At the end of the year, the prestigious Journal of Neuroinflammation (IF 9.3) published an international study entitled “Human-derived air-liquid interface cultures decipher Alzheimer’s disease-SARS-CoV-2 crosstalk in the olfactory mucosa” (open in a new window), which was co-authored by a team of authors from the Department of Genetic Toxicology and Epigenetics in collaboration with international colleagues from the University of Eastern Finland, Kuopio University Hospital and the University of Helsinki. The authors of the IEM CAS include Jan Topinka, Táňa Závodná and Zdeněk Krejčík.
In this study, the researchers investigated the relationship between Alzheimer’s disease (AD) and SARS-CoV-2 infection using an in vitro model of the olfactory mucosa. This was created from cultured olfactory mucosa cells that were collected from healthy individuals and AD patients. The results showed that both groups were equally susceptible to SARS-CoV-2 infection. However, an analysis assessing gene activity in cells from both groups infected under laboratory conditions with SARS-CoV-2 virus showed increased oxidative stress, suppression of inflammation, attenuation of immune responses and changes in olfactory-related genes in cells derived from individuals with AD. These findings suggest that people with AD may face more severe consequences of SARS-CoV-2 infection due to less efficient processes that suppress viral infection.
The full study can be found on the Spinger Link website (open in a new window).