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Recent Advances on the Role of GSK3ß in the Pathogenesis of Amyotrophic Lateral Sclerosis.
Choi, Hyun-Jun; Cha, Sun Joo; Lee, Jang-Won; Kim, Hyung-Jun; Kim, Kiyoung.
Afiliación
  • Choi HJ; Department of Integrated Biomedical Science, Soonchunhyang University, Cheonan 31151, Korea.
  • Cha SJ; Department of Medical Science, Soonchunhyang University, Asan 31538, Korea.
  • Lee JW; Department of Integrated Bio-industry, Sejong University, Seoul 05006, Korea.
  • Kim HJ; Dementia Research Group, Korea Brain Research Institute (KBRI), Daegu 41068, Korea.
  • Kim K; Department of Medical Science, Soonchunhyang University, Asan 31538, Korea.
Brain Sci ; 10(10)2020 Sep 26.
Article en En | MEDLINE | ID: mdl-32993098
Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disease characterized by progressive motor neuron degeneration. Although several studies on genes involved in ALS have substantially expanded and improved our understanding of ALS pathogenesis, the exact molecular mechanisms underlying this disease remain poorly understood. Glycogen synthase kinase 3 (GSK3) is a multifunctional serine/threonine-protein kinase that plays a critical role in the regulation of various cellular signaling pathways. Dysregulation of GSK3ß activity in neuronal cells has been implicated in the pathogenesis of neurodegenerative diseases. Previous research indicates that GSK3ß inactivation plays a neuroprotective role in ALS pathogenesis. GSK3ß activity shows an increase in various ALS models and patients. Furthermore, GSK3ß inhibition can suppress the defective phenotypes caused by SOD, TDP-43, and FUS expression in various models. This review focuses on the most recent studies related to the therapeutic effect of GSK3ß in ALS and provides an overview of how the dysfunction of GSK3ß activity contributes to ALS pathogenesis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Etiology_studies Idioma: En Revista: Brain Sci Año: 2020 Tipo del documento: Article Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Etiology_studies Idioma: En Revista: Brain Sci Año: 2020 Tipo del documento: Article Pais de publicación: Suiza