Background: Experimental models of neurocysticercosis (NCC) are helpful for an improved understanding of the pathophysiological mechanisms of human diseases and for testing novel therapeutic approaches. Controlling inflammation without reducing the effectiveness of anthelmintics is an important challenge in treating neurocysticercosis. This study investigates the effects of currently used drugs (Albendazole and Dexamethasone) in treating murine extraparenchymal NCC. Methods: Twenty-two rats were inoculated with Taenia crassiceps in the subarachnoid space. The animals underwent magnetic resonance imaging to ascertain the success of infection 3 months after inoculation. The infected animals were randomly assigned to one of the three groups (five rats each): control (no treatment), Albendazole (ABZ), or Albendazole + Dexamethasone (ABZ + DXM) for 14 days. The animals were subsequently euthanised for morphological assessment 2 weeks after the end of treatment. Results: Macroscopically integrated cysts were found in all animals. The ABZ + DXM animals demonstrated lower ventricular sizes, lymphocyte infiltration rates, and immunopositivity for IL-6, with statistical differences in lymphocytes within the arachnoid region. Conclusions: This experimental model, which has previously shown similarities to human infections, is also helpful in reproducing the morphological changes upon treatment with Albendazole and Dexamethasone.

Oxidative stress is associated with several infectious diseases, as well as the severity of inflammatory reactions. The control of inflammation during parasite destruction is a target of neurocysticercosis treatment, as inflammation is strongly related to symptom severity. In this study, we investigated the presence of malondialdehyde and protein carbonyl, two by-products of reactive oxygen species (ROS), in an experimental model of extraparenchymal neurocysticercosis. Twenty male and twenty female rats were inoculated with 50 cysts of Taenia crassiceps in the subarachnoid space of the cisterna magna. Ten animals (five males and five females) were used as controls. Three months after inoculation, their brains were harvested for oxidative stress and histological assessments. Infected animals had higher scores for inflammatory cell infiltrates, malondialdehyde, and protein carbonyl. These results encourage future efforts to monitor oxidative stress status in neurocysticercosis, particularly in the context of controlling inflammation.

Purpose Experimental models might help understand the pathophysiology of neurocysticercosis-associated hydrocephalus. The present study aimed to compare the extent of hydrocephalus and tissue damage in rats with subarachnoid inoculation of different concentrations of Taenia crassiceps cyst proteins. Methods Sixty young rats were divided into two groups: low- and high-concentration groups. The animals in the low concentration group received 0.02 ml of 2.4 mg/ml T. crassiceps cyst proteins while those in the high concentration group received 0.02 ml of 11.6 mg/ml T. crassiceps cyst proteins. The animals underwent magnetic resonance imaging at 1, 3, and 6 months postinoculation to assess the ventricle volume. Morphological assessment was performed at the end of the observation period. Results Repeated measures of ventricle volumes at 1, 3, and 6 months showed progressive enlargement of the ventricles. At 1 and 3 months, we observed no differences in ventricle volumes between the 2 groups. However, at 6 months, the ventricles were larger in the high concentration group (median = 3.86 mm³, range: 2.37–12.68) compared with the low concentration group (median = 2.00 mm³, range: 0.37–11.57), p = 0.003. The morphological assessment revealed a few inflammatory features in both groups. However, the density of oligodendrocytes and neurons within the periventricular region was lower in the high concentration group (5.18 versus 9.72 for oligodendrocytes and 15.69 versus 21.00 for neurons; p < 0.001 for both). Conclusion Our results suggest that, in rats, a higher concentration of T. crassiceps cyst proteins in the subarachnoid space could induce ventricle enlargement and reduce the number of neurons within the periventricular area. Objetivo Modelos experimentais podem ajudar a entender a fisiopatologia da hidrocefalia associada à neurocisticercose. O presente estudo teve como objetivo comparar a extensão da hidrocefalia e dano tecidual em ratos com inoculação subaracnóidea de diferentes concentrações de proteínas de cistos de Taenia crassiceps. Métodos Sessenta ratos jovens foram divididos em dois grupos: grupos de baixa e alta concentração. Os animais do grupo de baixa concentração receberam 0,02 ml de proteínas de cisto de T. crassiceps (2,4 mg/ml), enquanto os do grupo de alta concentração receberam 0,02 ml de proteínas de cisto de T. crassiceps (11,6 mg/ml). Os animais foram submetidos à ressonância magnética 1, 3 e 6 meses após a inoculação para avaliar o volume do ventrículo. A avaliação morfológica foi realizada no final do período de observação. Resultados Medidas repetidas dos volumes ventriculares aos 1, 3 e 6 meses mostraram aumento progressivo dos ventrículos. Após 1 e 3 meses, não observamos diferenças nos volumes ventriculares entre os 2 grupos. No entanto, aos 6 meses, os ventrículos foram maiores no grupo de alta concentração (mediana = 3,86 mm³, variação: 2,37–12,68) em comparação com o grupo de baixa concentração (mediana = 2,00 mm³, variação: 0,37–11,57; p = 0,003). A avaliação morfológica revelou algumas características inflamatórias nos dois grupos. No entanto, a densidade de oligodendrócitos e neurônios na região periventricular foi menor no grupo de alta concentração (5,18 versus 9,72 para oligodendrócitos e 15,69 versus 21,00 para neurônios; p < 0,001 para ambos). Conclusão Nossos resultados sugerem que, em ratos, uma maior concentração de proteínas do cisto de T. crassiceps no espaço subaracnóideo poderia induzir o aumento do ventrículo e reduzir o número de neurônios na área periventricular. Received: 03 July 2020 Accepted: 24 August 2020 Publication Date: 26 November 2020 (online) © 2020. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/). Thieme Revinter Publicações Ltda. Rua do Matoso 170, Rio de Janeiro, RJ, CEP 20270-135, Brazil

We read with great interest the recent article by Moura et al, titled “Demyelination in experimental intraventricular neurocysticercosis”¹. The authors are well-experienced with experimental neurocysticercosis, having previously published papers demonstrating inflammatory features in this model, as well as the effects of anti-parasitic drugs on the energetic metabolism of Taenia crassiceps^2,3,4.