COVID-19 changes gene activity in olfactory mucosal cells in Alzheimer’s

Distinct immune responses after infection between AD patients and healthy individuals.

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COVID-19’s impact on the brain raises worries about lasting effects, like a higher chance of Alzheimer’s disease. There’s also a suggestion that brain inflammation and Alzheimer ‘s-related issues might make someone more vulnerable to severe COVID-19 infection.

A recent study found changes in the transcriptomic signatures in human olfactory mucosal cells in people with Alzheimer’s after getting COVID-19. This could play a role in making COVID-19 worse for individuals with Alzheimer’s. The study was a collaboration between the University of Eastern Finland and the University of Helsinki.

The study was motivated by concerns about how COVID-19 affects people with pre-existing conditions like Alzheimer’s disease. Both COVID-19 and Alzheimer’s are linked to problems with the sense of smell. Researchers focused on the olfactory mucosa, the nose part connecting the outside world and the brain. They aimed to understand how SARS-CoV-2 interacts with Alzheimer’s in this area, exploring if it could be a possible way for the virus to enter the brain.

The study used a unique 3D model of the olfactory mucosa, the nose part related to smell. They used cells from healthy and Alzheimer ‘s-diagnosed individuals cultivated in a controlled environment mimicking real conditions. Olfactory mucosal biopsies were collected in collaboration with Kuopio University Hospital. Experts in molecular and cellular biology, neurology, and virology worked together to examine how different SARS-CoV-2 variants affect the olfactory mucosa.

Surprisingly, cells from healthy and Alzheimer ‘s-diagnosed individuals showed similar vulnerability to SARS-CoV-2 infection, suggesting no significant difference in initial infection rates. However, a notable distinction appeared in the gene activity of infected cells from Alzheimer’s patients. Their cells exhibited increased oxidative stress, changed immune responses, and significant alterations in genes related to the sense of smell compared to cells from cognitively healthy individuals.

Ali Shahbaz, a doctoral researcher in Professor Katja Kanninen’s research group at the University of Eastern Finland and the first author of the study, said“The results suggest a plausible scenario where individuals affected by AD might face potentially more severe COVID-19 outcomes due to pre-existing inflammation in the olfactory mucosa.”

Journal Reference:

  1. Shahbaz, M.A., Kuivanen, S., Lampinen, R. et al. Human-derived air–liquid interface cultures decipher Alzheimer’s disease–SARS-CoV-2 crosstalk in the olfactory mucosa. J Neuroinflammation 20, 299 (2023). DOI: 10.1186/s12974-023-02979-4