Alzheimer's may worsen COVID-19 outcomes via olfactory mucosa changes

NewsGuard 100/100 Score

A new study identifies alterations in the transcriptomic signatures in human olfactory mucosal cells of individuals with Alzheimer's disease following SARS-CoV-2 infection, potentially contributing to exacerbated COVID-19 outcomes. The study was conducted at the University of Eastern Finland in collaboration with the University of Helsinki and published in Journal of Neuroinflammation.

The study was prompted by concerns about the impact of COVID-19 on individuals with pre-existing conditions such as Alzheimer's disease (AD). Olfactory dysfunction, characterized 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.

Employing an innovative 3D in vitro model of the olfactory mucosa, the study utilized 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. The collection of olfactory mucosal biopsies was conducted collaboratively with Kuopio University Hospital. This multidisciplinary research integrated expertise from molecular and cellular biology, neurology, and virology to investigate the effects of various SARS-CoV-2 variants on the olfactory mucosa.

Distinct immune responses after infection between AD patients and healthy individuals

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 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."

Ali Shahbaz, doctoral researcher in Professor Katja Kanninen's research group at the University of Eastern Finland and the first author of the study

The present study represents a pivotal advancement in understanding the intricate interplay between COVID-19 and AD.

The study was funded by the Academy of Finland.

Journal reference:

Shahbaz, M. A., et al. (2023). Human-derived air–liquid interface cultures decipher Alzheimer’s disease–SARS-CoV-2 crosstalk in the olfactory mucosa. Journal of Neuroinflammation.


The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
Does vitamin D have protective role against COVID-19?