A group of researchers at Seoul National University Bundang Hospital has found the gene involved in the occurrence of Alzheimer’s disease through a cohort study.

The team, led by Professor Park Young-ho of the Department of Neurology at the hospital, conducted a study of 661 people in the U.S. and 674 in Europe to discover that certain gene expressions related to inflammatory reactions from immune cells and virus infections can affect Alzheimer’s disease.  

​Researchers, led by Professor Park Young-ho of the Department of Neurology at Seoul National University Bundang Hospital, have found genes causing Alzheimer’s disease through a cohort study. (SNUBH)
​Researchers, led by Professor Park Young-ho of the Department of Neurology at Seoul National University Bundang Hospital, have found genes causing Alzheimer’s disease through a cohort study. (SNUBH)

The disease accounts for 70 percent of dementia’s causes and appears in the form of brain shriveling due to dwindling nerve cells. It is a degenerative brain disease in which the cognitive functions, including memory, gradually worsen.

The researchers confirmed the “Genome-Wide Association Study” (GWAS) results to identify causative genes. 

This method compares genetic information of a patient and non-patient group and finding genetic information related to the disease by appearing more frequently in the patient group.

The team first identified 22 genes closely related to Alzheimer’s disease using the GWAS method. Next, they summed up gene expressions in the blood. The team then assessed whether the differences in the amount of gene expressions could help diagnose Alzheimer’s disease and analyzed through which mechanism they get involved in the disease's occurrence.

As a result, the patient group showed a higher rate of genetic expressions than the normal group. In other words, more genes were expressed in the former group found to be related to Alzheimer’s when examined by the GWAS method. 

Particularly, genes called CD33 and PILRA contribute greatly to the occurrence of Alzheimer's disease. In a healthy human body, dietary cells protect the body by feasting on unnecessary substances, which suppresses the development of Alzheimer’s, as food cells operate on the substances that cause the disease.

However, the team found that CD33 hinders these dietary cells' response to the immune system, leading to Alzheimer’s disease. Also, PILRA is known to assist the herpes simplex virus (HSV) penetrate cells and make the body more vulnerable to infections. 

The research team expects to identify more causative genes of Alzheimer’s disease and develop prevention and possible cure.

“All diseases have unique causative genes that vary from patients. Therefore, treatments become different, too. That is why we analyzed the differences in gene expression to establish a foundation for precision medical treatment, providing customized care by examining genetic and clinical information, and lifestyle of individuals,” Professor Park said. 

Since the study was conducted on Western people, there are limitations to applying it to Korean patients right away. Since genetic analysis results can racially vary, the research team plans to design follow-up studies for Korean patients and continue to check on Alzheimer’s disease diagnosis, he added.

The study results were published in the online September issue of Neurology Genetics from the American Academy of Neurology.
 

Copyright © KBR Unauthorized reproduction, redistribution prohibited