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AAIC 2021: Insights into COVID-19 Impacts on Cognitive Health

AAIC 2021: Insights into COVID-19 Impacts on Cognitive Health

Symptoms of long COVID include neurological deficits such as brain fog, and a new study suggests that the infection leads to a rise in biomarkers of neuronal injury and Alzheimer’s. Photo courtesy the Alzheimer’s Association.

It has become increasingly apparent that COVID-19 can have significant long-term health impacts, with the potential of symptoms lingering for weeks and months after infection in a condition dubbed “long COVID.”

In addition to respiratory and gastrointestinal symptoms, long COVID-related impairments can include short- or long-term neurological symptoms such as loss of smell and taste, and cognitive and attention deficits known as “brain fog.” Researchers are attempting to understand the biological basis of these neuropsychiatric deficits after infection with SARS-CoV-2, and the overall impact of COVID-19 on cognitive health.

At the Alzheimer’s Association International Conference (AAIC) 2021, initial research insights into brain dysfunction following COVID-19 infection were presented. Among these included a study that found correlations between biological markers of brain injury, neuroinflammation, Alzheimer’s disease (AD) and Alzheimer’s Disease Related Dementias (ADRD), and neurological symptoms in COVID-19 patients.

In addition, preliminary findings from an international consortium of scientists working to collect and assess the long-term effects of COVID-19 on cognitive health and the central nervous system suggest that older adults are more likely to experience cognitive impairment — including persistent lack of smell — post-infection with SARS-CoV-2 than younger adults. These initial findings, based on data from Greece and Argentina, show that the effects could be long-lasting in some cases.

These observations and initial findings highlight the importance of understanding how this novel coronavirus targets the body, including the brain, and what the long-term implications of this can be on brain health.


Related: AAIC 2021 Coverage: Expert Panel Unveils Recommendations for Biogen’s Aduhelm


Alzheimer’s Association vice president of medical and scientific relations, Heather M. Snyder, PhD, said in a news release from the association that, “These new data point to disturbing trends showing COVID-19 infections leading to lasting cognitive impairment and even Alzheimer’s symptoms.”

“It is imperative that we continue to study what this virus is doing to our body and brain,” she added.

COVID-19 Leads to Spike in Neuroinflammatory and Alzheimer’s Disease Blood Biomarkers

Neuroinflammation, injury to the brain, neurodegeneration and Alzheimer’s disease are associated with certain biological markers that can be detected in the blood. These include tau (t-tau); neurofilament light (NfL); glial fibrillary acid protein (GFAP); ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1); and species of amyloid beta (Aβ40, Aβ42) and phosphorylated tau (pTau-181).

In a study conducted at New York University Langone Health, researchers wanted to see whether these neurological plasma biomarkers could be detected in older patients (>60 years of age) hospitalized with COVID-19, comparing the presence and levels of these markers in those who had new neurological symptoms associated with infection, and those that did not.

Led by Thomas Wisniewski, MD, a professor of neurology, pathology and psychiatry at New York University Grossman School of Medicine, the researchers evaluated plasma samples from 310 patients who were admitted to New York University Langone Health with COVID-19. All of the patients were positive for SARS-CoV-2 and of them, 158 had neurological symptoms while 152 did not have any. The most common neurological symptom was confusion due to toxic-metabolic encephalopathy (TME).

The researchers found higher levels of t-tau, NfL, GFAP, pTau 181 and UCH-L1 in cognitively normal COVID-19 patients with TME compared to those without TME. There were no significant differences between the patients with respect to Aβ1-40; however, the pTau/Aβ42 ratio displayed significant differences in patients with TME. Additionally, tau, NfL, UCHL1, and GFAP significantly correlated with markers of inflammation such as C-reactive peptide, which could indicate a disrupted blood-brain barrier due to inflammation accompanying neuronal/glial injury.

The strong correlation of these serum biomarkers of neuronal injury, neuroinflammation and Alzheimer’s disease with the presence of neurological symptoms in COVID-19 patients suggest that COVID-19 patients could experience an acceleration of AD/ADRD symptoms and pathology.

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