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Cognitive impairment was correlated with persistent anosmia in older people recovering from SARS-CoV-2 infection, the first results of a large international consortium show.
The severity of cognitive impairment was significantly correlated with the severity of olfactory dysfunction (χ2= 13.82, P= 0.003) but not with the severity of acute COVID-19, Gabriel de Erausquin, MD, PhD, MSc, University of Texas Health Science Center in San Antonio, reported in 2021 International Conference of the Alzheimer’s Association (AAIC), held virtually and in Denver.
In other research presented to AAIC, biomarkers of brain damage, neuroinflammation and Alzheimer’s disease were strongly correlated with the presence of neurological symptoms in COVID-19 patients, reported Thomas Wisniewski, MD , New York University Grossman School of Medicine.
Additionally, people with cognitive decline after infection with SARS-CoV-2 were more likely to have low oxygen saturation after brief physical exertion, as well as general poor physical condition, according to George Vavougios, MD. , PhD, from the University of Thessaly in Greece.
“We do not know anything about the course of the disease with COVID-19,” said de Erausquin MedPage today.
“It can progress like dementia, stay stable over time or even improve,” he said. “The studies are intended to answer this question.”
In their study, de Erausquin and his co-researchers assessed olfactory dysfunction and chronic cognitive impairment after SARS-CoV-2 infection in 233 elderly people from the Andes mountains in Argentina, comparing them to 64 matched controls without history of COVID. Participants were studied between 3 and 6 months after infection with SARS-CoV-2. The average age of the participants was 67 years and the average education was 9.35 years of formal learning.
More than half of the people had persistent and serious problems with forgetting. About a quarter had additional cognition problems, including language and executive dysfunction. The only predictor of cognitive impairment was anosmia which persisted for at least 3 to 6 months, said de Erausquin.
“In this study, we are looking at just one age group, people over 60,” he said. “So far, we haven’t looked at biomarkers for inflammation or brain damage, although we have the plasma samples to do so. We are looking at a specific ethnic group, the Native Americans. We don’t have any imagery data, and we don’t. we still have longitudinal data, although we will follow up with the same people in 1 year. “
“We are starting to see clear links between COVID-19 and cognitive issues months after infection,” noted de Erausquin. “It is imperative that we continue to study this population, and others around the world, for a longer period of time to better understand the long-term neurological impacts of COVID-19. “
Rise in Alzheimer’s biomarkers
Wisniewski and colleagues evaluated plasma biomarkers total tau (t-tau), neurofilament lumen (NfL), glial fibrillar acid protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) and species amyloid (Aβ40, Aβ42) and phosphorylated tau (ptau-181) – indicators of brain damage, neuroinflammation and Alzheimer’s disease – in COVID-19 patients.
The researchers evaluated plasma samples from 310 patients admitted to New York University Langone Health. All were positive for SARS-CoV-2: 158 people had neurological symptoms and 152 did not. People with new neurological symptoms were older (median age 71 versus 63).
The most common neurologic symptom was confusion due to toxic metabolic encephalopathy (TME), which accounted for 51% of new neurologic diagnoses.
Among people who were initially cognitively normal, researchers found higher levels of t-tau, NfL, GFAP, ptau-181, and UCH-L1 in COVID-19 patients with MTCT compared to COVID-19 patients without MTCT . There were no significant differences in Aβ1-40, but the ptau / Aβ42 ratio showed significant differences in patients with MTCT.
Tau, NfL, UCH-L1, and GFAP were also significantly correlated with markers of inflammation, including the C-reactive peptide. This may suggest a disruption of the blood-brain barrier linked to the inflammation accompanying neuronal or glial injury, Wisniewski noted.
“These results indicate that patients with COVID-19 may have an acceleration of symptoms and pathology related to Alzheimer’s disease, but this clearly requires longer follow-up,” he said.
Cognitive decline and post-COVID health
In the study by Vavougios’ group, which was also part of the global SARS-CoV-2 consortium, researchers investigated cognitive impairment and health measures in 32 mild to moderate COVID-19 patients previously hospitalized 2 months after discharge. . Participants had an average age of 62 years and no history of neurodegenerative disease or stroke prior to SARS-CoV-2 infection.
More than half (56.2%) of the participants experienced cognitive decline, as indicated by a MoCA Note less than 24 years old. The predominant models of cognitive impairment were short-term memory impairment or multidomain disorder without short-term memory deficit.
Worse cognitive test scores were correlated with higher age, waist circumference, and waist-to-hip ratio. Poorer memory and thinking scores were independently associated with lower oxygen saturation levels on a 6-minute walk test, after adjusting for age and gender.
“An oxygen-deprived brain is not healthy, and persistent deprivation may very well contribute to cognitive difficulties,” observed Vavougios. “These data suggest some common biological mechanisms between the dyscognitive spectrum of COVID-19 and post-COVID-19 fatigue that have been reported anecdotally in recent months. “
“These new data point to disturbing trends showing COVID-19 infections leading to lasting cognitive impairment and even Alzheimer’s symptoms,” noted Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association.
“With more than 180 million cases and nearly 4 million deaths worldwide, COVID-19 has devastated the whole world,” she said. “It is imperative that we continue to study what this virus is doing to our bodies and brains. “
Last updated on July 29, 2021
Disclosures
The study presented by de Erausquin was funded by the Alzheimer’s Association, the Fundación de Lucha contra los Trastornos Neurológicos y Psiquiátricos en Minorías (FULTRA), the Zachry Foundation Distinguished Chair for Clinical Care and Research in Disease Alzheimer’s and the Distinguished University Chair of the Greehey Family Foundation.
The work presented by Wisniewski was supported by the National Institutes of Health, National Institute on Aging.
The research presented by Vavougios was funded by a National Strategic Reference Framework grant.
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