a-synuclein seeding activity in the olfactory mucosa followi

Deposits of misfolded proteins are the cause of frequent neurological diseases such as Alzheimer`s or Parkinson`s disease. In Parkinson`s disease, the misfolded protein alpha-synuclein is found in the olfactory mucosa of the nose, which contains nerve cells responsible for smell perception, from which the misfolded alpha-synuclein spreads further into the brain. The mechanisms that lead to this misfolding and the resulting damage to the nervous system are still unclear. One hypothesis is that inflammatory processes such as viral infections trigger the misfolding of alpha-synuclein in Parkinson`s disease and can lead to its deposition. Based on this assumption and the striking involvement of the sense of smell in SARS-CoV-2 infection (COVID-19), the aim of this study is to investigate the olfactory epithelium of the nasal mucosa of COVID-19 patients for possible alpha- synuclein deposits by using nasal swabs.

This pilot study explored whether SARS-CoV-2 infection might lead to harmful -synuclein protein aggregates in the olfactory mucosa-the tissue responsible for our sense of smell-potentially increasing the risk of neurological disorders like Parkinson's disease. We found that -synuclein aggregates were present in over 80% of Parkinson's disease patients, in about 23% of subjects after SARS-CoV-2 infection, and in about 12% of healthy individuals. Although overall positivity rates between subjects after SARS-CoV-2 infection and healthy controls did not differ significantly, a notable finding was that individuals experiencing persistent subjective smell loss after SARS-CoV-2 infection had higher rates of these protein aggregates compared to those without subjective smell problems and compared to healthy controls. While the study does not conclusively establish long-term neurological risks, it highlights an important area for ongoing research into the neurological implications of SARS-CoV-2 infection.