Toxoplasma gondii-induced neuronal alterations.
The zoonotic pathogen Toxoplasma gondii infects over 30% of the human population. The intracellular parasite can persist lifelong in the CNS within neurons modifying their function and structure, thus leading to specific behavioural changes of the host. In recent years, several in vitro studies and murine models have focused on the elucidation of these modifications. Furthermore, investigations of the human population have correlated Toxoplasma seropositivity with changes in neurological functions; however, the complex underlying mechanisms of the subtle behavioural alteration are still not fully understood. The parasites are able to induce direct modifications in the infected cells, for example by altering dopamine metabolism, by functionally silencing neurons as well as by hindering apoptosis. Moreover, indirect effects of the peripheral immune system and alterations of the immune status of the CNS, observed during chronic infection, might also contribute to changes in neuronal connectivity and synaptic plasticity. In this review, we will provide an overview and highlight recent advances, which describe changes in the neuronal function and morphology upon T. gondii infection.
Institute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University, Magdeburg, Germany.
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D000818:Animals; D000953:Antigens, Protozoan / Q000276:immunology; D017209:Apoptosis / Q000276:immunology; D001921:Brain / Q000469:parasitology / Q000473:pathology*; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D001523:Mental Disorders / Q000469:parasitology; D051379:Mice; D009474:Neurons / Q000469:parasitology* / Q000473:pathology / Q000502:physiology; D015800:Protozoan Proteins / Q000276:immunology; D014122:Toxoplasma / Q000276:immunology / Q000502:physiology*; D016781:Toxoplasmosis, Cerebral / Q000150:complications / Q000469:parasitology / Q000473:pathology*
D000953:Antigens, Protozoan; D015800:Protozoan Proteins; D004298:Dopamine
Toxoplasma gondii; behavioural manipulation; chronic CNS infection; neuronal alteration