Table of contents

  1. Front Matter
  2. Thomas Nyström
    Pages 1-16
  3. S. Michal Jazwinski
    Pages 39-59
  4. Michael Breitenbach, Frank Madeo, Peter Laun, Gino Heeren, Stefanie Jarolim, Kai-Uwe Fröhlich et al.
    Pages 61-97
  5. Bart P. Braeckman, Koen Houthoofd, Jacques R. Vanfleteren
    Pages 99-144
  6. Howard Thomas
    Pages 145-171
  7. Vladimir P. Skulachev
    Pages 191-238
  8. Wen-Hsing Cheng, Patricia L. Opresko, Cayetano von Kobbe, Jeanine A. Harrigan, and Vilhelm A. Bohr
    Pages 239-268
  9. Olivier Toussaint, Michel Salmon, Véronique Royer, Jean-François Dierick, Joao Pedro de Magalhaes, Frédéric Wenders et al.
    Pages 269-294
  10. Back Matter

About this book


Aging is the progressive decline in biological functions over time. This decline targets macromolecules, cells, tissues and, as a consequence, whole organisms. Despite considerable progress in the development of testable hypothesis concerning aging in an evolutionary context, a unifying theory of the molecular/physiological mechanistic causes of aging has not been reached. In fact, is it not clear to what extent aging is a programmed or stochastic process.

This book takes the reader from unicellular bacterial deterioration via senescence in yeast and worms to aging in rodents and humans, allowing a comparative view on similarities and differences in different genetic model systems. The different model systems are scrutinized in the light of contemporary aging hypothesis, such as the free radical and genomic instability theories.


aging free radicals genetic model systems stress apoptosis bacteria biological functions development fungi macromolecules metabolism mitochondria prokaryotes tissue

Bibliographic information

  • DOI
  • Copyright Information Springer-Verlag Berlin Heidelberg 2004
  • Publisher Name Springer, Berlin, Heidelberg
  • eBook Packages Springer Book Archive
  • Print ISBN 978-3-540-02490-3
  • Online ISBN 978-3-540-37005-5
  • Series Print ISSN 1610-2096
  • Series Online ISSN 1610-6970
  • Buy this book on publisher's site