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Overview

The Fifth Edition of the Handbook of the Biology of Aging continues the tradition of providing a comprehensive overview of some of the most important topics in biomedical gerontology. Beginning with an introduction to concepts and theories of aging, the book is then divided into three main sections covering cellular processes in organismic aging, systemic factors in organismic aging, and models of retarded aging. The book closes with a look at the future of biomedical research as it relates to aging, health, and longevity.
The Handbook will be of interest to biologists involved in aging research, gerontologists, medical researchers, psychologists, sociologists, and practitioners dealing with an aging population.
The Fifth Edition:

* opens with a broad introduction to theories and concepts of aging

* provides new insight into the cellular and systemic aspects of aging

* features new chapters on cellular proliferation, apoptosis, and environment-gene interactions

Audience: Students and researchers of gerontology and biology.

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Editorial Reviews

Doody's Review Service
Reviewer: David O. Staats, MD (University of Oklahoma Health Sciences Center)
Description: This is the fifth edition of a popular multiauthored review of our contemporary understanding of the biological nature of aging.
Purpose: The editors' aim is to provide synposes of current understanding of the nature of aging. They state that in an area with exponential growth of data and ideas, this book provifdes a way to bring a wide audience up-to-date on the current advances in the field. This is true.
Audience: The audience is primarily researchers in aging, graduate students in aging, and practitioners. This book presupposes a fairly broad understanding of molecular biology. All the authors are first-class experts in their fields.
Features: The outstanding aspects of this book are the thorough coverage of the topics and the organization of the book, which gives a comprehensive look at the molecular biology of aging. After a broad opening chapter on theories of aging, there then follow chapters on oxidation, protein turnover, DNA repair, mitochondrial factors, gene expression, mitogen-activated protein kinase signaling pathways, cell proliferation, apoptosis, effect of the neuroendocrine and immune systems, models to retard aging and a concluding chapter from a leading geriatrician. All of this is presented in several hundred pages total, so the information is digestible. The bibliographic citations are all pertinent.
Assessment: This wonderful book remains a leading standard in the field. Unlike the fourth and previous editions, the charming chapter on understanding studies of human aging is left out. If this book is about the molecular biology of aging, why leave out the trees and the invertebrates? On the other hand, the inclusion of comments only on neuroendocrine and immune factors leaves out lots on the nature of human aging at the organ system level. Given that the other handbooks in the series deal with psychological aspects of human aging and social aspects of human aging, perhaps a separate book on the physiologic changes of human aging would complement the series. Given the explosive growth in the data and conceptualization about human aging, theoretical and experimental, I do not fault the editors for choosing to concentrate on molecular biology — that's where the action is.
Gerontologist
Many of the chapters provide outstanding coverage of their subject areas...
Newsletter Of The Assocation For Gerontology In Higher Education
The Fifth Edition... continues the tradition of providing a comprehensive overview of some of the most important topics biomedical gerontology.
From the Publisher
"This is an important and timely book on an extremely critical subject, and although its technical excellence and depth will challenge those without a formal background in molecular biology, the rewards I believe will be deeply commensurate with the effort… However, with that qualification in mind, the articles are uniformly of high quality and address critical issues in the science of aging-several, if not many, of these reviews are good enough to be considered benchmark reviews, cogently summarizing the state of the science… For those interested in a benchmark series of reviews on aging, this volume has much to offer. I recommend it highly. For geriatric neuropsychologists, sophistication about the biology of aging should be considered a required area of competence."—Archives of Clinical Neuropsychology

3 Stars from Doody
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Product Details

  • ISBN-13: 9780124782600
  • Publisher: Elsevier Science & Technology Books
  • Publication date: 5/4/2001
  • Series: Handbooks of Aging
  • Edition description: REV
  • Edition number: 5
  • Pages: 534
  • Product dimensions: 6.90 (w) x 9.98 (h) x 1.07 (d)

