Hospitalized patients with COVID-19 and no prior history of dementia had elevated levels of brain injury biomarkers, an observational study showed.
Blood levels of total tau (t-tau), phosphorylated tau181 (p-tau181), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL) were significantly elevated in COVID-19 patients with encephalopathy and those who died in the hospital, reported Thomas Wisniewski, MD, of New York University Grossman School of Medicine in New York City, and co-authors.
Levels of NfL, GFAP, and ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) were as high or higher in the short term among hospitalized COVID-19 patients without a history of dementia than they were among Alzheimer’s patients who never had COVID-19, Wisniewski and colleagues wrote in Alzheimer’s & Dementia.
NfL, a marker of axonal injury, was 179% higher in COVID-19 patients than in Alzheimer’s patients (73.2 vs 26.2 pg/ml). GFAP, a sign of glial or astrocytic injury, was 65% higher (443.5 vs 275.1 pg/ml); UCHL1, an enzyme found in nerve cells, was 13% higher (43 vs 38.1 pg/ml).
These findings indicate a “profound neurological insult in these patients,” researchers wrote.
“Traumatic Brain Injury, which is also related with increases in these biomarkers does not mean that patients will develop Alzheimer’s disease or related dementia later but it does increase the chance of it,” Wisniewski stated in a statement.
“Whether that kind of relationship exists in those who survive severe COVID-19 is a question we urgently need to answer with ongoing monitoring of these patients,” he added.
The effect of COVID-19 on the brain is a complex question, noted Heather Snyder, PhD, of the Alzheimer’s Association, who wasn’t involved with the study. “There’s a lot that may be happening, and work like this is helping us better understand what underlying biology may be affected in some individuals who experience COVID-19,” she told MedPage Today.
” I don’t believe we know the long-term implications of this,” Snyder said. It will be crucial to track these individuals and others like them in order to understand how they may be affected and why. This could also help us understand their long-term risk of developing Alzheimer’s or other brain diseases. “
The researchers looked at data from 251 hospitalized COVID-19 patients without a history of dementia, assessing seven serum markers of neurodegeneration: t-tau, p-tau181, GFAP, NfL, UCHL1, amyloid beta 40, and amyloid beta 42. The pandemic began in March and ended in May 2020.. Patients were admitted to New York City hospitals. At hospital admission, blood samples were taken.
Biomarker levels of hospitalized COVID patients also were compared with 161 controls without COVID-19, including 54 people with no cognitive impairment, 54 people with mild cognitive impairment, and 53 people with Alzheimer’s disease dementia. Blood samples from the control population were taken before January 2020,, which was before the first SARS-CoV-2 case in New York City. Control samples were of plasma, not serum; this limited some comparisons with COVID-19 patients.
Median age of COVID-19 patients was 71 and 63% were men. In contrast, people in the Alzheimer’s dementia group had a median age of 82 and 40% were men.
Of the hospitalized COVID-19 patients, 31% required mechanical ventilation, 25% d