NEW YORK (StudyFinds.org) – Could COVID-19 actually be doing more harm to the human brain than Alzheimer’s disease? A new study reveals older patients contracting COVID have more signs of brain damage than people who develop the neurodegenerative disease.
Specifically, a team from NYU Grossman School of Medicine found significantly higher levels of certain blood proteins which typically rise when someone suffers neurological damage among COVID patients. Researchers said, over the short-term course of their infections, seven markers of brain damage were noticeably higher among COVID patients than non-COVID patients with Alzheimer’s. One of these markers was more than twice as high among coronavirus patients.
“Our findings suggest that patients hospitalized for COVID-19, and especially in those experiencing neurological symptoms during their acute infection, may have levels of brain injury markers that are as high as, or higher than, those seen in people who have Alzheimer’s disease,” said lead author Jennifer Frontera, MD, a professor in the Department of Neurology, in a university release.
Which blood markers should COVID patients worry about?
Study authors said the main sign of brain damage among the COVID patients was the condition toxic metabolic encephalopathy (TME). Symptoms range from confusion to coma, due to toxins created by the immune system reacting (sepsis), the kidneys failing, and not enough oxygen in the tissue.
The team examined 251 people hospitalized for COVID-19 during the first few months of the pandemic in 2020. The average age of the participants was 71 years-old, but all were in generally good health with no history of dementia or cognitive decline before their COVID infection. Researchers separated these patients into two groups, those with and without neurological symptoms due to COVID-19.
From there, the team compared these individuals to a group of control patients from the Clinical Core cohort of NYU Langone’s Alzheimer’s Disease Research Center. This group is part of NYU’s long-term study of dementia and included 54 healthy people, 54 with mild cognitive decline, and 53 with Alzheimer’s disease. None of the control patients contracted COVID-19 during the study.
When it comes to what scientists were looking for, three blood markers — ubiquitin carboxy-terminal hydrolase L1 (UCHL1), total tau, and phosphorylated-tau-181 (ptau181) — all measure the death or disruption of neurons in the brain.
Levels of neurofilament light chain increase when the brain’s axons take damage. These are branch-like extensions coming from the neurons. Glial fibrillary acidic protein (GFAP) levels measure the damage to glial cells, another type of brain cell that supports the neurons. Lastly, amyloid beta 40 and 42 are common markers which usually build up in people with Alzheimer’s.
Results show the seven brain damage markers were over 60% higher among COVID patients with TME than those without the neurological symptoms.
Brain damage even worse among fatal COVID cases
Concerningly, study authors found the markers for brain damage were even worse among patients that did not survive their coronavirus infection. Markers among patients who died from COVID were 124% higher than those who eventually left the hospital.
In comparison to patients with Alzheimer’s, results show markers for neurofilament light chain were 179% higher among coronavirus patients over the short-term. Levels of GFAP were also 65% higher among COVID patients in comparison to those with dementia.
“Traumatic brain injury, which is also associated with increases in these biomarkers, does not mean that a patient will develop Alzheimer’s disease or related dementias later on, but does increase the risk of it,” said senior author Thomas Wisniewski, MD, director of the Center for Cognitive Neurology at NYU Langone. “Whether that kind of relationship exists in those who survive severe COVID-19 is a question we urgently need to answer with ongoing monitoring of these patients.”
The study is published in the Alzheimer’s & Dementia®: The Journal of the Alzheimer’s Association.