Nearly two full years into the COVID-19 pandemic, researchers are still in the process of learning what’s really going on inside the heads of COVID-19 survivors. From brain fog or sensory issues (like losing one’s sense of smell) to sudden strokes or lasting delirium, the virus can, in some people, cause a range of neuropsychiatric symptoms. In “long-haul” patients, these symptoms persist for months, and past pandemics point to the possibility that brain damage could be life-long.
The link between COVID-19 and the onset of dementia or even Alzheimer’s is not yet known — and researchers will need years more to understand any relationship there in full — but, evidence is growing that the diseases do share the biomarkers of brain damage. And according to a new study, COVID-19 appears to bring higher levels of blood proteins linked to neurodegeneration than Alzheimer’s disease does in the short term.
Researchers at the NYU Grossman School of Medicine analyzed two months of data gathered at the start COVID-19 pandemic, from March to May 2020. Results were published this month in the journal of the Alzheimer’s Association. The researchers found higher levels of seven different biomarkers of neurodegeneration in COVID-19 patients with neurological symptoms than in those without neurological symptoms. The level of these biomarkers were by far the highest in patients who died in the hospital than in those who recovered, indicating a relationship between the severity of the disease and the severity of the brain damage. A second analysis found that a subset of the damage markers in patients hospitalized with COVID-19, over the short term, were significantly higher than in patients diagnosed with Alzheimer’s disease. In one case, these biomarker levels were more than twice as high in a person with COVID-19 than they were in people living with Alzheimer’s.
“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,” the study’s lead author Dr. Jennifer A. Frontera, a professor at NYU’s neurology department, said in a statement.
The current study identified 251 cognitively healthy people, averaging 71 years of age, who were hospitalized for COVID-19. The researchers looked at the study participants who had neurological symptoms related to COVID-19, and where possible, they compared these patients neurodegenerative biomarker levels to 161 participants without COVID-19 who were part of an ongoing, long-term study of Alzheimer’s at NYU Langone’s Alzheimer’s Disease Research Center
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The team then measured all participants’ degree of brain injury using a precise new diagnostic technology to track seven different biomarkers for neurodegeneration — all of which are known associated with the death or disabling of neurons — in blood plasma and serum. The biomarkers included two beta-amyloid proteins (a biomarker of Alzheimer’s which happens to be associated with loss of one’s sense of smell) and two tau proteins, which are also known to aggregate in the brains of people with Alzheimer’s and other dementias.
The most dramatic difference between the two groups was in levels of neurofilament light chain — a neuronal protein associated with a number of neurodegenerative diseases, including Alzheimer’s. Past research has shown that the presence of NfL may increase three to four times faster in people living with Alzheimer’s than in cognitively health individuals. In COVID-19 patients, NYU’s study found, NfL was nearly another two times higher than in people with Alzheimer’s — a difference of 179 percent.
What they found was that the participants who had been hospitalized for COVID-19 had an average of more than 60 percent higher presence of neurodegeration-related biomarkers in their blood than the participants with Alzheimer’s. People who died of COVID had more than double the level of these brain damage biomarkers than people who survived it.
“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 and neurology professor Dr. Thomas M. Wisniewski at 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.”
Some of these findings were presented in July at the 2021 Alzheimer’s Association International Conference as the researchers probed why COVID-19 appeared to accelerate the onset of Alzheimer’s symptoms.
“These new data point to disturbing trends showing COVID-19 infections leading to lasting cognitive impairment and even Alzheimer’s symptoms,” Heather Snyder, Alzheimer’s Association vice president of medical and scientific relations, said of the studies presented at the conference at the time. “With more than 180 million cases and nearly 4 million deaths worldwide, COVID-19 has devastated the entire world,” she added. “It is imperative that we continue to study what this virus is doing to our body and brain.
This study took place at the very start of the pandemic, and as Alzheimer’s can take years from the appearance of the first biomarkers to the first symptoms to appear, there is no way to know what association will eventually come to light, if any, between having survived COVID-19 with neurological symptoms, and developing Alzheimer’s or a related dementia. Any determination of whether patients with COVID-19 are at increased risk for future Alzheimer’s disease, or instead recover over time, the researchers stated, will need to await the outcomes of long-term studies.