It is now known that people suffering from COVID-19 temporarily lose their sense of smell and taste. This assumes that the viruses invade the olfactory bulb of the brain (Bulbus olfactorius = BO).
The BO contains a large number of ACE2 receptors, which are known to be the entry point of the SARS CoV-2 virus into the cell. The distribution of the ACE2 receptors in mice and humans was recently examined in more detail by Chen et al (2020).
At the same time, the number of ACE2 receptors is reduced in Alzheimer’s disease, see the work of Kehoe et al (2016). Furthermore, Evans et al. (2020) could show that ACE2-enhancing activation helps in Alzheimer’s disease.
Thus, the replication pathway of the SARS CoV-2 virus via the ACE2 receptor and the protection against Alzheimer’s are in contrast to each other. It is therefore quite possible that COVID-19 promotes the risk of Alzheimer's. On the other hand, a deficiency of ACE2 receptors in existing Alzheimer’s disease may even be protective against COVID-19, especially in older patients with previous diseases, which is quite typical for Alzheimer's disease.
As was reported on March 11, 2020, a 100-year-old man in China with pre-existing conditions and Alzheimer's disease was able to recover from a COVID-19 disease, but only after receiving blood plasma from recovered COVID-19 patients as a transfusion, so that the antibodies contained in it apparently worked well. It is likely that this was the cause of his recovery. This is because in a similar case in Germany, in which a 33-year-old nurse without previous illnesses became ill with COVID-19 and almost died, the patient was also saved by a blood transfusion.