Meet the Author

Edward J. Masoro was the recipient of the 1989 Allied-Signal Achievement Award in Aging Research. In 1990, he received the Geriatric Leadership Academic Award from the National Institute on Aging and the Robert W. Kleemeier Award from the Gerontological Society of America. In 1991, he received a medal of honor from the University of Pisa for Achievements in Gerontology. In 1993, Dr. Masoro received the Distinguished Service Award from the Association of Chairmen of Departments of Physiology. He received the 1995 Irving Wright Award of Distinction of the American Federation for Aging Research and the 1995 Glenn Foundation Award. He served as the President of the Gerontological Society of America from 1994-1995, as the Chairman of the Aging Review Committee of the National Institute on Aging (NIA), and as Chairman of the Board of Scientific Counselors of the NIA. Dr. Masoro received his Ph.D. from the University of California at Berkeley. He has held faculty positions at Queens University (Canada), Tufts University School of Medicine, University of Washington,and Medical College of Pennsylvania. From 1973 through May 1991, he served as Chairman of the Department of Physiology at the University of Texas Health Science Center at San Antonio. He presently continues his duties as Professor in the Department of Physiology and is the Director of the newly created Aging Research and Education Center. On April 1, 1996, he became Professor Emeritus. Dr. Masoro was a Wellcome Visiting Professor in Basic Medical Sciences for the 1992-1993 Academic Year. His research has been in lipid metabolism, cold exposure, membrane biochemistry, and biological gerontology. Since 1975, Dr. Masoros research has focused on the influence of food restriction on aging. He has or is serving in an editorial role for ten journals, and in January 1992, he became the Editor of the Journal of Gerontology: Biological Sciences.

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Read an Excerpt

Handbook of the Biology of Aging


Academic Press

Copyright © 2011 Elsevier Inc.
All right reserved.

ISBN: 978-0-12-378639-5


Chapter One

The Genetic Network of Life-Span Extension by Dietary Restriction

Eric Greer, Anne Brunet Department of Genetics and Cancer Biology Program, Stanford University, Stanford, California, USA

CHAPTER CONTENTS

Introduction 3 The DR Network in C. elegans 4 DR Regimens in C. elegans 4 DR Pathways in C. elegans 5 Criteria 5 Energy Sensors: Insulin–PI3K, SIR2, AMPK, TOR 9 Transcriptional Regulators: FoxO/daf-16, FoxA/pha-4, NFE2/skn-1, HIF-1, HSF-1,CBP-1 10 Other Genes Important for DR: Mitochondrial Genes, Autophagy Genes 12 DR Nodes Conserved in Other Species 12 Yeast DR: SIR2 and TOR 12 Fly DR: SIR2, TOR, and FoxO 12 DR in Mammals: SIR2, TOR, Insulin–FoxO, NFE2 13 Why are there Differences between DR Regimens? 14 Type of Nutrients 14 Temporal Effects 15 Tissue Specificity 15 Non-DR Parameters 16 DR Mimetics 16

Conclusions 17

References 17

Introduction

Restriction of nutrients without malnutrition extends life span in a wide range of species (Masoro, 2005). Dietary restriction (DR) does not solely extend life span, it also prolongs the youthful and disease-free period of life by delaying the onset of a number of age-related pathologies, including cancer and neuro-degenerative diseases (Maswood et al., 2004; Michels & Ekbom, 2004; Wang et al., 2005). While the effects of DR on longevity and disease prevention have been known for almost a century (Rous, 1914; McCay et al., 1935), the genetic mechanisms by which DR extends life span are just beginning to be deciphered (Mair & Dillin, 2008).

Given the diversity of food regimens in different species, it is not surprising that the DR regimens used in the laboratory vary significantly between species. More surprisingly, there exist radically different methods of implementing DR within the same species (Table 1.1) (Dilova et al., 2007; Greer et al., 2007; Piper & Partridge, 2007; Mair & Dillin, 2008). Whether different methods of DR always alter total caloric content is not entirely clear in invertebrates. Thus, caloric restriction may be one of several ways by which dietary manipulations extend life span. The existence of various DR paradigms raises the important question of whether different DR regimens evoke a single universal "DR pathway" or whether they elicit independent pathways that act in a "DR network," with different hubs of the network synergizing with one another. In this chapter, we focus on the genetic pathways that mediate longevity induced by various DR regimens in Caenorhabditis elegans and provide evidence that these pathways are relatively independent, but interact to form a DR network. We also highlight the most conserved nodes of the DR network throughout species. Finally, we provide possible explanations as to why distinct DR regimens trigger different genetic pathways to promote longevity and discuss how these different pathways might be harnessed to mimic DR.

THE DR NETWORK IN C. ELEGANS

Dr Regimens in C. Elegans

C. elegans normally live in the soil and feed on bacteria, for example, those present on rotten fruits. In the laboratory, worms are traditionally grown on a thin film of Escherichia coli bacteria spread on solid agar plates. Twelve DR regimens have been developed in C. elegans, and they all extend life span, albeit to different degrees (Table 1.1).

