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Background  Toxocariasis is a worldwide zoonotic parasitic disease mainly caused by  Toxocara canis . Humans can be infected by accidental ingestion of  T. canis  embryonated ovum-contaminated food, water, or encapsulated larvae in paratenic hosts’ viscera or meat. Since humans and mice are paratenic hosts of  T. canis , the wandering larvae might cause mechanical tissue damage and excretory-secretory antigens may trigger inflammatory injuries to local organs. Long-term residence of  T. canis  larvae in a paratenic host’s brain may cause cerebral toxocariasis (CT) that contributes to cerebral damage, neuroinflammation and neuropsychiatric disorders in mice and clinical patients. Since the hippocampus has been long recognized as being responsible for learning and memory functions, parasitic invasion of this site may cause neuroinflammatory and neurodegenerative disorders. The present study intended to assess pathological changes, expressions of neurodegeneration-associated factors (NDAFs), including transforming growth factor (TGF)-β1, S100B, glial fibrillary acidic protein (GFAP), transglutaminase type 2 (TG2), claudin-5, substance P (SP) and interleukin (IL)-1β, and the ubiquitin-proteasome system (UPS) function in the hippocampus and associated cognitive behavior in ICR mice orally inoculated with a high, medium or low-dose of  T. canis  embryonated ova during a 20-week investigation.    Results  Results indicated although there were insignificant differences in learning and memory function between the experimental mice and uninfected control mice, possibly because the site where  T. canis  larvae invaded was the surrounding area but not the hippocampus per se. Nevertheless, enhanced expressions of NDAF, persistent UPS impairment and excess amyloid β (Aβ) accumulation concomitantly emerged in the experimental mice hippocampus at 8, 16 and 20 weeks post-infection.    Conclusions  We thus postulate that progressive CT may still progress to neurodegeneration due to enhanced NDAF expressions, persistent UPS impairment and excess Aβ accumulation in the hippocampus.    Electronic supplementary material  The online version of this article (10.1186/s13071-017-2578-6) contains supplementary material, which is available to authorized users.

parasites and vectors

Enhanced expressions of neurodegeneration-associated factors, UPS impairment, and excess Aβ accumulation in the hippocampus of mice with persistent cerebral toxocariasis