Coronavirus particles, illustration - SARS-CoV-2 virus

New research from investigators in the U.K. has shown that markers of brain injury are present many months after COVID-19 infection, despite standard blood testing that is normal. The research, published in Nature Communications, helps provide potential therapy pathways for patients that experience cognitive difficulties after recovering from COVID-19 by indicating that these ongoing symptoms are likely due to dysregulation of the innate and adaptive immune response to the SARS-CoV-2 virus and not direct infiltration of the central nervous system.

“During the COVID-19 pandemic it became apparent that neurological complications were occurring in a significant proportion of hospitalized patients and even in those with mild COVID-19 infection,” said Prof. Benedict Michael, director of the University of Liverpool’s Infection Neuroscience Laboratory and the study’s principal investigator. “While some neurological ‘symptoms’ were often mild (headache and muscle aches [myalgia]), it became clear that more significant and potentially life-changing new neurological ‘complications’ were occurring, including encephalitis (brain inflammation), seizures, and stroke.”

For this study investigators from the University of Liverpool and King’s College London led COVID-19 Clinical Neuroscience Study (COVID-CNS). The investigators analyzed samples from more than 800 patients hospitalized with COVID-19 in England and Wales. Half of those in the study had new neurological symptoms and investigators measured brain injury markers across the entire cohort including serum inflammatory proteins (cytokines), antibodies, and brain (neuroglial) injury proteins.

The findings showed that during the acute, rapidly developing phase of COVID-19 that the body is producing key inflammatory proteins and brain injury proteins. It also showed that, months after infection and hospital discharge, there was a surprising level of biomarker evidence of neuroglial injury. These markers were more prominent in patients who had shown neurological dysfunction while hospitalized and continued in the recovery phase of patients who had exhibited acute neurological complications.

Since the biomarkers identified in the early acute phase of COVID-19 are associated with abnormal immune response, the investigators suggest these could be targets for treatment of COVID-19-related neurological complications, as well as other infections known to cause acute brain dysfunction.

“Our study shows that markers of brain injury are present in the blood months after COVID-19, and particularly in those who have had a COVID-19-induced brain complication (e.g. inflammation, or stroke), despite resolution of the inflammatory response in the blood,” Michael added. “This suggests the possibility of ongoing inflammation and injury inside the brain itself which may not be detected by blood tests for inflammation.”

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