One of the most commonly used methods to mimic DR is a genetic mutation (eat-2) that reduces the pharyngeal pumping rate of the worms, thereby leading to reduced nutrient consumption (Avery, 1993; Lakowski & Hekimi, 1998) (Table 1.1). In addition to this genetic way of inducing DR, there are four DR methods in which the source of nutrient is altered in liquid media (Table 1.1). While liquid cultures are not the typical conditions for growing worms, they allow an easier manipulation of the nutrients. The most frequently used liquid method of DR, devised by Klass in 1977, consists in simply diluting E. coli bacteria in liquid cultures and has been termed bacterial DR (BDR) (Klass, 1977; Houthoofd et al., 2003; Panowski et al., 2007). Importantly, the worms do not compensate for the dilution in bacteria by eating more in this DR regimen (Mair et al., 2009). This BDR method has been further refined to include both a solid support and a liquid dilution of bacteria, and we will term this DR regimen LDR, for liquid DR, in this review (Bishop & Guarente, 2007). DR-like phenotypes can also be induced by two chemically defined liquid media: the axenic medium and the chemically defined liquid medium (CDLM) (Vanfleteren & Braeckman, 1999; Houthoofd et al., 2002; Szewczyk et al., 2006).

Seven methods of DR have been implemented on solid agarose-containing plates—the more traditional way of growing C. elegans in the laboratory (Table 1.1). In an initial method devised in the 1980s, the reduction of bacteria is obtained by the dilution of peptone in the agarose (Hosono et al., 1989). However, peptone dilution leads to an increase in worm fertility, which contrasts with the conserved ability of DR to decrease reproduction, raising the possibility that peptone dilution is not a bona fide DR regimen. Later, another method of DR on agarose plates, termed solid DR (sDR), was developed (Greer et al., 2007). In this method, worms are exposed to serial dilutions of feeding bacteria on agarose plates at day 4 of adulthood, which corresponds to the very end of the reproductive period in the worms (Greer et al., 2007; Greer & Brunet, 2009; Park et al., 2009a). sDR does not cause the worms to eat more to compensate for the lack of food (Greer et al., 2007). N ote that sDR is provided in the absence of 5-fluoro-2'-deoxyuridine (FUdR), a drug often used in worm life-span assays to facilitate adult worm counting by inhibiting progeny production. Three variants of sDR have been implemented. In the first of these, termed modified sDR (msDR), bacteria are also serially diluted on plates, but restriction is initiated at day 1 of adulthood and FUdR is used to inhibit progeny production (Chen et al., 2009). In the second variation of sDR, which we will term sDR(H) in this review, restriction is initiated at day 2 of adulthood, and FUdR is also used (Honjoh et al., 2009). In the third variation of sDR, which we will term sDR(C) in this review, restriction is initiated at day 5 of adulthood and FUdR is also used (Carrano et al., 2009). Importantly, the total absence of bacteria on plates (bacterial deprivation, BD, or dietary deprivation, DD) in the presence of FUdR also extends life span (T. L. Kaeberlein et al., 2006; Lee et al., 2006). BD/DD has also been shown to extend the life span of wild-derived C. elegans strains, as well as C. remanei strains (Sutphin & Kaeberlein, 2008). Finally, the most recently devised method to induce DR in worms involves feeding worms only once every 2 days in the presence of FUdR and has been termed intermittent fasting (IF) (Honjoh et al., 2009).

It is important to note that in all DR methods—with the exception of sDR—worms are treated with FUdR, a compound that inhibits DNA synthesis and can even extend life span in some cases (Mitchell et al., 1979). FUdR is used because it makes counting worms easier by inhibiting the production of new progeny. However, progeny production is an energy-costly biological process that can be linked with life span, so altering this process by adding FUdR may affect the response of somatic cells to DR. O n the other hand, FUdR could also help reveal a longevity phenotype in specific cases (Shaw et al., 2007), because FUdR limits matricide (the hatching of worms inside the mother), which is a confounding factor for worm life span (Mitchell et al., 1979). In addition FUdR slows the growth of bacteria on the agar plates (Bertani & Levy, 1964) and may thereby alter the food concentration for worms. Thus, there is a complex interaction between FUdR, life span, and bacteria, which should be taken into account when results are compared across various methods of DR.

DR Pathways in C. elegans

Studies using a variety of DR regimens in C. elegans have uncovered a growing number of genes that mediate the beneficial effects of DR on life span (Table 1.2, Figure 1.1). These DR genes encode proteins that act as energy sensors, transcriptional regulators, mitochondrial components, and autophagy proteins. We will discuss each of these in turn using a series of defined criteria.

