According to a new study conducted by researchers at the University of California-Riverside, infection with toxoplasmosis triggers an accumulation of the neurotransmitter glutamate in the brain, which could cause neurodegenerative diseases in predisposed individuals. The results of the research were published in the journal, PLOS Pathogens.
Toxoplasmosis is caused by the relatively-common parasite, Toxoplasmosis gondii. While it’s estimated that 60 million people in the US are infected with the parasite, a healthy immune system is usually sufficient to avoid experiencing symptoms.
Complications of toxoplasmosis – including damage to the eyes and brain – usually only occur in immunocompromised individuals. According to the current study however, toxoplasmosis may also be associated with the development of neurodegenerative diseases.
Researchers, led by Emma Wilson – an associate professor in the Division of Biomedical Sciences at the UC-Riverside School of Medicine, came to this conclusion after studying the effects of toxoplasmosis on glutamate production in the brain. Glutamate is an amino acid produced by neurons, which acts as a neurotransmitter between cells. While normal levels of glutamate are necessary to facilitate this cell-to-cell signaling, excess glutamate can be harmful.
ndividuals who have experienced a traumatic brain injury, as well as those with neurodegenerative diseases like multiple sclerosis and amyotrophic lateral sclerosis, all show a build-up of glutamate. This excess glutamate accumulates outside the neurons, where central nervous system cells known as astrocytes work to regulate the amount of the neurotransmitter present. A glutamine transporter known as GLT-1 is used by the astrocytes to convert excess glutamate into glutamine, which acts as an energy source for cells.
“When a neuron fires, it releases glutamate into the space between itself and a nearby neuron,” said Wilson. “The nearby neuron detects this glutamate, which triggers a firing of the neuron. If the glutamate isn’t cleared by GLT-1 then the neurons can’t fire properly the next time and they start to die.”
In studying mice infected with toxoplasmosis gondii, the researchers found an increase in the levels of glutamate. The glutamate accumulation was explained by the impaired ability of astrocytes to clear the neurotransmitter in the presence of the parasite.
Wilson and her colleagues also found that GLT-1 expression was diminished in animals with toxoplasmosis, leading to a build-up of unconverted glutamate. This accumulation may cause neuronal cell death, and lead to the onset of neurodegenerative disease.
“These results suggest that in contrast to assuming chronic toxoplasmosis infection as quiescent and benign, we should be aware of the potential risk to normal neurological pathways and changes in brain chemistry,” said Wilson. “More direct and mechanistic research needs to be performed to understand the realities of this very common pathogen.”