A new brain imaging study suggests that long COVID may not be primarily driven by persistent inflammation in the brain, challenging one of the leading theories behind the condition.

Researchers from the University of Turku in Finland found no signs of widespread neuroinflammation in patients experiencing prolonged symptoms after COVID-19 infection. Instead, people with more severe symptoms showed increased activity in brain regions associated with emotion, stress, and memory.

The findings, published in the Journal of Neurology, are based on advanced PET and MRI brain scans performed on 14 long COVID patients, alongside healthy volunteers and people with multiple sclerosis (MS), a neurological disease known to involve brain inflammation.

Scientists have long suspected that lingering inflammation caused by SARS-CoV-2 could explain symptoms such as fatigue, “brain fog,” anxiety, and depression. However, the new study found that inflammatory activity in long COVID patients was significantly lower than in MS patients and not meaningfully different from healthy participants.

Researchers also analyzed blood samples for markers linked to nerve cell damage and neurodegeneration but found no major abnormalities in the long COVID group.

The study did reveal another important pattern. Patients reporting higher levels of anxiety, depression, and poorer quality of life showed increased cellular activity in the hippocampus and amygdala — brain regions involved in emotional regulation, memory, and stress responses.

According to lead researcher Professor Laura Airas, inflammation may still play a role during the earlier stages after infection before gradually decreasing over time.

The findings suggest that persistent long COVID symptoms could be linked more closely to altered brain activity in emotional and stress-related networks rather than ongoing widespread inflammation.

Researchers say the results may help guide future treatment strategies. Some patients could potentially benefit more from therapies focused on emotional regulation and stress management instead of treatments aimed solely at suppressing inflammation.

Scientists emphasized that further research is needed to better understand the complex biological mechanisms behind long COVID and develop more targeted therapies.