{"title":"前言/前页","authors":"L. Guarente, L. Partridge, D. Wallace","doi":"10.1101/087969824.51.i","DOIUrl":null,"url":null,"abstract":"The past decade or so has witnessed an explosion in knowledge about the molecular basis of the aging process and its modulation by genes and diet. This book was designed to capture the field of aging research at this exciting moment in its history. The chapters were chosen to represent many of the important threads that are woven together to provide the current framework of our understanding of aging, at the level of molecules, cells, tissues, and the whole organism. One group of chapters focuses on the model organisms that have been used to dissect the genetics and molecular biology of aging in recent years. These include yeast, C. elegans, Drosophila , and mice. The strengths and weaknesses of each system are on display, and the major findings that have emerged are described in detail. Several of the pathways identified show evolutionary conservation among these model systems, and are hence candidates for modulation of human aging. The roles of stress resistance and of DNA repair are discussed, as are genomic systems and population genetic approaches currently used to investigate aging in model organisms and humans. Human aging may have unique features that are not shared by the model organisms, and this is also addressed. Another theme in this book is the interaction between diet, metabolism, and life span. It has been known for about 75 years that a low calorie diet, termed calorie restriction or CR, can extend lifespan in rodents and in an expanding range of organisms, and these physiological","PeriodicalId":10493,"journal":{"name":"Cold Spring Harbor Monograph Archive","volume":"5 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Preface/Front Matter\",\"authors\":\"L. Guarente, L. Partridge, D. Wallace\",\"doi\":\"10.1101/087969824.51.i\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The past decade or so has witnessed an explosion in knowledge about the molecular basis of the aging process and its modulation by genes and diet. This book was designed to capture the field of aging research at this exciting moment in its history. The chapters were chosen to represent many of the important threads that are woven together to provide the current framework of our understanding of aging, at the level of molecules, cells, tissues, and the whole organism. One group of chapters focuses on the model organisms that have been used to dissect the genetics and molecular biology of aging in recent years. These include yeast, C. elegans, Drosophila , and mice. The strengths and weaknesses of each system are on display, and the major findings that have emerged are described in detail. Several of the pathways identified show evolutionary conservation among these model systems, and are hence candidates for modulation of human aging. The roles of stress resistance and of DNA repair are discussed, as are genomic systems and population genetic approaches currently used to investigate aging in model organisms and humans. Human aging may have unique features that are not shared by the model organisms, and this is also addressed. Another theme in this book is the interaction between diet, metabolism, and life span. It has been known for about 75 years that a low calorie diet, termed calorie restriction or CR, can extend lifespan in rodents and in an expanding range of organisms, and these physiological\",\"PeriodicalId\":10493,\"journal\":{\"name\":\"Cold Spring Harbor Monograph Archive\",\"volume\":\"5 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2008-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cold Spring Harbor Monograph Archive\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/087969824.51.i\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cold Spring Harbor Monograph Archive","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/087969824.51.i","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The past decade or so has witnessed an explosion in knowledge about the molecular basis of the aging process and its modulation by genes and diet. This book was designed to capture the field of aging research at this exciting moment in its history. The chapters were chosen to represent many of the important threads that are woven together to provide the current framework of our understanding of aging, at the level of molecules, cells, tissues, and the whole organism. One group of chapters focuses on the model organisms that have been used to dissect the genetics and molecular biology of aging in recent years. These include yeast, C. elegans, Drosophila , and mice. The strengths and weaknesses of each system are on display, and the major findings that have emerged are described in detail. Several of the pathways identified show evolutionary conservation among these model systems, and are hence candidates for modulation of human aging. The roles of stress resistance and of DNA repair are discussed, as are genomic systems and population genetic approaches currently used to investigate aging in model organisms and humans. Human aging may have unique features that are not shared by the model organisms, and this is also addressed. Another theme in this book is the interaction between diet, metabolism, and life span. It has been known for about 75 years that a low calorie diet, termed calorie restriction or CR, can extend lifespan in rodents and in an expanding range of organisms, and these physiological