RGD Reference Report - Increased tau phosphorylation and receptor for advanced glycation endproducts (RAGE) in the brain of mice infected with Leishmania amazonensis. - Rat Genome Database

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Increased tau phosphorylation and receptor for advanced glycation endproducts (RAGE) in the brain of mice infected with Leishmania amazonensis.

Authors: Gasparotto, J  Senger, MR  Kunzler, A  Degrossoli, A  De Simone, SG  Bortolin, RC  Somensi, N  Girardi, CS  De Souza, CD  Calabrese, KD  Dal-Pizzol, F  Moreira, JC  Silva-Jr, FP  Gelain, DP 
Citation: Gasparotto J, etal., Brain Behav Immun. 2014 Jul 8. pii: S0889-1591(14)00389-4. doi: 10.1016/j.bbi.2014.06.204.
RGD ID: 8695986
Pubmed: PMID:25014011   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbi.2014.06.204   (Journal Full-text)

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-alpha, IL-1beta, and IL-6 levels were not different from control animals; however, increased protein carbonylation, decreased IFN-gamma levels and impairment in antioxidant defenses were detected. Systemic antioxidant treatment (NAC 20mg/kg, i.p.) inhibited tau phosphorylation and recovered IFN-gamma 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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
leishmaniasis  ISOAger (Mus musculus)8695986; 8695986protein:increased expression:brainRGD 
leishmaniasis  IEP 8695986protein:increased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Mus musculus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Homo sapiens)
AGER  (advanced glycosylation end-product specific receptor)


Additional Information