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

Gasparotto, Juciano and Senger, Mario Roberto and de Sa Moreira, Emilio Telles and Brum, Pedro Ozorio and Kessler, Flavio Gabriel Carazza and Peixoto, Daniel Oppermann and Panzenhagen, Alana Castro and Ong, Lin Kooi ORCID: https://orcid.org/0000-0001-8664-0540 and Soares, Marlene Campos and Reis, Patricia Alves and Schirato, Giuliana Viegas and Valente, Walter Cesar Goes and Montoya, Bogar Omar Araujo and Silva, Floriano P. and Moreira, Jose Claudio Fonseca and Dal-Pizzol, Felipe and Castro-Faria-Neto, Hugo C. and Gelain, Daniel Pens (2021) Neurological impairment caused by Schistosoma mansoni systemic infection exhibits early features of idiopathic neurodegenerative disease. Journal of Biological Chemistry, 297 (2):100979. pp. 1-17.

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Abstract

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.


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Item Type: Article (Commonwealth Reporting Category C)
Refereed: Yes
Item Status: Live Archive
Faculty/School / Institute/Centre: No Faculty
Faculty/School / Institute/Centre: No Faculty
Date Deposited: 10 Jun 2022 01:09
Last Modified: 13 Jun 2022 01:35
Uncontrolled Keywords: Amyloid-beta peptides; Central nervous systems; Learning and memory; Neglected tropical disease; Neurologic function; Schistosoma mansoni; Social development; Synergistic effect
Fields of Research (2020): 32 BIOMEDICAL AND CLINICAL SCIENCES > 3204 Immunology > 320499 Immunology not elsewhere classified
32 BIOMEDICAL AND CLINICAL SCIENCES > 3214 Pharmacology and pharmaceutical sciences > 321405 Pharmaceutical sciences
32 BIOMEDICAL AND CLINICAL SCIENCES > 3209 Neurosciences > 320902 Cellular nervous system
Socio-Economic Objectives (2020): 20 HEALTH > 2001 Clinical health > 200105 Treatment of human diseases and conditions
Identification Number or DOI: https://doi.org/10.1016/j.jbc.2021.100979
URI: http://eprints.usq.edu.au/id/eprint/48231

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