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Study finds no widespread brain inflammation in long COVID

2 hours ago
Study finds no widespread brain inflammation in long COVID

By AI, Created 12:30 PM UTC, May 22, 2026, /AGP/ – A new University of Turku brain imaging study found no evidence of widespread brain inflammation in people with long COVID, even as the most severe symptoms tracked with higher activity in mood- and emotion-related brain regions. The findings could shift attention toward stress, emotional regulation and other non-inflammatory drivers of persistent symptoms.

Why it matters: - The study challenges a leading explanation for long COVID symptoms: persistent brain inflammation after SARS-CoV-2 infection. - The findings suggest long COVID may involve different biological pathways, which could change how clinicians think about diagnosis and treatment. - The results point away from inflammation-only treatments for some patients with prolonged symptoms.

What happened: - Researchers at the University of Turku in Finland used advanced brain imaging to study whether long COVID patients showed signs of brain inflammation. - The study included 14 people with long COVID, 11 healthy controls and 13 patients with multiple sclerosis, a neurological disease known to involve brain inflammation. - The study found no evidence of widespread brain inflammation in long COVID patients compared with healthy controls. - The study by Laura Airas and colleagues was published in the Journal of Neurology.

The details: - Participants underwent PET imaging sensitive to neuroinflammation and MRI to assess brain structure and white matter changes. - Blood samples were analyzed for biomarkers of neuronal and glial damage. - Compared with patients with multiple sclerosis, long COVID patients showed significantly lower inflammatory activity in brain white matter. - No differences appeared in markers of brain inflammation or neurodegeneration between the long COVID group and healthy controls. - In people scanned within 16 months of infection, white matter inflammatory activity was higher than in those with longer disease duration. - Laura Airas said the pattern suggests inflammation may be more prominent early after infection and decline over time. - Higher depression and anxiety levels, along with lower quality of life, were linked to increased cellular activity in the hippocampus and amygdala. - The hippocampus and amygdala are involved in memory, emotional regulation and stress responses.

Between the lines: - The findings refine the picture of long COVID by separating early inflammatory effects from the persistent symptoms seen later in some patients. - The study does not rule out brain involvement in long COVID; it suggests the most severe symptoms may be tied more closely to activity in emotion-regulating regions than to widespread inflammation. - The results also support a more mixed long COVID model, where different patients may have different underlying mechanisms. - The researchers suggested some patients may benefit more from treatments targeting stress and emotional regulation than from therapies focused only on inflammation.

What’s next: - Researchers said more work is needed to understand the biological mechanisms driving long COVID and to develop targeted treatments. - Further studies may help identify which patients are most likely to have early inflammatory changes and which are more affected by mood- and stress-related brain activity. - The University of Turku said InFLAMES is a joint initiative with Åbo Akademi University and is part of the Research Council of Finland’s Flagship Programme. - Long COVID remains a recognized condition affecting millions worldwide, with symptoms that can last for months or years after the initial infection.

The bottom line: - Widespread brain inflammation does not appear to explain persistent long COVID symptoms in this study, but mood- and emotion-related brain activity may still help explain symptom severity for some patients.

Disclaimer: This article was produced by AGP Wire with the assistance of artificial intelligence based on original source content and has been refined to improve clarity, structure, and readability. This content is provided on an “as is” basis. While care has been taken in its preparation, it may contain inaccuracies or omissions, and readers should consult the original source and independently verify key information where appropriate. This content is for informational purposes only and does not constitute legal, financial, investment, or other professional advice.

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