“The research is still tremendously split. Most are still in agreement that the protein beta-amyloid, which forms harmful accumulations in the brain, has a central role,” says Katarina Kågedal, reader in experimental pathology at Linköping University.
Together with people such as Ann-Christin Brorsson, reader in molecular biotechnology, she is now publishing a study of the interaction between lysozyme and beta-amyloid. In the article, in Neurobiology of Disease, evidence is presented that lysozyme appears to protect the brain’s nerve cells from toxic beta-amyloid structures.
The researchers first looked at tissue samples from deceased Alzheimer’s patients. They discovered that the level of lysozyme in their spinal fluid was significantly higher than in persons who did not have the illness. They also saw that lysozyme accumulated on the plaque that had formed in the brain.
That part of the study, however, said nothing on whether this was good or bad for the development of the illness. To get further, experiments were conducted on banana flies infected with beta-amyloid.
“The research clearly shows that overexpression of lysozyme curbs the development of the illness. The flies lived longer and became more active,” Ms Brorsson says.
The researchers also saw that lysozyme prevents the genesis of harmful accumulations of beta-amyloid.
First and foremost, they believe that analysis of the lysozyme levels in spinal column samples could be used as biomarkers for Alzheimer’s disease, especially in its early phase. Today, diagnoses are made primarily in the form of memory tests at health clinics, and in severe cases with what is called ‘PET scanning’ of the brain.
Over the long term, lysozyme tracks can also open the way for a strategy for preventative treatment.
“The dream is to be able to pay a visit to the doctor sometime during the year and remove the plaque, somewhat like going to the dentist,” Ms Kågedal says.
Article: Protective properties of lysozyme on β-amyloid pathology: implications for Alzheimer disease by L. Helmfors, A. Boman, L. Civitelli, S. Nath, L. Sandin, C. Janefjord, H. McCann, H. Zetterberg, K. Blennow, G. Halliday, A-C. Brorsson, K. Kågedal. Neurobiology of Disease 83 (2015). doi:10.1016/j.nbd.2015.08.024