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COVID-19 patients have higher blood markers of brain cell damage in the short term than Alzheimer’s

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A new study indicates that patients hospitalized for COVID-19 had greater levels of blood proteins known to rise with neurological damage in the short term than non-COVID-19 individuals diagnosed with Alzheimer’s disease.

The new study conducted between March-May 2020, led by researchers at NYU Grossman School of Medicine, discovered significantly higher levels of seven markers of brain damage (neurodegeneration) in COVID-19 patients with neurological symptoms than in those without, as well as significantly higher levels in patients who died in the hospital compared to those who were discharged and sent home.

A second analysis discovered that a subset of damage markers in COVID-19 individuals were much greater in the short term than in patients diagnosed with Alzheimer’s disease, and in one case more than twice as high.

“Our findings suggest that patients hospitalized for COVID-19, and especially in those experiencing neurological symptoms during their acute infection, may have levels of brain injury markers that are as high as, or higher than, those seen in patients with Alzheimer’s disease,” said lead author Jennifer A. Frontera, MD.                     

The current study included 251 individuals who, while being 71 years old on average, had no history or signs of cognitive decline or dementia prior to being hospitalized with COVID-19. These patients were subsequently split into two groups: those who had neurological symptoms during their acute COVID-19 infection and those who did not, depending on whether they recovered and were discharged or died.

The researchers also compared biomarker levels in the COVID-19 group to patients in the NYU Alzheimer’s Disease Research Center (ADRC) Clinical Core cohort, a long-term study at NYU Langone Health, where possible. COVID-19 was not detected in any of the 161 control patients (54 cognitively normal, 54 with mild cognitive impairment, and 53 with Alzheimer’s disease). Single molecule array (SIMOA) technology was used to assess brain injury, which can track minute blood levels of neurodegenerative indicators in picograms (one trillionth of a gram) per milliliter of blood (pg/ml), which prior technologies could not.

Three of the study markers – ubiquitin carboxy-terminal hydrolase L1 (UCHL1), total tau, and ptau181 – are established indicators of neuron death or impairment. When neurons’ axons, or extensions, are damaged, their levels of neurofilament light chain (NFL) rise. Damage to glial cells, which sustain neurons, is measured by glial fibrillary acidic protein (GFAP). Amyloid Beta 40 and 42 are proteins that have been linked to the development of Alzheimer’s disease. Previous research suggests that total tau and phosphorylated-tau-181 (p-tau) are also unique indicators of Alzheimer’s disease, although their significance in the disease is still unknown.

The COVID patients’ blood markers were measured in blood serum (the liquid part of blood that has been prepared to clot), whereas the Alzheimer’s patients’ blood markers were measured in plasma (the liquid blood fraction that remains when clotting is prevented). Due to technological constraints, NFL, GFAP, and UCHL1 levels could be compared between the COVID-19 group and Alzheimer’s disease patients, however total tau, ptau181, Amyloid beta 40, and amyloid beta 42 levels could be compared only within the COVID-19 patient group (neuro symptoms or not; death or discharge).

Furthermore, toxic metabolic encephalopathy, or TME, was the primary indicator of neurological damage in COVID-19 patients, with symptoms ranging from confusion to coma and caused by toxins produced when the immune system overreacts (sepsis), kidneys fail (uremia), and oxygen delivery is compromised (hypoxia). In hospitalized patients with TME, the average percentage increase in levels of the seven markers was 60.5 percent as compared to those without neurological symptoms. When comparing individuals who were safely sent home from the hospital to those who died in the hospital, the average percentage increase was 124 percent for the same markers within the COVID-19 group.

A second set of data came from comparing levels of NFL, GFAP, and UCHL1 in COVID-19 patients’ serum to those of the same markers in non-COVID Alzheimer’s patients’ plasma (figure 3). In COVID-19 patients, NFL was 179 percent greater (73.2 versus 26.2 pg/ml) than in Alzheimer’s patients in the short run. COVID-19 patients had 65 percent greater GFAP (443.5 against 275.1 pg/ml) than Alzheimer’s patients, while UCHL1 was 13 percent higher (43 versus 38.1 pg/ml).

“Traumatic brain injury, which is also associated with increases in these biomarkers, does not mean that a patient will develop Alzheimer’s or related dementia later on, but does increase the risk of it,” added senior author Thomas M. Wisniewski, MD. “Whether that kind of relationship exists in those who survive severe COVID-19 is a question we urgently need to answer with on-going monitoring of these patients.”

Source: 10.1002/alz.12556

Image Credit: Getty

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