2023-11-20 05:30:23
Effect of amyloid precursor C-terminal truncation (APP-C31) on the function of Alzheimer’s pathology factors
[충청뉴스 이성현 기자] A toxic protein that causes Alzheimer’s disease has been discovered by a domestic research team.
At the Korea Advanced Institute of Science and Technology (KAIST), Professor Mi-hee Lim’s research team from the Department of Chemistry is conducting joint research with Dr. Young-ho Lee’s research team from the Bio Convergence Research Department at the Korea Basic Science Institute (KBSI), Professor Moo-hyeon Baek’s research team from the KAIST Department of Chemistry, and Professor Jin-joo Han’s research team from the Graduate School of Medical Sciences, and the Korea Research Institute of Bioscience and Biotechnology (KAIST) is conducting research on rare and difficult-to-treat diseases. It was announced on the 20th that the participation of Dr. Lee Da-yong’s research team at the Disease Research Center presented a new pathological network related to Alzheimer’s disease by discovering intracellular proteins that promote the toxicity of Alzheimer’s disease-causing factors.
A typical pathological phenomenon that appears in the brains of Alzheimer’s disease patients is the accumulation of senile spots. The main component of senile spots is amyloid-beta peptide, which binds to intracellular substances and causes cell damage. Therefore, the correlation between these aggregates and cell death is being actively studied. However, much remains unknown regarding the direct interaction between amyloid-beta and apoptosis-inducing factors.
A new drug for Alzheimer’s disease recently approved by the U.S. FDA was developed to primarily target cellular damage caused by amyloid-beta peptide aggregates that cause age-related spots. However, due to limited use (especially side effects), researchers are keenly aware of the need for change in direction and improvement in the development of new drugs.
Professor Lim Mi-hee’s research team discovered that the ‘amyloid precursor C-terminal truncated protein’, which is overexpressed in Alzheimer’s disease and causes neuronal death of unknown causes, binds to amyloid-beta and metal-amyloid-beta complexes to promote aggregation and acts as a toxicity accelerator. announced the world’s first research proving that
The results of this study suggest that the amyloid precursor C-terminal truncated product itself or a complex bound to amyloid-beta can act as a new biomarker for Alzheimer’s disease and that they can also be targets for new drug development.
This study, in which Dr. Namju Nam (Ph.D. in Chemistry from KAIST, researcher at Brigham and Women’s Hospital and Harvard Medical School) from Professor Mihee Lim’s research team participated as the first author, was conducted to identify amyloid precursor C-terminal truncated forms of amyloid-beta within cells through intracellular protein microinjection technology. The research team confirmed its role in promoting cohesion.
Furthermore, the phenomenon of amyloid-beta-related cell death, neuron damage, and inflammatory response in neuron cells and rodent brains was confirmed to be further increased by amyloid precursor C-terminal truncation, attracting worldwide attention.
Professor Lim Mi-hee said, “The results of this study are significant in discovering previously unknown in vivo amyloid-beta aggregation and toxicity promoters in Alzheimer’s disease,” adding, “This research result suggests new biomarkers and treatment targets.” did.
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