Published in the Journal of Neuroinflammation, the study identified alterations in the human olfactory mucosal cells of individuals with Alzheimer’s following SARS-CoV-2 infection, potentially contributing to exacerbated Covid-19 outcomes.
Olfactory dysfunction, characterised by an impaired sense of smell, is commonly associated with Covid-19 and is also observed in persons with AD.
Exploring the olfactory mucosa as a direct interface between the external environment and the brain, the research aimed to investigate the interaction between SARS-CoV-2 infection and AD within the olfactory mucosa, assessing the potential for this tissue to serve as a plausible entry route for the virus into the brain.
“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,” said Ali Shahbaz, a doctoral researcher at the University of Eastern Finland.
The team employed an innovative 3D in vitro model of the olfactory mucosa. They utilised primary cells obtained from voluntary donors, including both cognitively healthy individuals and those diagnosed with AD. These cells were cultivated at the air-liquid interface (ALI), a technique providing a controlled environment that closely mimics physiological conditions.
Contrary to expectations, cells derived from healthy individuals and those with AD exhibited comparable susceptibility to infection by SARS-CoV-2 virus, indicating no significant difference in initial infection rates between the two groups.
However, a significant contrast emerged in the gene activity of infected cells from individuals with AD. Their cells displayed heightened oxidative stress, altered immune responses, and substantial changes in genes related to olfaction when compared to olfactory mucosal cells from cognitively healthy individuals, the researchers said.
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