New study on how a common parasite infection affects human behavior might aid in the development of schizophrenia and other neurological illnesses therapies. Toxoplasmosis is caused by T. gondii, which infects 2.5 billion individuals globally.
New study on the effects of a common parasite infection on human behavior might aid in the development of medicines for schizophrenia and other neurological illnesses.
According to scientists, persons afflicted with T. gondii, which infects 2.5 billion people globally and causes the illness, modify their behavior. Toxoplasmosis may be associated to decreased levels of norepinephrine, a stress-related neurotransmitter secreted in the brain. Neuroinflammation, or the activation of the brain’s immune system to fight infection, is likewise controlled by norephinephrine.
Neuropsychological illnesses such as schizophrenia, Alzheimer’s disease, and ADHD are linked to norepinephrine and neuroinflammation.
Although T. gondii infection is normally asymptomatic in humans, it may induce headaches, disorientation, and seizures in certain people, as well as an elevated risk of schizophrenia — and it can be deadly in immunocompromised individuals.
T. gondii can only reproduce sexually in cats. It creates cysts in the cat’s feces, which are then excreted. Ingestion of anything contaminated by these cysts, such as water, soil, or vegetables; blood transfusions from unpasteurized goat’s milk; eating raw or undercooked meat; or transmission from mother to fetus are all ways it spreads to new hosts.
The infection enters a latent period after a few weeks, during which cysts grow in the brain. They may stay there for a long time, potentially for the rest of their lives. Infection causes the brain’s immune response regulator norepinephrine to diminish during this period.
The processes through which the parasite influences brain function remain a mystery. However, new study from the University of Leeds and the Université de Toulouse reveals that the parasite’s capacity to lower norepinephrine disrupts immune system activation regulation, allowing for an excessive immune response that may affect the host’s cognitive processes.
The results were reported in Trends in Immunology as “Noradrenergic Signaling and Neuroinflammation Crosstalk Regulates Toxoplasma gondii-Induced Behavioral Changes.”
The study’s lead author, Glenn McConkey, Associate Professor of Heredity, Disease, and Development at Leeds’ School of Biology, said: “Our discovery bridges the gap between two competing hypotheses about how Toxoplasma modifies host behavior, and it might be applied to other nervous system diseases. The immunological response to illness, according to one school, causes behavioral abnormalities, whereas changed neurotransmitters, according to the other.”
“This study will help fill a critical gap in our knowledge of how brain inflammation affects cognition, which is critical for the development of antipsychotic medications in the future.”