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Aging and aging related neurodegenerative disease models and drug screening based on Caenorhabditis elegans:research progress / 中国药理学与毒理学杂志
Article in Zh | WPRIM | ID: wpr-613829
Responsible library: WPRO
ABSTRACT
Caenorhabditis elegans is a very important model organism in life sciences. C. elegans has been widely used in research on life sciences, especially in drug screening and the mechanism of drugs, thanks to some of their prominent characteristics, including a short life,short generation cycle, and easy culture and observation. Aging is a complex process, which is the result of multiple factors. There are mainly three types of anti-aging signal pathways in C. elegans, including insulin-insulin-like growth factor-1 signal pathway, diet-restricted signaling pathway and mitochondrial respiratory chain/ATP synthesis pathway. In this paper, we reviewed the aging models based on the above three signaling pathways and the progress in anti-aging drugs based on the above aging models. In addition, a number of C. elegans models of aging-related neurodegenerative diseases can be obtained by using transgenic or chemical mutagenesis. Thus, this paper reviewed the transgenic models of C. elegans associated with neurodegenerative diseases, including theα-synuclein transgenic model of Parkinson disease, theβ-amyloid deposition model of Alzheimer disease, and the polyQ of Huntington disease, and summa?rized the effective drugs based on the above disease models. This review will provide reference for the study of C. elegans in the future screening of anti-aging drugs and drug screening for the prevention and treatment of neurodegenerative diseases.
Key words
Full text: 1 Index: WPRIM Type of study: Diagnostic_studies / Prognostic_studies / Screening_studies Language: Zh Journal: Chinese Journal of Pharmacology and Toxicology Year: 2017 Type: Article
Full text: 1 Index: WPRIM Type of study: Diagnostic_studies / Prognostic_studies / Screening_studies Language: Zh Journal: Chinese Journal of Pharmacology and Toxicology Year: 2017 Type: Article