Cats are the final hosts of the toxoplasmosis pathogen. About the excrement of the animal, the disease can be transmitted to humans.

© Alena Ozerova –

Wed. 07. November 2018

Toxoplasmosis is one of the most common infectious diseases worldwide. Researchers from Magdeburg have now found that the parasite affects the metabolism in the brain. This could lead to diseases like depression, schizophrenia and autism.

When mice get infected with the toxoplasmosis virus, something strange happens: they lose their natural fear of cats. Where this behavioral change comes from, researchers from the University of Magdeburg and the Leibniz Institute of Neurobiology have now found out: Apparently, the synapses in the brain of animals after an infection with the parasite called Toxoplasmose gondii, as reported in the journal Journal of Neuroinflammation. These findings could also be relevant to humans. "They support the assumption that Toxoplasma gondii is a risk factor for neuropsychiatric diseases," says Prof. Dr. med. Ildiko Rita Dunay, Director of the Institute for Inflammation and Neurodegeneration of the University of Magdeburg. Because the malfunction of synapses in the brain is associated with neuropsychiatric disorders such as depression, schizophrenia and autism, explains the physician. Toxoplasmosis is widespread worldwide, both in animals and in humans. About 30 to 50 percent of people become infected in the course of their lives, often without realizing it. "In healthy people, the infection triggers short-term cold symptoms such as chills, fever and body aches, which can be dangerous for pregnant women or people with weakened immune systems," says Dr. Dunay. So far there is no therapy to get rid of the parasite once it has attacked the brain. So once you're infected, it will last a lifetime. To inhibit the propagation of parasites, currently the active ingredient sulfadiazine is used. The treatment also seems to have an influence on the altered brain metabolism, as the researchers were able to show: the changes in the brain of the mice were again comparable after sulfadiazine therapy with that of uninfected animals. The inflammatory activity also decreased measurably. NK
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