Toxocara canis belongs to one of zoonotic parasites that commonly infects canines worldwide, and its eggs in host faeces may contaminate the food, water, soil and their fur as well as the larvae entrapped in the granuloma can infect paratenic hosts including mice and humans. Survivability of T. canis embryonated eggs under moist, cool conditions may be as long as 2–4 years or more. In paratenic hosts such as mice and humans, T. canis L3 larvae neither moult, grow, nor replicate and will wander through a number of internal organs in humans so as to cause Th2-dominant pathology in various internal organs as leading to neurotoxocariasis (NT), ocular toxocariasis (OT), or visceral larva migrans (VLM). Although the systemic immune response to T. canis has been widely reported, the immune response in the brain has received little attention. Differential cytokine expression and other brain injury-associated biomarkers or neurodegeneration-associated factors have been observed in infected versus uninfected outbred and inbred mice. Preliminary data have also suggested a possible link between significant memory impairment and cytokine production associated with T. canis infection in the hippocampus which has been long recognised as being responsible for learning and memory functions. Notably, it remains an enigma concerning cerebral invasion by T. canis larvae rarely induces a recognisable neurological syndrome or its involvement in neuropathological disorders in humans. Exploration of the relationship between host and parasite in the brain may elucidate the cryptic symptoms of human cerebral toxocariasis, with patients presenting with mental retardation, epilepsy, neurodegeneration and other central nervous system (CNS) disorders.