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COVID-19 lockdowns may have triggered brain inflammation even in people who didn’t get infecting with the virus, research from Massachusetts General Hospital shows.
The societal and lifestyle disruptions caused by the pandemic may have triggered inflammation in the brain that can affect mental health, according to the study. The impacts manifest as symptoms including fatigue, brain fog and mental distress.
Scientists looked at brain imaging, behavioral tests and blood samples from 57 people before and 15 people after stay-at-home measures were in place.
After the lockdown, the participants had higher levels of two neuroinflammation markers. People who noticed mood changes and fatigue had higher levels of a protein that also indicates inflammation.
The evidence supports the notion that stress and brain inflammation can go hand-in-hand, noted senior author Dr. Marco Loggia, co-director of the Center for Integrative Pain NeuroImaging at MGH and Harvard Medical School. The new information can help treat the symptoms in many cases with exercise and possibly medication.
“This could have important implication for developing interventions for a broad number of stress-related disorders,” Loggia added.
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Human study measuring pandemic-related neuroinflammation in individuals negative to COVID-19 antibodies.
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Multimodal PET/MR brain imaging shows elevation in two independent putative markers of glial activation.
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PET signal increases are associated with physical/mental fatigue indices.
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Imaging transcriptomics analyses reveal a spatial overlap with the expression of genes related to neuroimmune responses.
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Marginally elevated serum inflammatory markers correlate with neuroimaging markers.
Abstract
While COVID-19 research has seen an explosion in the literature, the impact of pandemic-related societal and lifestyle disruptions on brain health among the uninfected remains underexplored. However, a global increase in the prevalence of fatigue, brain fog, depression and other “sickness behavior”-like symptoms implicates a possible dysregulation in neuroimmune mechanisms even among those never infected by the virus.
We compared fifty-seven ‘Pre-Pandemic’ and fifteen ‘Pandemic’ datasets from individuals originally enrolled as control subjects for various completed, or ongoing, research studies available in our records, with a confirmed negative test for SARS-CoV-2 antibodies. We used a combination of multimodal molecular brain imaging (simultaneous positron emission tomography / magnetic resonance spectroscopy), behavioral measurements, imaging transcriptomics and serum testing to uncover links between pandemic-related stressors and neuroinflammation.
Healthy individuals examined after the enforcement of 2020 lockdown/stay-at-home measures demonstrated elevated brain levels of two independent neuroinflammatory markers (the 18 kDa translocator protein, TSPO, and myoinositol) compared to pre-lockdown subjects. The serum levels of two inflammatory markers (interleukin-16 and monocyte chemoattractant protein-1) were also elevated, although these effects did not reach statistical significance after correcting for multiple comparisons. Subjects endorsing higher symptom burden showed higher TSPO signal in the hippocampus (mood alteration, mental fatigue), intraparietal sulcus and precuneus (physical fatigue), compared to those reporting little/no symptoms. Post-lockdown TSPO signal changes were spatially aligned with the constitutive expression of several genes involved in immune/neuroimmune functions.
This work implicates neuroimmune activation as a possible mechanism underlying the non-virally-mediated symptoms experienced by many during the COVID-19 pandemic. Future studies will be needed to corroborate and further interpret these preliminary findings.
