Medical and Health Science for Co-prosperity
The Relationship Between GSK3Βeta Activity and TDP-43 Me-diated Neuritis in Neurodegenerative Diseases
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- 통권
- Proceedings of THE 6th INTERNATIONAL CONFERENCE OF HYOJEONG ACADEMY (2025.08)바로가기
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- 페이지
- pp.126-131
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- 저자
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- 언어
- 영어(ENG)
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- URL
- https://www.earticle.net/Article/A489380
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원문정보
초록
- 영어
- TDP-43-positive inclusions have also been reported to be associated with the hippocampal CA1 Lewy-body pa-thology of familial Parkinson’s disease patients bearing a Parkin mutant suggesting that there is likely a link between Parkin and TDP-43. Also, it is known that loss of the nuclear RNA binding protein TAR DNA binding protein-43 (TDP-43) into cytoplasmic inclusions is the strongest correlate to neurodegeneration in frontotemporal degeneration (FTD) and amyotrophic lateral sclerosis (ALS). TDP-43, TAF15, and FUS are DNA/RNA binding proteins, and these lead to neurodegenerative disease when inducing cytoplasmic aggregates. Selective expression of TDP-43 in rat astrocytes also leads to non-cell autonomous neuronal toxicity. TDP-43 is ubiquitously expressed in many tissues and cell types, including glial cells of the central nervous system. Glycogen Synthase Kinase 3β (GSK3β) is a Serine/Threonine protein kinase that phosphorylate either threonine or serine and participates in a variety of cellular processes such glycogen metabolism, gene transcription, apoptosis and micro-tubule stability. To identify the mechanism of neuroinflammatory induction through over-expression GSK3β in astrocyte using Shaggy which is the homolog of GSKβ in Drosophila model. This experiment revealed that we were able to suppress astrocytes-induced neuroinflammation by regulating GSK3β activity in the TDP-43 ALS model.
목차
Abstract
1. Introduction
2. Materials and Methods
3. Results
3.1. GSK3β / Shaggy enzyme activity was increased in TDP-43-induced drosophila degenerative model
3.2. Inhibition of Shaggy restored the abnormal wing posture in TDP-43-induced drosophila degenerative model
3.3. Inhibition of Shaggy restored the locomotor activity of adult flies in TDP-43-induced drosophila degenerative model
3.4. Cytoplasmic TDP-43 was decreased by the knockdown of GSK3β
3.5. Astrocyte-derived TDP43 aggregates are spread and propagation to neurons
3.6. Inhibition of Shaggy in the TDP-43-expressing flies restored the decreased number of boutons and size at the Neuromuscular Junction
4. Discussion & Conclusions
References
키워드
Glycogen Synthase Kinase 3β (GSK3β) 1 TDP-43 (TAR DNA binding protein-43) 2 Amyotrophic lateral sclerosis (ALS) 3저자
간행물 정보
발행기관
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- 발행기관명
- 선문효정학술연구회 [Sun Moon Hyojeong Academy Society]
- 설립연도
- 2023
- 분야
- 복합학>학제간연구
- 소개
- Journal of Hyojeong Academia aims to serve as a global platform where researchers and scholars of various disciplines can contribute ideas for our sustainable global community of Co‐existence, Co‐prosperity, and Co‐righteousness. The journal is a multidisciplinary, open‐access, internationally peer‐reviewed academic journal, and it invites all areas of research conducted in the spirit of post materialism including studies centering on God, studies unifying religions and sciences, and studies on all aspects of Co‐existence, Co‐prosperity, and Co‐righteousness.
간행물
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- 간행물명
- 선문효정학술연구회 학술대회 프로시딩
- 간기
- 반년간
- 수록기간
- 2023~2026
- 십진분류
- KDC 238 DDC 289
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