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A new study finds that patients hospitalized with COVID-19 have higher blood protein levels in the short term than non-COVID-19 patients diagnosed with Alzheimer's, and blood protein levels are known to increase with nerve damage.
Importantly, the current report, published online today (January 13, 2022) in Alzheimer's and Dementia: A Journal of the Alzheimer's Association, was published during the pandemic (March-May 2020).
A new study led by researchers at NYU School of Medicine, led by Grossman, found that COVID-19 patients with brain damage (neurodegeneration) had elevated levels of seven markers compared to those without the damage, and deaths were also higher than recoveries and discharges.
A second analysis found that patients hospitalized with COVID-19 had significantly higher levels of impairment markers in the short term than patients diagnosed with Alzheimer's disease, and in one case was twice the latter times more
"Our findings suggest that patients hospitalized with COVID-19, especially those experiencing neurological symptoms during acute infection, may have as high or higher levels of brain injury markers as Alzheimer's patients
Study structure/details
The current study identified 251 patients with an average age of 71 who had no record or symptoms of cognitive decline or dementia prior to being hospitalized with COVID-19
When possible, the research team also compared marker levels in the COVID-19 cohort with patients in the NYU Alzheimer's Disease Research Center (ADRC) clinical core cohort
Three of the markers studied—ubiquitin carboxy-terminal hydrolase L1 (UCHL1), total tau protein, pta181—are known measures of death or loss of function in neurons, the cells that carry information to neural pathways
Blood markers in the covid-19 patient group were measured in serum (the fluid portion of blood that has been made into a clot), while blood markers in the Alzheimer's study were measured in plasma (the portion of blood that remains when the clot is blocked) liquid blood part)
In addition, the main measure of neurological damage in COVID-19 patients is toxic metabolic encephalopathy (TME), with symptoms ranging from confusion to coma, caused by an overreactive immune system (sepsis), kidney failure (uremia), and impaired oxygen delivery (hypoxia) ) toxins produced by severe infections
A moderate set of findings came from comparing NFL, GFAP and UCHL1 levels in the plasma of non-COVID Alzheimer's patients with the same markers as the serum levels of COVID-19 patients (Figure 3)
"Traumatic brain injury is also associated with an increase in these biomarkers, but that doesn't mean the patient will develop Alzheimer's or related dementia later in life, but it does increase the risk
Reference: "Comparison of Serum Neurodegenerative Biomarkers in Hospitalized COVID-19 Patients and Patients with Normal Cognitive Function, Mild Cognitive Impairment, or Alzheimer's Disease", Alzheimer's, January 13, 2022 Hymer's Disease and Dementia
Drs