Taenia solium development and host interactions in neurocysticercosis: a narrative mini review on mechanistic pathways to epileptogenesis

Abstract

Neurocysticercosis (NCC), a central nervous system infection caused by the larval stage of Taenia solium, remains a leading cause of acquired epilepsy in endemic regions. Mounting evidence indicates that seizure development in NCC is not solely driven by host inflammatory responses but reflects complex, dynamic interactions between parasite development, host neuroimmune processes, and neuronal network remodeling. This narrative mini-review integrates experimental and clinical data to demonstrate that T. solium larvae actively shape the cerebral microenvironment through stage-specific immune modulation, blood–brain barrier disruption, and the release of neuroactive excretory–secretory products. During cyst degeneration, parasite antigens and excitatory amino acids drive microglial and astrocytic activation, amplify glutamatergic signaling, and destabilize inhibitory neurotransmission, collectively reducing seizure thresholds. These acute events are followed by chronic structural alterations, including perilesional gliosis, synaptic reorganization, and persistent network hyperexcitability, particularly around parenchymal and calcified lesions that serve as enduring epileptogenic foci. Integrating parasite developmental biology with neuroimmune and neuroexcitatory mechanisms, this review reconceptualizes NCC epileptogenesis as an active, multilevel dialogue between parasite, host, and neuron, rather than a passive, inflammation-driven consequence of infection. This integrated mechanistic framework highlights opportunities for biomarker discovery and therapeutic strategies that look beyond mere parasite eradication to address sustained neural dysfunction. It further underscores the critical need for One Health-oriented interventions to disrupt the T. solium transmission cycle and alleviate the long-term burden of NCC-associated epilepsy.