According to a new study, patients admitted with COVID-19 had higher short-term levels of blood protein known to be elevated in neurological damage than non-COVID-19 patients diagnosed with Alzheimer’s disease. rice field.
Important is the current report published online on January 13th. Alzheimer’s disease and dementia: The Journal of the Alzheimer’s Association was held for two months in the early days of the pandemic (March-May 2020).Determining whether Patience With COVID-19, you have to wait for the results of long-term studies as it increases your risk of future Alzheimer’s disease or instead recovers over time.
In this new study, led by researchers at the NYU Grossman School of Medicine, patients with COVID-19 with neurological symptoms have higher levels of seven markers of brain damage (neurodegenerative disease) than those without them. It was found to be at a much higher level than in patients who died in the hospital. For those who have left the hospital and returned home.
The second analysis found that the subset of injury markers in patients admitted with COVID-19 was significantly higher in the short term than in patients diagnosed with Alzheimer’s disease, and in one case more than twice as high. ..
“Our findings show that in patients hospitalized with COVID-19, especially those experiencing neurological symptoms during acute infection, brain damage markers equal to or higher than those found in patients with Alzheimer’s disease. It suggests that it may have a level of. ”Leading author Jennifer A. Frontera, Ph.D., states that she is a professor of neurology at NYU Langone Health.
Research structure / details
The current study identified 251 patients, who averaged 71 years of age, but had no records or symptoms of cognitive decline or dementia prior to admission with COVID-19. These patients were then divided into groups with and without neurological symptoms during acute COVID-19 infection, and the patients recovered and were discharged or died.
The research team also compared marker levels in the COVID-19 group, if possible, with patients in the NYU Alzheimer’s Disease Research Center (ADRC) clinical core cohort. This is an ongoing long-term study at NYU Langone Health. None of these 161 control patients (54 cognitively normal, 54 with mild cognitive impairment, 53 diagnosed with Alzheimer’s disease) had COVID-19. Brain damage was measured using single molecule array (SIMOA) technology. It can track microblood levels of neurodegenerative markers in picograms (1/1 trillion grams) per milliliter (pg / ml) of blood.
Three of the research markers, ubiquitin carboxy-terminal hydrolase L1 (UCHL1), total tau, and ptau181 are known measures of neuronal death or nullification, which are cells that allow neural pathways to carry messages. Neurofilament light chain (NFL) levels increase with damage to axons, neuronal elongation. Glial fibrous acidic protein (GFAP) is a measure of damage to glial cells that support neurons. Amyloid beta 40 and 42 are proteins known to accumulate in patients with Alzheimer’s disease. Past research results claim that total tau and phosphorylated tau-181 (p-tau) are also specific measures of Alzheimer’s disease, but their role in the disease is still controversial.
Blood markers for the COVID patient group were measured in serum (the liquid portion of coagulated blood), and blood markers in the Alzheimer study were measured in plasma (the liquid blood fraction that remains when coagulation is prevented).For technical reasons, this difference meant that NFL, GFAP, and UCHL1 levels could be compared between the COVID-19 group and patients with Alzheimer’s disease, but total tau, ptau181, amyloid beta 40, and Amyloid beta 42 could only be compared within the COVID-19 patient group (neurosymptomatic, death or secretions).
Moreover, Neurological injury In patients with COVID-19, toxic metabolic encephalopathy (TME) with symptoms ranging from confusion to coma, immune system overreaction (sepsis), renal dysfunction (uremia), and decreased oxygen supply (hypoxia). Caused during severe infection with toxins produced by encephalopathy). ).Specifically, the average rate of increase in the levels of the seven markers in inpatients with TME compared to inpatients without TME. Neurological symptoms (Figure 2 of the survey) was 60.5%. For the same marker in the COVID-19 group, the average increase was 124% when comparing patients who were successfully discharged from the hospital with those who died in the hospital.
A secondary set of findings was obtained by comparing NFL, GFAP, and UCHL1 levels in serum of COVID-19 patients with the same marker levels in plasma of non-COVID Alzheimer’s disease patients (Figure). 3). NFL was 179% higher in the short term in patients with COVID-19 than in patients with Alzheimer’s disease (73.2 vs. 26.2 pg / ml). GFAP was 65% higher in COVID-19 patients (443.5 vs 275.1 pg / ml) than in Alzheimer’s disease patients, whereas UCHL1 was 13% higher (43 vs 38.1 pg / ml).
“Traumatic brain injury, which is also associated with an increase in these biomarkers, does not mean that the patient later develops Alzheimer’s disease or associated dementia, but increases its risk,” said the senior author. Thomas M. Wisnievsky, Doctor of Medicine, said. Gerald J. and Dorothy R. Friedman are professors of neurology and director of the Cognitive Neurology Center at NYU Langone. “Whether such a relationship exists in people who have survived severe COVID-19 is an urgent question to be answered with continuous monitoring of these patients.”
With the doctor. Authors of Frontera, Wisniewski and NYU Langone Health include lead authors Allal Boutajangout, Arjun Masurkarm, Yulin Ge, Alok Vedvyas, Ludovic Debure, Andre Moreira, Ariane Lewis, Joshua Huang, Sujata Thawani, Laura Balcer and Steven Galetta. I did. The author was Rebecca Betensky of NYU School of Global Public Medicine.
Jennifer A. Frontera et al, Comparison of serum neurodegenerative biomarkers between hospitalized COVID-19 patients and non-COVID subjects with normal cognition, mild cognitive impairment, or Alzheimer’s disease, Alzheimer’s disease and dementia (2022). DOI: 10.1002 / alz.12556
NYU Langone Health
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