{"title":"评估转基因秀丽隐杆线虫阿尔茨海默病模型中的淀粉样蛋白聚集和毒性。","authors":"Leticia Priscilla Arantes, Larissa Marafiga Cordeiro, Félix Alexandre Antunes Soares","doi":"10.1016/bs.mcb.2024.06.001","DOIUrl":null,"url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms. Caenorhabditis elegans (C. elegans) is a simple and valuable organism to study the dynamics of Aβ. It may contribute to advancing our comprehension of AD development and progression, as well as to discovering new treatments. Herein, we describe usual protocols for evaluating Aβ aggregation and toxicity in transgenic C. elegans models of AD (CL2006, CL4176, GMC101, and CL2355 strains) through the visualization and quantification of the peptide with specific fluorescent dyes, in addition to the analysis of particular behaviors (paralysis and chemotaxis associated with learning).</p>","PeriodicalId":18437,"journal":{"name":"Methods in cell biology","volume":"192 ","pages":"189-202"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Evaluating amyloid-beta aggregation and toxicity in transgenic Caenorhabditis elegans models of Alzheimer's disease.\",\"authors\":\"Leticia Priscilla Arantes, Larissa Marafiga Cordeiro, Félix Alexandre Antunes Soares\",\"doi\":\"10.1016/bs.mcb.2024.06.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms. Caenorhabditis elegans (C. elegans) is a simple and valuable organism to study the dynamics of Aβ. It may contribute to advancing our comprehension of AD development and progression, as well as to discovering new treatments. Herein, we describe usual protocols for evaluating Aβ aggregation and toxicity in transgenic C. elegans models of AD (CL2006, CL4176, GMC101, and CL2355 strains) through the visualization and quantification of the peptide with specific fluorescent dyes, in addition to the analysis of particular behaviors (paralysis and chemotaxis associated with learning).</p>\",\"PeriodicalId\":18437,\"journal\":{\"name\":\"Methods in cell biology\",\"volume\":\"192 \",\"pages\":\"189-202\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Methods in cell biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.mcb.2024.06.001\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/7/9 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Methods in cell biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.mcb.2024.06.001","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/9 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
Evaluating amyloid-beta aggregation and toxicity in transgenic Caenorhabditis elegans models of Alzheimer's disease.
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms. Caenorhabditis elegans (C. elegans) is a simple and valuable organism to study the dynamics of Aβ. It may contribute to advancing our comprehension of AD development and progression, as well as to discovering new treatments. Herein, we describe usual protocols for evaluating Aβ aggregation and toxicity in transgenic C. elegans models of AD (CL2006, CL4176, GMC101, and CL2355 strains) through the visualization and quantification of the peptide with specific fluorescent dyes, in addition to the analysis of particular behaviors (paralysis and chemotaxis associated with learning).
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For over fifty years, Methods in Cell Biology has helped researchers answer the question "What method should I use to study this cell biology problem?" Edited by leaders in the field, each thematic volume provides proven, state-of-art techniques, along with relevant historical background and theory, to aid researchers in efficient design and effective implementation of experimental methodologies. Over its many years of publication, Methods in Cell Biology has built up a deep library of biological methods to study model developmental organisms, organelles and cell systems, as well as comprehensive coverage of microscopy and other analytical approaches.
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