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Identification of new neurodegenerative mechanisms of dementia



Dr. Hyung-Chun Kim and Jin-Ri Lee, Korea Brain Research Institute, present the international journal Autophagy
Anti-dementia therapies expect abnormal protein removal

Kim Hyung-unun, Korea Research Institute in Korea, Lee Yin-researcher, and Professor Kim Ki-young (left) at Songhungyang University remove the dementia fruit fly model from the fruit incubator.
Kim Hyung-unun, Korea Research Institute in Korea, Lee Yin-researcher, and Professor Kim Ki-young (left) at Songhungyang University remove the dementia fruit fly model from the fruit incubator.

Korea Scientific EconomicsThe Korea Brain Research Institute (KBRI) on the 12th announced that a home research team with Kim Hyung-un, Lee Yin-rio and Professor Kim Ki-young of Sunjiang University published a new molecular mechanism that prevents non-neuronal death. cells during dementia and Lou Gerrig's disease.

The research results were published in the November issue of the international journal Autophagy (IF = 11.059).

Neuronal cells in patients with dementia or Lou Gerig's disease often have abnormal aggregates that contain accumulated TDP-43 * proteins, causing damage to the intracellular protein quality control system (UPS) that removes damaged or unnecessary protein. Causes neurodegeneration;

The Ubiquitin Proteasome System (UPS) is part of protein quality control (a mechanism that removes or restores abnormal proteins to keep proteins intact) and is known to inhibit cell death by abnormal protein degradation.

TDP-43 is a protein that contributes to RNA stability and function and is known to be a major pathogen such as Lou Gerrig's disease (ALS), frontal lobe dementia (JDD) and Alzheimer's Dementia (AD).

The team has found a new role for the three proteins (PTK2, TBK1, SQSTM1) that can inhibit neuronal degeneration with TDP-43, and their interactions are another system for controlling the quality of proteins in cells in the event of UPS damage. The first in the world has been shown to be able to inhibit neuronal degeneration by improving the phagolysosomal pathway (ALP) *. "

Autophagy Lysosome Pathway (ALP) is an intracellular scavenger that acts as an intracellular scavenger that disassembles and recycles organelles or parts that are not needed in cells.

This study reveals a molecular mechanism of a new pathway that can reverse the neurodegenerative symptoms caused by the TDP-43 protein, which is the cause of various dementia and disease of Lou Gerrig, thereby eliminating abnormal proteins accumulated in neurons of the patient's neurons. . It is estimated that a new treatment strategy has been introduced.

Hyung Jun Kim, lead researcher at the Korea Brain Research Institute, said: "The results of this study proved the mechanism at the basic level of research, and the verification process is crucial at the clinical level for the development of treatment." cooperation with domestic and overseas brain banks and hospitals. We are forming a verification team in the organization and will conduct further research. "

The Korea Brain Research Institute signed a contract in August this year with King's College University in London, the Dementia Research Center in London (UK DRI). Will be strengthened.

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