Memory impairment in chronic experimental Chagas disease: Benznidazole therapy reversed cognitive deficit in association with reduction of parasite load and oxidative stress in the nervous tissue

dc.creatorPereira, Glaucia Vilar
dc.creatorBarrios, Leda Castaño
dc.creatorSilva, Andrea Alice da
dc.creatorBatista, Angelica Martins
dc.creatorPereira, Isabela Resende
dc.creatorMoreira, Otacílio Cruz
dc.creatorBritto, Constança
dc.creatorSantos, Hilton Antônio Mata dos
dc.creatorVieira, Joseli Lannes
dc.date2021-03-30T19:51:52Z
dc.date2021-03-30T19:51:52Z
dc.date2021
dc.date.accessioned2023-09-26T20:36:12Z
dc.date.available2023-09-26T20:36:12Z
dc.identifierPEREIRA, Glaucia Vilar et al. Memory impairment in chronic experimental Chagas disease: Benznidazole therapy reversed cognitive deficit in association with reduction of parasite load and oxidative stress in the nervous tissue. Plos One, v. 16, n.1, e0244710, 21p, Jan. 2021.
dc.identifier1932-6203
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/46469
dc.identifier10.1371/journal.pone.0244710
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8860401
dc.descriptionMemory impairment has been associated with chronic Chagas disease (CD), a neglected tropical disease caused by the protozoan parasite Trypanosoma cruzi. In degenerative diseases, memory loss has been associated with increased oxidative stress, revealed as enhanced lipid peroxidation, in the cerebral cortex. Benznidazole (Bz), a trypanocidal drug efficient to reduce blood parasite load in the acute and chronic phases of infection, showed controversial effects on heart disease progression, the main clinical manifestation of CD. Here, we evaluated whether C57BL/6 mice infected with the Colombian type I T. cruzi strain present memory deficit assessed by (i) the novel object recognition task, (ii) the open field test and (iii) the aversive shock evoked test, at 120 days post infection (dpi). Next, we tested the effects of Bz therapy (25mg/Kg/day, for 30 consecutive days) on memory evocation, and tried to establish a relation between memory loss, parasite load and oxidative stress in the central nervous system (CNS). At 120 dpi, T. cruzi-infected mice showed memory impairment, compared with age-matched non-infected controls. Bz therapy (from 120 to 150 dpi) hampered the progression of habituation and aversive memory loss and, moreover, reversed memory impairment in object recognition. In vehicle-administered infected mice, neuroinflammation was absent albeit rare perivascular mononuclear cells were found in meninges and choroid plexus. Bz therapy abrogated the infiltration of the CNS by inflammatory cells, and reduced parasite load in hippocampus and cerebral cortex. At 120 and 150 dpi, lipid peroxidation was increased in the hippocampus and cortex tissue extracts. Notably, Bz therapy reduced levels of lipid peroxidation in the cerebral cortex. Therefore, in xperimental chronic T. cruzi infection Bz therapy improved memory loss, in association with reduction of parasite load and oxidative stress in the CNS, providing a new perspective to improve the quality of life of Chagas disease patients.
dc.formatapplication/pdf
dc.languageeng
dc.publisherPublic Library of Science
dc.rightsopen access
dc.subjectDoença de Chagas
dc.subjectTerapia de benznidazol
dc.subjectCarga de parasitas
dc.subjectEstresse oxidativo
dc.subjectTecido nervoso
dc.subjectComprometimento da memória em experimentos crônicos
dc.subjectChagas disease
dc.subjectBenznidazole therapy
dc.subjectParasite load
dc.subjectOxidative stress
dc.subjectNervous tissue
dc.subjectMemory impairment in chronic experimental
dc.titleMemory impairment in chronic experimental Chagas disease: Benznidazole therapy reversed cognitive deficit in association with reduction of parasite load and oxidative stress in the nervous tissue
dc.typeArticle


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