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COVID-19 Associated With Long-Term Cognitive Dysfunction, Acceleration of Alzheimer’s Symptoms

COVID-19 Associated With Long-Term Cognitive Dysfunction, Acceleration of Alzheimer’s Symptoms

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Publish Date:
29 July, 2021
Category:
Covid
Video License
Standard License
Imported From:
Youtube



Much has been learned about SARS-CoV-2, the virus that causes the novel coronavirus, since the start of the COVID-19 pandemic. However, questions remain about the long-term impact of the virus on our bodies and brains. New research reported at the 2021 Alzheimer’s Association International Conference® (AAIC®) held virtually and in Denver found associations between COVID-19 and ongoing cognitive impairment, including the acceleration of Alzheimer’s disease pathology and symptoms.

In addition to the respiratory and gastrointestinal symptoms associated with COVID-19, many people with the virus experience short- and/or long-term neuropsychiatric symptoms, including loss of smell and taste, and cognitive and attention deficits known as “brain fog.” . For some, these neurological symptoms persist, and researchers are trying to understand the mechanisms by which this brain dysfunction occurs, and what that means for long-term cognitive health.

Scientific leaders, including the Alzheimer’s Association and representatives from nearly 40 countries – with technical guidance from the World Health Organization (WHO) – are part of an international, multidisciplinary consortium to examine the long-term impact of COVID-19 on the central nervous system, as well as the differences between countries . The first findings of this consortium, presented at AAIC 2021 from Greece and Argentina, suggest that older adults often suffer from persistent cognitive impairment, including a persistent lack of smell, after recovering from SARS-CoV-2 infection.

Other key results reported at AAIC 2021 include:

Biological markers of brain injury, neuroinflammation and Alzheimer’s disease strongly correlate with the presence of neurological symptoms in COVID-19 patients. Individuals who experienced cognitive decline after COVID-19 infection were more likely to have low blood oxygen levels after brief physical exertion and poor overall physical condition.

“These new data point to troubling trends showing that COVID-19 infections lead to lasting cognitive impairment and even Alzheimer’s symptoms,” said Heather M. Snyder, Ph.D., vice president of medical and scientific relations for the United States. Alzheimer’s Association. “With more than 190 million cases and nearly 4 million deaths worldwide, COVID-19 has devastated the entire world. It is imperative that we continue to study what this virus is doing to our bodies and our brains. The Alzheimer’s Association and its partners are leading the way, but more research is needed.”

Cognitive impairment correlates with persistent loss of smell in recovered COVID-19 patients

Gabriel de Erausquin, MD, Ph.D., M.Sc., of the University of Texas Health Science Center at San Antonio Long School of Medicine, along with colleagues from the Alzheimer’s Association-led global SARS-CoV 2 consortium, studied cognition and sense of smell in a cohort of nearly 300 elderly adult Native Americans from Argentina who had COVID-19.

The participants were examined three to six months after being infected with COVID-19. More than half had persistent problems with forgetfulness, and about one in four had additional problems with cognition, including language and executive dysfunction. These problems were associated with ongoing odor function problems, but not with the severity of the original COVID-19 disease.

“We are starting to see clear links between COVID-19 and problems with cognition months after infection,” Erausquin said. “It is imperative that we continue to study this population, and others around the world, over an extended period of time to better understand the long-term neurological effects of COVID-19.”

COVID-19 infection associated with increase in Alzheimer’s disease biomarkers in the blood

Certain biological markers in blood – including total tau (t-tau), neurofilament light (NfL), glial fibrillary acid protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) and types of amyloid beta (Aβ40, Aβ42) and phosphorylated tau (pTau-181) – are indicators of brain injury, neuroinflammation and Alzheimer’s disease.

To study the presence of these blood biomarkers, neurodegeneration, and neuroinflammation in elderly patients hospitalized with COVID-19, Thomas Wisniewski, MD, a professor of neurology, pathology, and psychiatry at New York University Grossman School of Medicine, and colleagues collected plasma samples from 310 patients admitted with COVID-19 at New York University’s Langone Health. Of the patients, 158 were positive for SARS-CoV-2 with neurological symptoms and 152 were positive for SARS-CoV-2 without neurological symptoms. The most common neurological symptom was confusional state due to toxic metabolic encephalopathy (TME).

In patients who were initially cognitively normal with and without TME related to COVID-19 infection, the researchers found higher levels of t-tau, NfL, GFAP, pTau-181, and UCH-L1 in COVID-19 patients with TME compared with COVID. -19 patients without TME. There were no significant differences with Aβ1-40, but the pTau/Aβ42 ratio showed significant differences in patients with TME. In addition, t-tau, NfL, UCH-L1, and GFAP significantly correlated with markers of inflammation such as C-reactive peptide, suggesting an inflammation-related disruption of the blood-brain barrier associated with neuronal/glial damage.

“These findings suggest that patients who had COVID-19 may have an acceleration of Alzheimer’s-related symptoms and pathology,” Wisniewski said. “However, more longitudinal research is needed to study how these biomarkers affect cognition in individuals who had long-term COVID-19.”

Individuals recovered from COVID-19 who experience cognitive decline are more likely to have poor physical fitness, low oxygen saturation

George Vavougios, MD, Ph.D., postdoctoral researcher for the University of Thessaly (UTH), and colleagues studied cognitive impairment and related health measures in 32 previously hospitalized mild-to-moderate COVID-19 patients two months after discharge from the hospital. Hopital. Among them, 56.2% presented cognitive decline. Short-term memory impairment and multidomain impairment without short-term memory deficits were the predominant patterns of cognitive impairment.

Poorer cognitive test scores correlated with older age, waist circumference, and waist-to-hip ratio. After adjusting for age and gender, poorer memory and thinking scores were independently associated with lower levels of oxygen saturation during the 6-minute walk test, which is commonly used to assess the functional capacity of people with cardiovascular disease.

“A brain without oxygen is not healthy, and continued deprivation can very well contribute to cognitive problems,” Vavougios said. “These data suggest some common biological mechanisms between the dyscognitive spectrum of COVID-19 and post-COVID-19 fatigue that have been anecdotally reported in recent months.”

This cohort is also part of the global SARS-CoV-2 consortium.

About the Alzheimer’s Association International Conference (AAIC)

The Alzheimer’s Association International Conference (AAIC) is the world’s largest gathering of researchers from around the world focusing on Alzheimer’s disease and other forms of dementia. As part of the Alzheimer’s Association research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community.