The researchers from Australia's La Trobe University believe they are on the path to uncovering the cause of "brain fog", which is a common symptom of people with long COVID. Their study reveals similarities between the effects of the coronavirus and the early stages of neurodegenerative diseases such as dementia.
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Their report, published in Nature Communications and revealed on Thursday, provides the first indications that some long-COVID symptoms are being caused by amyloid clumps in the brain that are similar to those found among sufferers of Alzheimer's and Parkinson's disease. Those toxic clumps are comprised of hard protein plaques that interfere with nerve cells in the brain.
Biophysical chemist Nick Reynolds said the protein clumps may be responsible for some of long-COVID's most debilitating symptoms. Long-COVID, which has been estimated to have impacted more than 100 million people since the pandemic began, is marked by inflictions such as memory loss, sensory confusion, severe headaches, and even stroke.
However, the researchers cautioned that the implications of the changes were unclear and did not necessarily suggest people might have lasting damage or that the changes might profoundly affect thinking, memory, or other functions. If further studies confirmed the clumps were contributing to that "brain fog", then drugs already used to combat Alzheimer's and Parkinson's may prove effective.
"It may be possible that existing drugs may be used to treat the brain fog that affects a significant portion of people experiencing long-COVID having been infected with SARS-CoV-2," Reynolds said.
There had been an "enormous amount of research" into those disorders over the past 30 years which could eventually also provide invaluable insights into battling long-COVID. During their research, the scientists investigated if similar amyloid clumps could be formed from fragments of SARS-CoV-2 protein, and found two such protein fragments ORF6 and ORF10, which were highly toxic to brain cells grown in their laboratory.
The researchers said that while there was evidence that the virus could enter the brain of infected people, the precise mechanisms causing the neurological symptoms remained unknown. The next step in their work would be to partner with Australian and international medical researchers to confirm their hypothesis.