In a recent study published in Nature Neuroscience, scientists at Trinity College in Ireland utilized blood tests to assess specific biological markers and employed specialized brain imaging techniques.
With their findings revealed that individuals with long COVID experiencing brain fog exhibited greater permeability or "leakiness" of the blood-brain barrier.
This study marks the initial biological evidence suggesting that the symptom may stem from underlying changes in the brain.
Brian Fog Symptoms in Long COVID Patients
Dr. Leah Croll, a neurologist and assistant professor at Temple University, emphasized the significance of this research, challenging the common dismissal of long COVID symptoms, particularly brain fog, as mere psychological issues.
The study's identification of a tangible biological mechanism behind these symptoms offers validation for individuals experiencing them.
While acknowledging the study's limited scale, its implications could contribute valuable insights to ongoing research aimed at understanding and treating long COVID, a condition affecting millions.
Presently, there are no established tests or treatments for this debilitating condition.
The study involved 32 participants who had contracted COVID-19 in 2020, with brain imaging revealing increased blood-brain barrier permeability in those with long COVID and brain fog.
Cognitive tests further indicated mild-to-moderate cognitive impairment in participants with brain fog.
Additionally, the researchers examined blood markers related to inflammation and blood clotting in 76 individuals hospitalized for acute COVID-19 in 2020.
Those reporting brain fog during their acute infection showed a significant increase in a marker associated with blood-brain barrier dysfunction.
This suggests that inflammation affecting the blood-brain barrier may contribute to brain fog in both acute and long COVID cases.
Further Research into Long COVID Brain Fog Treatment
Despite the study's limitations, conducted on a small scale at one Irish hospital during the early stages of the pandemic, it provides valuable insights and warrants further investigation.
Researchers emphasize the need for more extensive studies to confirm these findings and comprehend their implications.
Dr. Croll expressed optimism that the study contributes to unraveling the biological foundations of COVID-related brain fog, paving the way for improved tests and treatments in the future.
Professor Matthew Campbell, Head of Genetics at Trinity and Principal Investigator at FutureNeuro, highlighted the significance of identifying leaky blood vessels and a hyperactive immune system as potential drivers of brain fog in long COVID.
Understanding these underlying causes could pave the way for targeted therapies in the future.
Professor Colin Doherty, Head of the School of Medicine at Trinity and Principal Investigator at FutureNeuro, commended the research's execution amid a national crisis, noting its potential to change the landscape of post-viral neurological conditions.
Dr. Chris Greene, the study's first author, anticipates further studies exploring the molecular events contributing to post-viral fatigue and brain fog, believing that similar mechanisms may underlie neurological dysfunction in various viral infections.
Origins of Brain Fog
In the quest to understand the origins of brain fog, researchers concentrated on serotonin and engaged in a thorough examination of the disease process.
Commencing with mouse experiments, they postulated that "viral persistence," a significant element in long COVID, could be associated with serotonin depletion.
Existing studies propose that, even after the initial illness wanes, certain long COVID patients retain lingering infections in specific body areas, often termed "viral reservoirs," potentially contributing to persistent symptoms.
Maayan Levy, a senior author and assistant professor of microbiology at the University of Pennsylvania, clarified that they sought proof of viral persistence by analyzing the stool of long COVID individuals for viral genetic material.
Approximately 30% of patients exhibited viral RNA in their gastrointestinal tract, prompting the team to replicate this scenario in mouse models.
The experiments illustrated that a prolonged viral infection, employing lymphocytic choriomeningitis virus as a substitute for SARS-CoV-2, resulted in diminished serotonin levels, implicating the body's immune response in this phenomenon.
Subsequent inquiries concentrated on a cytokine named type 1 interferon, exposing its pivotal role in promoting inflammation and disrupting serotonin levels in the bloodstream.
Given that the gut contributes to 90% of serotonin production in the body, the inflammatory response in the gut obstructed the absorption of tryptophan, a crucial amino acid and serotonin precursor.
Consequently, decreased tryptophan levels led to reduced serotonin production.
Moreover, these cytokines induced blood platelet clotting, further depleting circulating serotonin levels stored in platelets.
