Australian-led research may have uncovered the cause of the neurological conditions seen in patients with long-COVID, such as brain fog.
A study conducted by a team of researchers from Swinburne University of Technology, La Trobe University and Luxembourg University has revealed that fragments of proteins from the SARS-CoV-2 virus can form amyloid clumps in the brain that look similar to the amyloids found in patients with neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Furthermore, the study authors showed that these amyloids are highly toxic to brain cells.
Dr Mirren Charnley, a postdoctoral researcher at Swinburne, designed, performed and analysed the biochemical flow cytometry assays used to determine the mechanism of brain cell death triggered by the amyloids and assisted with physical characterisation of the amyloids at the Australian Synchrotron.
“If further studies are able to prove that the formation of these amyloids is causing long-COVID then anti-amyloid drugs developed to treat Alzheimer’s might be used to treat some of the neurological symptoms of long-COVID,” Dr Charnley says.
Dr Mirren Charnley collecting data at the Australian synchrotron.
Long-COVID is marked by neurological symptoms, such as memory loss, sensory confusion, severe headaches, and even stroke.
These neurological symptoms are similar to the early stages of neurodegenerative diseases such as Alzheimer’s and Parkinson’s, which are characterised by the presence of clumps of ordered proteins – known as amyloids – in the brain.
The long-COVID symptoms can persist for months after the infection is over.
While there is evidence that the virus can enter the brain of infected people, the precise mechanisms causing these neurological symptoms are unknown.
The research has been published in Nature Communications.