The COVID-19 pandemic revealed that there is a loss of smell in many patients, including in infected but otherwise asymptomatic individuals. The underlying mechanisms for the olfactory symptoms are unclear. Using a mouse model, we determined whether cells in the olfactory epithelium express the obligatory receptors for entry of the SARS-CoV-2 virus by using RNAseq, RT-PCR, in situ hybridization, Western blot, and immunocytochemistry. We show that the cell surface protein ACE2 and the protease TMPRSS2 are expressed in sustentacular cells of the olfactory epithelium but not, or much less, in most olfactory receptor neurons. These data suggest that sustentacular cells are involved in SARS-CoV-2 virus entry and impairment of the sense of smell in COVID-19 patients. We also show that expression of the entry proteins increases in animals of old age. This may explain, if true also in humans, why individuals of older age are more susceptible to the SARS-CoV-2 infection.

For over 30 years, a large volume of data has been collected indicating the possibility of an infectious form of Alzheimer’s disease (AD). Using various AD animal models and patients’ brain extracts it has been demonstrated that amyloid Aβ (Aβ) can be an infectious agent. The similarities of Aβ and PrPsc prion protein (PrPsc) have been an important indicator of a potentially infective nature of AD. Nonetheless, the majority of epidemiological data have not yet supported the hypothesis of the infectious nature of this disease. It must be emphasized that AD is a very complex disease which is most likely unique to humans. The strong evidence on the infectivity and propagation of Aβ in animal models is accompanied by the uncertainty of whether the observed symptoms can be recapitulated in humans. Therefore, using currently available AD models it may not be feasible to collect data of sufficient quality clearly and unambiguously demonstrating the infectivity of the disease. We postulate that in order to gather stronger evidence for AD infectivity in humans, new experimental strategies must be considered. This approach should also lead to better understanding of the peripheral routes of Aβ infection. The aim of this review is to present the current state of knowledge and existing doubts in this important area of neurobiology and medicine. In the light of available data, AD infectivity has still not been proven, yet it should be seriously considered. The confirmation that some forms of AD are infectious may result in significant scientific, medical and social consequences.