Institute of Experimental Medicine CAS

Published 21. 04. 2022

A new international study on the ionic imbalance of bio-metals in the olfactory mucosa of patients with Alzheimer's disease (AD) has been published in the „International Journal of Molecular Sciences“ (IF 5,924). In addition to researchers from Finland, Australia and Italy, scientists from the IEM CAS, namely Ing. et Mgr. Táňa Závodná, Ph.D., Ing. Zdeněk Krejčík, Ph.D. and Ing. Jan Topinka, CSc., DSc. took part in the study. 

The function of sense of smell, which is provided by the cells of the olfactory epithelium, is already impaired in the early stage of AD. Biogenic ions play an important role in the proper function of olfactory cells, but very little is known about the homeostasis of biochemicals in the olfactory mucosa. Therefore, this study aimed to assess whether there are changes in the concentrations of selected bio-metals in AD patients, and to identify new biomarkers and risk groups of patients. 

In the initial phase of the study, the researchers focused on a more detailed investigation of genes related to bio-metal binding and metabolism. Using gene expression (mRNA) of olfactory epithelial cells, they identified changes in the 17 genes in a study group of AD patients compared to a control group of healthy individuals. In the next phase, the researchers analyzed the concentrations of selected biometals in the olfactory epithelial cells in more detail.  

The results showed that higher levels of zinc, calcium and sodium were found in AD patients, along with changes in the expression of 17 genes whose function is related to biochemicals and significantly higher levels of the protein alpha-2-macroglobulin. The results thus confirmed the researchers' hypothesis that the olfactory mucosa cells of AD patients copy specific changes related to neurodegenerative processes that occur directly in brain tissue. 

The detection of changes in biometal homeostasis at the level of olfactory mucosa cells opens new possibilities for the early diagnosis of AD.