A new study published by Neuroscience Applied suggests that cannabidiol (CBD) may help reduce neuroinflammation linked to long COVID by altering the inflammatory signals carried between brain cells.
The research, conducted by scientists from Universidade de São Paulo, focused on extracellular vesicles, tiny lipid-bound particles released by cells that play a key role in cell-to-cell communication. In recent years, these vesicles have been increasingly implicated in the spread of inflammation and neurological damage associated with SARS-CoV-2 infection, particularly in patients who experience persistent cognitive and mood-related symptoms after recovery.
Using human SH-SY5Y neuroblastoma cells, researchers infected the cells with a clinical isolate of SARS-CoV-2 and then treated them with low concentrations of CBD. After 24 hours, extracellular vesicles were isolated and analyzed to determine how infection and CBD exposure altered their contents.
The results showed that infection significantly increased levels of inflammatory markers carried within the vesicles, including TNF-α, IL-6 and IL-1β. Treatment with CBD sharply reduced all three, bringing inflammatory signaling closer to baseline levels. At the same time, CBD increased levels of brain-derived neurotrophic factor, a protein involved in neuronal survival and cognitive function, which had been suppressed by viral infection.
CBD treatment also increased vesicle levels of ACE-2, a receptor involved in viral entry, suggesting that the compound may influence how infected cells package viral-related proteins during infection. Importantly, exposure to these vesicles did not reduce the viability of healthy brain cells, indicating that CBD-modified vesicles were not toxic.
Further analysis showed that most of the observed changes could be explained by a shift away from pro-inflammatory signaling toward a more neuroprotective profile. According to the researchers, these findings support the idea that CBD may help blunt long COVID–related neurological effects by reshaping inflammatory communication between brain cells, though they emphasized that further research is needed to confirm whether similar effects occur in humans.
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