Korean researchers identify the mechanism of interaction between Alzheimer’s causative proteins and high-risk genes

Alzheimer’s disease cause protein deposition group
Depending on the presence of high-risk genes
Identify different brain function connectivity activation patterns

Yeouido St. Mary’s Hospital Brain Health Center Professor Lim Hyun-guk (left), Seoul St. Mary’s Hospital Department of Psychiatry Professor Kang Dong-gu.

湲 蹂肄

[아시아경제 이관주 기자] A Korean research team has revealed a mutual pathological mechanism between the ‘APOE4’ gene, a major risk factor for Alzheimer’s disease, and the degree of amyloid beta protein deposition in normal cognitive groups.

The research team led by Professor Hyunguk Lim of the Brain Health Center at the Catholic University of Korea Yeouido St. Mary’s Hospital and Professor Dongwoo Kang of the Department of Psychiatry at Seoul St. Mary’s Hospital classified the level of beta-amyloid protein accumulation as below or above the threshold, and then the brain function and cognitive changes according to the level of deposition were determined by APOE4 (APOE4). It was confirmed on the 31st that it was confirmed that there was a significant difference depending on the presence or absence of the gene.

Alzheimer’s disease, a typical neurodegenerative disease, accumulates amyloid beta protein in the brain 10 to 15 years before the onset of symptoms, which causes gradual changes in brain function and structure, and cognitive decline. Therefore, a period in which amyloid beta protein is deposited occurs even in a normal cognitive state, which is attracting attention as a period that can increase the possibility of early diagnosis and treatment. In the case of ‘Sporadic Alzheimer’s disease’, which accounts for 99% of Alzheimer’s disease, multiple factors influence the pathogenesis of the disease. In particular, it is known that the severity of pathological progression and the risk of developing dementia depend on the presence or absence of the Apoi4 gene.

The research team classified the elderly group (182 people) in the normal cognitive function category into a group with beta-amyloid protein above the threshold (72 people) and a group with beta-amyloid protein below the threshold (110 people), and then the degree of beta-amyloid protein deposition and the functional connectivity of the resting cranial neural network. , the presence or absence of the Apoi4 gene, a high-risk gene for sporadic Alzheimer’s disease, was evaluated. In addition, the main neural networks involved in cognitive function changes were extracted and the intra-network connectivity and inter-network connectivity were analyzed.

As a result, when carrying the Apoi4 gene, neural network connectivity was enhanced in the precuneus and cerebellum crus in the subthreshold amyloid beta deposition group, whereas the neural network in the insula in the above-threshold deposition group was enhanced. As a result, connectivity was weakened. In the case of carrying the Apoi4 gene, the patterns of changes in neural network connectivity in the two groups were different, but it was found that these changes in both groups contributed to improvement in executive ability and memory.

Professor Lim Hyeon-guk said, “It is essential to establish the basis for early treatment of dementia to closely identify the cause of amyloid-beta protein on brain function and clinical indicators at the earliest stage when it begins to be deposited in the brain. It is meaningful in that the effect of protein deposition on the brain function impairment process was evaluated compared to the threshold abnormal deposition group, and the interaction with high-risk genes was considered.”

This study was published in ‘frontiers in Aging Neuroscience’.


Reporter Lee Kwan-ju leekj5@asiae.co.kr


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