Studies show that protozoal toxoplasmosis can interfere with brain function. The disease is associated with schizophrenia, depression and autism. Rats infected with the parasite that causes toxoplasmosis behave in a strange way, losing the natural fear of cats, the ultimate host of protozoan that causes this disease. Studies show that cats exposed to the smell of smell seem to be attracted to the predator itself.
As in mice, studies show that protozoal toxoplasmosis can also cause changes in behavior in humans. The parasite is associated with schizophrenia, depression, autism, and even an increased risk of participating in road accidents.
New research has revealed how this protozoan can interfere with the functioning of the brain. Researchers from the Otto von Guericke University in Magdeburg and the Leibniz Institute of Neurobiology have discovered how this parasite affects host brain metabolism.
Toxoplasmosis is caused by Toxoplasma gondii, which exists throughout the world. It infects birds and mammals, including humans. However, the parasite can only reproduce sexually in the digestive system of cats and cats that are their ultimate carriers.
The toxoplasmosis pathogen is eliminated along with faeces. Transmission of the disease occurs through contact with contaminated feces or after ingestion of contaminated food and water.
It is estimated that half of the planet's adult population is infected with this protozoan, but in most cases its presence goes unnoticed and causes flu-like symptoms such as fever, fatigue and muscle pain as well as diarrhea. However, toxoplasmosis is dangerous for people with weakened immune systems as well as during pregnancy.
After being infected, the parasite is placed in muscle tissues and in the brain and remains dormant for the rest of its life, in what they call occult doctors.
According to a German study published in the journal Journal of Neuroinflammation, the parasite changes the molecular structure of synapses, which are responsible for the transmission of brain signals.
"Toxoplasma gondii is absorbed by humans through digestion, enter the bloodstream, and migrates to the brain, entering nerve cells until the end of their lives," said Karl-Heinz Smalla from the Special Laboratory of Molecular Biology at LIN.
In collaboration with the Helmholtz Center for Research on Infection, the researchers were able to prove that the infection changes the number of 300 synaptic proteins in the rat brain.
In particular, the animals showed less proteins near the stimulating receptors that release glutamate. At the same time, there is an increase in proteins involved in immune responses.
"The abnormal functioning of glutamatergic synapses is associated with depression, schizophrenia and autism, and the components of these diseases are also associated with these diseases," says Ildiko Rita Dunay, who worked on this study. "This suggests that immune reactions can cause synapse changes that can lead to neurological disorders," he adds.
Researchers also found that sulfadiazine, an antibiotic used to treat toxoplasmosis, can normalize the metabolism in the brain of infected mice. "All analyzed proteins responsible for glutamatergic signaling returned to normal, and inflammatory activity also decreased measurably," said Björn Schott, a scientist who worked on the research.
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Deutsche Welle is a German international broadcaster and creates independent journalism in 30 languages.