Model Systems in Aging

ISBN-13: 9783642056987 / Angielski / Miękka / 2010 / 301 str.

Thomas Nystrom; Heinz D. Osiewacz

Opis

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 fungi 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.

Spis treści

Conditional Senescence in Prokaryotes.- Aging and Mitochondrial Dysfunction in the Filamentous Fungus Podospora anserina.- Caulobacter: Model for Prokaryotic Replicative Senescence and Trade-off Theories of Aging.- Mitochondria, Metabolism and Aging: the Retrograde Response and Calorie Restriction.- Mitochondrial ROS production and Apoptosis-like Processes in Yeast.- Energy Metabolism, Anti-oxidant Defense and Aging in Caenorhabditis elegans.- Do Green Plants Age and, if so, How? Mammalian Aging, Oxygen Radicals and Restricted Feeding.- Aging and the Programmed Death Phenomena.- The Human Werner Syndrome as a Model for Aging.- Towards a Role of Subcytotoxic Stress in Tissue Ageing.-

Blurb

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.