How Toxoplasma gondii Alters Brain Cell Communication

A recent study published in the journal PLOS Pathogens reveals how the tiny parasite Toxoplasma gondii can significantly impair brain function by disrupting the communication pathways between neurons and supportive glial cells. Conducted by researchers at the University of California, Riverside, the research shows that even a small number of infected neurons can alter crucial cellular signaling mechanisms, potentially leading to neurological issues.

Toxoplasma gondii has a remarkable ability to infect nearly all warm-blooded animals, with a preference for neurons where it forms cysts that can persist for decades. The researchers discovered that infected neurons release fewer extracellular vesicles (EVs)—small, membrane-bound packets essential for cell-to-cell communication. This decrease in EV signaling hampers the coordination between neurons and astrocytes, a critical type of glial cell that maintains neural environment stability.

Professor Emma H. Wilson, the lead author, explained that this disruption can disturb neurotransmitter balance, notably elevating glutamate levels. Elevated glutamate can cause neural hyperexcitability, seizures, and damage, as well as affecting overall brain connectivity.

An important finding is that even a handful of infected neurons can shift the brain's neurochemical equilibrium, highlighting the vulnerability of neural communication to parasitic interference. This has significant implications, considering that up to 30% of individuals in the U.S. harbor latent Toxoplasma infections, mostly acquired through undercooked meat or exposure to cat feces. While the immune system generally contains the parasite, it can become reactivated in immunocompromised individuals, leading to serious health issues.

Currently, diagnostic tools can identify whether someone has been exposed to Toxoplasma by detecting antibodies but cannot determine whether the parasite remains in the brain or how it influences brain function. The study suggests that EVs could serve as biomarkers for active brain infection, which could be detected from blood samples.

Wilson pointed out that in healthy brains, astrocytes regulate neurotransmitters like glutamate, preventing neural overexcitation. But when infected neurons cease to send proper EV signals, this regulation fails, increasing the risk of neurological symptoms. The researchers aim to analyze human blood samples to identify EVs associated with Toxoplasma and to explore the glial cells’ response to parasite proteins.

The research emphasizes that the parasite’s interference with neural communication could play a broader role in neurological and behavioral disorders than previously thought. Wilson remarked that understanding how the brain’s defenses detect and respond to infection could lead to novel therapies or vaccines. Importantly, she reassured that most infections remain asymptomatic, and prevention involves proper food handling and hygiene, particularly avoiding contact with young cats and their feces.

Further studies are underway to better understand these mechanisms and develop strategies for early detection and intervention, ultimately aiming to safeguard brain health from covert parasitic infections.