Murine Study Alarmingly Shows That COVID-19 Virus Fragments Disrupts Brain Signals!
Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 04, 2025 5 hours, 8 minutes ago
Medical News: In a breakthrough animal study, researchers have found that exposure to virus-like particles (VLPs) of the SARS-CoV-2 virus—the virus responsible for COVID-19—can significantly disrupt brain activity patterns in mice.
Murine Study Alarmingly Shows That COVID-19 Virus Fragments Disrupts Brain Signals
These VLPs, which mimic the virus’s structure without containing its genetic material, were shown to interfere with how neurons in the brain fire, particularly in areas responsible for motor control and sensory input.
This
Medical News report comes from a collaboration between scientists at the Cleveland Clinic Foundation’s Lerner Research Institute and the Oregon Health & Science University, including its Vaccine and Gene Therapy Institute and Division of Neuroscience. The researchers used specially engineered mice to explore whether VLPs alone—without active viral infection—can affect the brain. Their findings are raising alarm about the potential long-term neurological effects of COVID-19 exposure.
Virus Like Particles Trigger Strong Short Term Brain Activity Spikes
To safely simulate COVID-19 exposure, the researchers used SARS-CoV-2 VLPs containing all major structural proteins (spike, envelope, membrane, and nucleocapsid) but no viral RNA. These particles were injected into two groups of mice: normal wild-type (WT) mice and genetically modified mice that express the human tau protein, a hallmark of Alzheimer’s disease.
Shortly after exposure, both types of mice showed a surge in brain activity, especially in regions involved in movement and sensory perception. Using advanced two-photon microscopy, the team recorded neuron firing patterns over several weeks. They discovered that:
-In wild-type mice, VLP exposure caused a dramatic 105–200% rise in stimulus-evoked brain activity.
-In tau-expressing mice, the spike was even more severe, with a 310% increase.
-Tau mice also displayed a 370% increase in spontaneous neuronal firing rates—unlike wild-type mice, whose spontaneous activity remained stable.
These results indicate that even without the live virus, the body’s exposure to virus-like proteins can provoke serious neurological effects.
Long Term Effects Reveal Lingering Neurological Changes
Over six weeks, the researchers continued to monitor brain activity in both groups. In wild-type mice, the heightened activity gradually subsided but did not fully return to pre-exposure levels. This suggested some long-lasting disruption in brain function. In contrast, tau-expressing mice showed a more complex and concerning response:
-Their initial hyperactivity slowly declined, but brain firing patterns never normalized.
-The number of neurons firing spontaneously remained higher than before exposure, suggesting a
lingering imbalance in the brain’s excitability.
-Even mice that received only the injection solution (without VLPs) showed abnormal brain patterns, indicating heightened sensitivity in the tau group.
This suggests that individuals with pre-existing neurological risks—such as those prone to Alzheimer’s disease—may be particularly vulnerable to long-term brain effects following exposure to COVID-19 viral proteins.
Immune System Activation Detected in the Brain
The study also confirmed that VLP exposure activated the immune system both systemically and within the brain. Corticosterone (a stress hormone) levels rose significantly in high-dose VLP-treated mice. Chemokines like CCL3, ICAM-1, and LIX—all markers of inflammation—were altered in the hippocampus, a region involved in memory.
These findings support the theory that even minimal exposure to viral proteins may trigger inflammation in the brain and interfere with neuron-to-neuron communication.
Tau Expression Increases Brain Susceptibility
Tau-expressing mice showed signs of more severe and prolonged neurological disruptions. According to the researchers, the presence of human tau protein in the brain made these mice more sensitive to the stress of viral protein exposure. Their neural circuits were more easily destabilized, which could mirror what happens in elderly people or those with neurodegenerative diseases who contract COVID-19.
This raises concerns that even mild or asymptomatic SARS-CoV-2 exposures in vulnerable populations might contribute to long COVID symptoms like brain fog, memory loss, and cognitive dysfunction.
Conclusion
The findings from this study reveal that SARS-CoV-2 virus-like particles alone—without an actual infection—are capable of causing significant, lasting changes to brain activity. Individuals with underlying neurological vulnerabilities may be at even greater risk of persistent neurological effects. These results underscore the urgent need for further research into how COVID-19 and its components affect the central nervous system and whether these effects contribute to long COVID symptoms or increase the risk of neurodegenerative diseases in the future.
The study findings were published in the peer reviewed journal: Communications Biology
https://link.springer.com/article/10.1038/s42003-025-08435-8
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