Criteria

In presenting results from many different groups, it is important to consider the terminology. In this review, we will write that a DR method is dependent (D in Table 1.2) on gene X or that gene X is necessary for longevity induced by a DR method when the ablation of gene X completely blocks the effects of dietary restriction on life span. We will write that a DR method is partially dependent (PD in Table 1.2) on gene X or that gene X is partially necessary for longevity induced by a DR method to indicate that inhibition or ablation of the gene partially, but significantly, blocks the protective effects of dietary restriction. Note that some groups have termed this second category "not dependent" (or "not entirely dependent") on gene X (Mair & Dillin, 2008). Finally, we will write that a method is independent (I in Table 1.2) of gene X or that gene X is not necessary for longevity induced by a DR method when the inhibition or ablation of the gene has no significant effect on the protective effects of dietary restriction.

Second, it is important to highlight that a gene could be necessary for DR but not mediate DR. A n example would be a gene that is important for the general health of the organism such that when the gene is abolished, DR can no longer exert its beneficial effect on life span. Thus, we will use the term mediate whenever a gene fits a series of criteria: (1) there is evidence that the gene or the gene product is regulated by DR itself; (2) the gene is at least partially necessary for the extension of life span (i.e., there is a significant difference in the way mutations in the gene affect life span under ad libitum conditions versus DR conditions in the same experiment); and (3) the ablation/inhibition of the gene specifically affects longevity in response to DR, but not in response to other longevity extension pathways.

Third, it is crucial to note that establishing the requirement of a gene in longevity by DR is difficult outside of the clear-cut case of a genetic null mutant (Gems et al., 2002). Hypomorph mutants, RNAi knockdown, or ectopic expression of a gene may all lead to faulty interpretations. The case of RNAi knockdown is further confounded by the fact that RNAi does not knock down genes uniformly in all cells in the worms—for example, neurons are quite resistant to the effect of RNAi in worms (Timmons et al., 2001). If DR still further extends the life span of a hypomorph mutant, or in the case of RNAi knockdown or of overexpression of gene X , which would normally suggest that this gene is not required for DR, this gene could in fact still be necessary for DR if it were completely abolished or overexpressed to the maximal amount. We indicate, in the text and in the figures, when hypomorph mutants, RNAi, or overexpressors have been used to draw conclusions on the implications of specific genes in the DR response.

Finally, examining the implication of a gene in DR using only two conditions (ad libitum and DR) may be misleading, as mutating a gene may only displace the optimum concentration at which DR is reached (Clancy et al., 2002; Mair et al., 2009). Methods that involve dilution of bacteria, such as BDR and sDR, allow the study of a gene mutation over a graded dilution of bacteria. To examine the specificity of the interaction between a gene and DR, it is also important to test if the effects of a specific knockdown or genetic mutation on longevity under DR conditions versus ad libitum conditions are statistically different (Gems et al., 2002). The interaction between food concentration and genotype can be assessed statistically by using proportional hazards regression tests (Tatar, 2007).

