How behavior-changing parasites inspire new mental health treatments
Toxoplasmosis is a disease caused by a common parasitic infection. Although it is suspected hundreds of millions of people around the world may be infected with the parasite, only a small volume display symptoms and go on to develop disease.
During the acute stages of an infection some people have been known to display cognitive or behavioral alterations. There has been a significant amount of research investigating the correlation between schizophrenia and toxoplasmosis, but there is still debate over whether the parasite can be causally connected to these kinds of neuropsychological disorders.
New research, led by a team from the University of Leeds and the Université de Toulouse, is presenting a robust hypothesis to explain how this kind of parasitic infection could influence certain neurological disorders and alter behavior. The article, published in the journal Trends in Immunology, provides new insights into how neurophysiological changes influence behavior, and points to novel therapeutic research targets.
“Our insight connects the two opposing theories for how T. gondii alters host behavior and this may apply to other infections of the nervous system,” explains Glenn McConkey, lead on the new research. “One school believes that behavior changes are invoked by the immune response to infection and the other that changes are due to altered neurotransmitters.”
The new research suggests infection with the toxoplasmosis-causing parasite downregulates a neurotransmitter called norepinephrine. This subsequently triggers pro-inflammatory mechanisms in brain cells by suppressing the signaling processes than control immune responses. The consequent behavioral and cognitive changes are thought to be caused by increased neuroinflammation.
Moving forward, further work is needed to understand whether restoring norepinephrine signaling can either prevent, or reverse, the behavioral abnormalities associated with a parasitic infection. Potential drug targets could hypothetically be developed to modulate this pathway and treat a number of neurological conditions that are underpinned by neuroinflammation.
"This research will contribute to the great need in understanding how brain inflammation is connected to cognition, which is essential for the future development of antipsychotic treatments,” says McConkey.
The new research was published in the journal Trends in Immunology.
Source: University of Leeds