Groundbreaking Research by KAIST Unveils New Pathological Network in Alzheimer’s Disease
The number of people suffering from Alzheimer’s disease has seen a rapid increase in recent years, but the identification of the cause and the development of treatments have been slow. However, a domestic research team has presented a breakthrough in the search for a clue to treatment.
The Korea Advanced Institute of Science and Technology (KAIST) announced on the 20th that Professor Mihee Lim’s research team in the Department of Chemistry has, through joint research, discovered intracellular proteins that promote the toxicity of factors that cause Alzheimer’s disease. This groundbreaking discovery has led to the presentation of a new version of a pathological network related to Alzheimer’s disease.
The research is the result of collaboration with Dr. Lee Youngho from the Department of Convergent Bio Research at the Korea Institute of Basic Science, Professor Moohyun Baek’s team from the Department of Chemistry at KAIST, and Professor Jinju Han’s team from the KAIST Graduate School of Medical Sciences. The research team of Dr. Lee Da-yong from the Korea Institute of Bioscience and Biotechnology Research Center for Rare and Incurable Diseases also participated in this groundbreaking study.
The accumulation of senile plaques is a characteristic pathological phenomenon that appears in the brains of Alzheimer’s disease patients. These senile plaques are composed of amyloid and beta peptide aggregates, which bind to intracellular substances and cause cell damage. However, the direct interaction between beta amyloid and factors that cause cell death has remained largely unknown.
The research team found that the ‘C-terminal amyloid precursor truncating protein’, which is overexpressed in Alzheimer’s disease and causes neuronal death of unknown causes, binds to amyloid-beta and metal-amyloid complexes to promote aggregation and acts as toxicity. This groundbreaking discovery suggests that the C-terminal amyloid precursor truncation product itself or the complex bound to amyloid-beta may serve as a new biomarker for Alzheimer’s disease and a potential target for new drug development.
Professor Lim Mihee stated, “We discovered previously unknown promoters of amyloid/beta aggregation and toxicity in vivo in Alzheimer’s disease.” She added, “The research results suggest new biomarkers and treatment targets.”
The results of the research were published on the 10th in the international academic journal ‘Advanced Science’.
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KAIST Professor Mihee Lim’s research team presents a new pathological network
(From left) Professor Mihee Lim, Professor Moohyun Baek, Professor Jinju Han, and Dr. Youngho Lee / KAIST
The number of people suffering from Alzheimer’s disease has increased rapidly, but although identification of the cause and development of treatments has been slow, a domestic research team has presented a clue to treatment.
The Korea Advanced Institute of Science and Technology (KAIST) announced on the 20th that Professor Lim Mi-hee’s research team in the Department of Chemistry, through joint research, discovered intracellular proteins that promote the toxicity of factors that cause Alzheimer’s disease, and presented a new version of a pathological network related to Alzheimer’s disease.
This is the result of joint research with the research team of Dr. Lee Young-ho from the Department of Convergent Bio Research of the Korea Institute of Basic Science, the research team of Prof. Baek Moo-hyun from the Department of Chemistry at KAIST, and the research team of Prof. Jin-joo Han from the KAIST Graduate School of Medical Sciences, and the participation of the research team of Dr. . Lee Da-yong of the Korea Institute of Bioscience and Biotechnology Research Center for Rare and Incurable Diseases.
A characteristic pathological phenomenon that appears in the brains of Alzheimer’s disease patients is the accumulation of senile spots. The main component of age spots are amyloid and beta peptide aggregates, which bind to intracellular substances and cause cell damage.
Although the correlation between these aggregates and cell death is being studied, much is still unknown about the direct interaction between beta amyloid and factors that cause cell death.
The research team found that the ‘C-terminal amyloid precursor truncating protein’, which is overexpressed in Alzheimer’s disease and causes neuronal death of unknown causes, binds to amyloid-beta and metal-amyloid complexes. beta to promote aggregation and acts as toxicity. published research proves it.
Through this, it has been suggested that the C-terminal amyloid precursor truncation product itself or the complex bound to amyloid-beta acts as a new biomarker for Alzheimer’s disease and may be a target for new drug development.
Professor Lim Mi-hee said, “We discovered previously unknown promoters of amyloid/beta aggregation and toxicity in vivo in Alzheimer’s disease,” and added, “The research results suggest biomarkers and treatment targets new.”
The results of the research were published on the 10th in the international academic journal ‘Advanced Science’.
Copyright © DementiaNews Reproduction and redistribution prohibited.
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