Neurological impairment caused by Schistosoma mansoni systemic infection exhibits early features of idiopathic neurodegenerative disease

• Autor(a) principal: Gasparotto, Juciano
• Data de Publicação: 2021
• Outros Autores: Senger, Mário Roberto, Moreira, Emilio Telles de Sá, Brum, Pedro Ozorio, Kessler, Flávio Gabriel Carazza, Peixoto, Daniel Oppermann, Panzenhagen, Alana Eduarda de Castro, Ong, Lin Kooi, Campos, Marlene Soares, Reis, Patricia Alves, Schirato, Giuliana Viegas, Valente, Walter César Góes, Montoya, Bogar Omar Araújo, Silva Junior, Floriano Paes, Moreira, Jose Claudio Fonseca, Dal Pizzol, Felipe, Faria Neto, Hugo Caire de Castro, Gelain, Daniel Pens
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/230768
• topic: Esquistossomose mansoni; Disfunção cognitiva; Praziquantel; Estresse oxidativo; Fosforilação; Proteínas tau; Encefalite

Schistosomiasis, a neglected tropical disease caused by trematodes of the Schistosoma genus, affects over 250 million people around the world. This disease has been associated with learning and memory deficits in children, whereas reduced attention levels, impaired work capacity, and cognitive deficits have been observed in adults. Strongly correlated with poverty and lack of basic sanitary conditions, this chronic endemic infection is common in Africa, South America, and parts of Asia and contributes to inhibition of social development and low quality of life in affected areas. Nonetheless, studies on the mechanisms involved in the neurological impairment caused by schistosomiasis are scarce. Here, we used a murine model of infection with Schistosoma mansoni in which parasites do not invade the central nervous system to evaluate the consequences of systemic infection on neurologic function. We observed that systemic infection with S. mansoni led to astrocyte and microglia activation, expression of oxidative stress-induced transcription factor Nrf2, oxidative damage, Tau phosphorylation, and amyloid-β peptide accumulation in the prefrontal cortex of infected animals. We also found impairment in spatial learning and memory as evaluated by the Morris water maze task. Administration of anthelmintic (praziquantel) and antioxidant (N-acetylcysteine plus deferoxamine) treatments was effective in inhibiting most of these phenotypes, and the combination of both treatments had a synergistic effect to prevent such changes. These data demonstrate new perspectives toward the understanding of the pathology and possible therapeutic approaches to counteract long-term effects of systemic schistosomiasis on brain function.