Energy Sensors: Insulin-PI3K, SIR2, AMPK, TOR

Insulin levels are potently regulated by nutrients, raising the possibility that the insulin signaling pathway—a well-known regulator of aging (Kenyon, 2005)—may play a role in mediating DR. While insulin levels are indeed decreased by DR in mammals (Ramsey et al., 2000), it is not clear whether insulin-like peptides or the activity of the insulin signaling pathway is decreased by DR in C. elegans. FoxO/daf-16 nuclear translocation, which is a consequence of the inactivation of the insulin signaling pathway, does not appear to be affected by many DR methods (Henderson & Johnson, 2001; Houthoofd et al., 2003; Greer et al., 2007), although starvation and IF both trigger FoxO/daf-16 nuclear translocation (Henderson & Johnson, 2001; Honjoh et al., 2009). Mutants of the insulin receptor daf-2 or of age-1, which encodes the C. elegans ortholog of the catalytic subunit of PI3K, still display an extension of life span in response to BDR that is equivalent to that of the wild type (WT) (Johnson et al., 1990; Houthoofd et al., 2003). S uch a result suggests that daf-2 and age-1 are not necessary for BDR to extend life span. Similarly, daf-2 mutants still display extension of life span to the same extent as WT in response to sDR (Greer et al., 2007), eat-2 (Lakowski & Hekimi, 1998), and BD/DD (T. L. Kaeberlein et al., 2006; Lee et al., 2006). A xenic medium and a modified form of BDR, termed LDR in this review, also extend the life span of daf-2 worms significantly more than that of WT worms (Houthoofd et al., 2003; Bishop & Guarente, 2007). Consistent with a limited involvement of the insulin signaling pathway in life-span extension by DR, the life span of FoxO/daf-16 null mutant worms is still increased by many methods of DR (Lakowski & Hekimi, 1998; Houthoofd et al., 2003; T. L. Kaeberlein et al., 2006; Lee et al., 2006; Bishop & Guarente, 2007; Chen et al., 2009; Zhang et al., 2009). However, interestingly, FoxO mutants no longer show life-span extension in response to sDR (Greer et al., 2007; Greer & Brunet, 2009) and have a decreased ability to show life-span extension in response to BDR (Houthoofd et al., 2003; Panowski et al., 2007; Greer & Brunet, 2009). In addition, because the daf-2 and the age-1 mutants are hypomorph mutants, it is possible that the DR and insulin pathways interact more than was initially thought. Intriguingly, the life span of one allele of daf-2, daf-2(e1368), was not at all extended by an alternate eat-2 mutation, suggesting that life-span extension due to eat-2 may also involve the insulin pathway under some conditions (Iser & Wolkow, 2007). In addition, the life span of daf-2 mutants is only mildly increased by IF (10.2% life-span extension) compared to the dramatic effect IF has on WT worms (56.6% life-span extension) (Honjoh et al., 2009). Taken together, these data indicate that the insulin pathway probably plays some role in the response to DR, even though this pathway does not seem to be the major mediator of longevity by DR.

SIR-2.1 is a NA D-dependent protein deacetylase of the S irtuin family and has been proposed to sense the metabolic state of a cell, in part via changes in the NA D:NADH ratio (Guarente, 2005). Whether SIR2 activity or levels are affected by DR methods in worms has never been tested. The sir-2.1 gene was found to be necessary for longevity triggered by the eat-2 mutation, a genetic mimic of DR (Wang & Tissenbaum, 2006). However, the role of SIR-2.1 in DR-induced longevity is still controversial, as another study has shown that the sir-2.1 gene is not necessary for longevity induced by eat-2 (Hansen et al., 2007). The basis for this discrepancy is not known, but may be due to the fact that ad libitum conditions might already activate the endogenous SIR-2.1 protein under some circumstances, thereby masking the effect of SIR-2.1 in longevity induced by the eat-2 mutation. Notwithstanding these differences, the involvement of SIR-2.1 in DR-induced longevity in worms is relatively limited, in that SIR-2.1 is not necessary for longevity induced by sDR, DD, BDR, and IF (T. L. Kaeberlein et al., 2006; Lee et al., 2006; Greer & Brunet, 2009; Honjoh et al., 2009; Mair et al., 2009). Thus, while SIR-2.1 may be a node of the DR network in worms, it is not a major mediator of DR-induced longevity in this organism. It is possible that the other SIR2 family members in worms may play a role in DR-induced longevity. A double mutant of sir-2.1 and sir-2.3 responded to BDR similar to wild-type worms (Mair et al., 2009), but sir-2.2 and sir-2.4 have not been tested yet for their role in life-span extension by DR.

(Continues...)



Excerpted from Handbook of the Biology of Aging Copyright © 2011 by Elsevier Inc.. Excerpted by permission of Academic Press. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

1 Reliability theory of aging and longevity 3
2 Are age-associated diseases an integral part of aging? 43
3 Dietary restriction, hormesis, and small molecule mimetics 63
4 Hematopoietic stem cells, aging, and cancer 105
5 Mitochondria : a critical role in aging 124
6 P53 and mouse aging models 149
7 Complex genetic architecture of Drosophila longevity 181
8 Evolutionary biology of aging : future directions 217
9 Senescence in wild populations of mammals and birds 243
10 Biodemography of aging and age-specific mortality in Drosophila melanogaster 267
11 Microarray analysis of gene expression changes in aging 295
12 Computer modeling in the study of aging 334
13 Dissecting the processes of aging using the nematode Caenorhabditis elegans 360
14 Genetic manipulation of life span in Drosophila Melanogaster 400
15 Juvenile and steroid hormones in Drosophila melanogaster longevity 415
16 A critical evaluation of nonmammalian models for aging research 449
17 Differential aging among skeletal muscles 470
18 Aging, body fat, and carbohydrate metabolism 498
19 Growth and aging : why do big dogs die young? 512
20 Growth hormone, insulin-like growth factor-1, and the biology of aging 534
21 Aging of the female reproductive system 570
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