, Alice
Degrossoli, Adriana
Simone, Salvatore Giovanni de
Bortolin, Rafael Calixto
Somensi, Nauana
Girardi, Carolina Saibro
Souza, Celeste da Silva Freitas de
Calabrese, Kátia da Silva
Dal-Pizzol, Felipe
Moreira, José Claudio Fonseca
Silva Junior, Floriano Paes
Gelain, Daniel Pens
Palavras-chave: Leishmaniasis
Oxidative stress
Neurodegenerative diseases
Estresse oxidativo
Doenças neurodegenerativas
Publicador: Elsevier, Academic Press
Data da publicação: Jan-2015
Referência: GASPAROTTO, J. et al. Increased tau phosphorylation and receptor for advanced glycation endproducts (RAGE) in the brain of mice infected with Leishmania amazonensis. Brain, Behavior and Immunity, Orlando, v. 43, p. 37-45, Jan 2015.
Abstract: Leishmaniasis is a parasitosis caused by several species of the genus Leishmania, an obligate intramacrophagic parasite. Although neurologic symptoms have been observed in human cases of leishmaniasis, the manifestation of neurodegenerative processes is poorly studied. The aim of the present work was to investigate if peripheral infection of BALB/c mice with Leishmania amazonensis affects tau phosphorylation and RAGE protein content in the brain, which represent biochemical markers of neurodegenerative processes observed in diseases with a pro-inflammatory component, including Alzheimer’s disease and Down syndrome. Four months after a single right hind footpad subcutaneous injection of L. amazonensis, the brain cortex of BALB/c mice was isolated. Western blot analysis indicated an increase in tau phosphorylation (Ser396) and RAGE immunocontent in infected animals. Brain tissue TNF-α, IL-1β, and IL-6 levels were not different from control animals; however, increased protein carbonylation, decreased IFN-γ levels and impairment in antioxidant defenses were detected. Systemic antioxidant treatment (NAC 20 mg/kg, i.p.) inhibited tau phosphorylation and recovered IFN-γ levels. These data, altogether, indicate an association between impaired redox state, tau phosphorylation and RAGE up-regulation in the brain cortex of animals infected with L. amazonensis. In this context, it is possible that neurologic symptoms associated to chronic leishmaniasis are associated to disruptions in the homeostasis of CNS proteins, such as tau and RAGE, as consequence of oxidative stress. This is the first demonstration of alterations in biochemical parameters of neurodegeneration in an experimental model of Leishmania infection.
Idioma: en_US
Aparece nas coleções:DSA - Artigos publicados em periódicos

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