The main variants of the SARS-CoV-2 virus currently in circulation are sub-variants of the Omicron strain that has generally been found to have milder symptoms. The virus is still a danger to at-risk patients and we do not know the long-term consequences of infection.

Dementia patients, particularly those in care homes, are at higher risk of infection with the virus which in turn may worsen their dementia. The vaccines targeting the SARS-CoV-2 virus provide protection and are an important strategy for protecting particularly high-risk groups such as dementia patients.

As a Biomedical Science researcher, I have been involved in studies of some of the biochemical mechanisms involved in Alzheimer’s disease and other related disorders. The pathology of Alzheimer’s disease involves the accumulation of amyloid-ß deposits in the brains of patients and this may contribute to the destruction of the brain regions involved in memory processes leading to dementia.

As part of my own research, I have studied the fascinating processes of amyloid formation in the laboratory. Incubation of the amyloid-ß peptide in a test tube overnight results in the formation of fibrils that can be seen using high-powered microscopes, the picture above shows what those fibrils look like and is taken from a collaborative study I undertook with colleagues in other laboratories.

In many human diseases amyloid deposits are considered the bad guys as they cause the death of cells surrounding the deposits. Studies have also shown that drug treatments which prevent the formation of amyloid deposits are highly effective and recent studies in Alzheimer’s patients have suggested that treatment with antibodies that bind amyloid-ß is potentially effective on Alzheimer’s dementia.

I recently penned an opinion piece for the Frontiers in Dementia journal as I found papers that suggested proteins made by the SARS-CoV-2 virus in infected cells have amyloid properties and could potentially form deposits in infected cells, in a similar way to the amyloid-ß in Alzheimer’s. The published literature also suggested that chemicals that target the amyloid-forming proteins made by the SARS-CoV-2 virus were effective at preventing infection.

The published literature has previously suggested that viral infections could be involved in the development of Alzheimer’s disease and also the ongoing deterioration in brain function. The studies I reviewed suggest that SARS-CoV-2 virus infection is capable of inducing changes in brain function, and it is known that people with Long-COVID-19 often complain of ‘brain fog’.

The SARS-CoV-2 virus is also capable of initiating changes in amyloid-ß that could trigger or enhance Alzheimer-like symptoms. The effects of the SARS-CoV-2 virus on breathing could also reduce the oxygen supply to the brain and cause changes similar to a Stroke, where the blood supply is cut off to part of the brain leading to a lack of oxygen for energy in the affected part of the brain.

The SARS-CoV-2 virus is also capable of getting directly into the brain and this could result in the deposition of SARS-CoV-2 protein-derived amyloid which in turn could trigger changes to brain function. Since some of the SARS-CoV-2 protein-derived amyloid is capable of sticking to amyloid-ß it could change the pathology of Alzheimer’s either directly or indirectly.

In my opinion article, I propose that the SARS-CoV-2 protein-derived amyloid has the potential to contribute to the symptoms of dementia in patients with pre-existing diseases such as Alzheimer’s and also potentially directly trigger dementia. I also proposed that the SARS-CoV-2 protein-derived amyloid could be a target for the development of treatments in the future.

Dr Nat Milton FRSB, FIBMS, FHEA, AcFIOEE is the Academic Lead in Biomedical Science and Associate Professor (Professional Practice) at Leeds Trinity University (Nat Milton — Leeds Trinity University).