This volume provides a timely and thorough review of the current state of understanding of a fascinating type of cell that is capable of forming many or all cells in the body. In humans and other mammals embryonic stem cells, the immediate offspring of the fertilized egg, are capable of forming any type of cell in the body. Moreover stem cells are present in many different tissues in adults that are capable of dividing and differentiating into the specific cell types that comprise the organ in which they reside.

A major focus of the book is to provide the reader with up-to-date information on the molecular mechanisms that regulate the proliferation, differentiation and survival of stem cells, and how aging and age-related disease impacts on stem cells. Leading authorities detail the properties and therapeutic potential of embryonic stem cells and stem cells of the nervous and immune systems, muscle and bone. Particularly exciting are emerging technologies for using stem cells to treat human age-related diseases including cardiovascular disease, diabetes, neurodegenerative disorders such as Parkinson's and Alzheimer's diseases.

This book will be a valuable reference for developmental biologists and for scientists and clinicians who study and treat a variety of diseases.

Experts in the fields of energy metabolism, aging and oxidative stress provide an integrated view of how mechanisms involved in regulating energy metabolism are linked to fundamental processes of aging including cellular stress resistance and free radical production.

During evolution signal transduction pathways and organ systems have been optimised for the efficient seeking, ingestion, storing and using of energy. These signalling pathways play prominent roles in lifespan determination with insulin and related signalling pathways being prime examples. The authors consider how lifespan and healthspan can be extended through knowledge of energy metabolism with the experimental model of dietary restriction being one example. The information in this volume of ACAG will foster novel approaches and experiments for further understanding the roles of energy metabolism in aging and disease.

The lipids of cellular membranes not only serve roles in controlling the structure and fluidity of the membrane, but are increasingly recognized for their roles as signalling molecules and modifiers of membrane protein function. Recent studies described in this volume reveal striking changes in membrane lipids during aging and in age-related diseases such as cancer, cardiovascular disease and neurodegenerative disorders. Lipids including inositol phospholipids, cholesterol, sphingolipids and ceramides play important roles in signalling cellular responses to stress and specific stimuli such as growth factors, cytokines and neurotransmitters. One or more of these lipid mediators has been linked to the pathogenesis of age-related diseases.

This book provides a comprehensive review of specific membrane lipid mediators and their roles in aging and age-related disease.

This volume of "Advances in Cell Aging and Gerontology" critically reviews the rapidly advancing area of telomerase research with a focus at the molecular and cellular levels. The clearly established function of telomerase is to maintain chromosome ends during successive rounds of cell division by adding a six base DNA repeat on to the telomeric ends of chromosomes. As presented in the chapters of this volume, the mechanisms that regulate telomerase expression and activity are complex. Moreover, emerging data suggest additional roles for telomerase in the regulation of cell differentiation and survival.

It is expected that this quite comprehensive volume will provide a valuable resource for graduate students and postdocs in the telomerase field and for established investigators in other fields who are beginning to study telomerase in their particular research program. With an increasing number of proteins being brought into the fold of telomerase research (e.g., DNA damage and repair response proteins, heat-shock proteins, and proteins in various signal transduction cascades) many new scientists are beginning to study this enzyme from novel vantage points.

Apoptosis, or programmed cell death, is an adaptive form of cell death that plays a critical role in turnover of mitotic cells and various tissues in the adult, including epithelial cells, fibroblasts and various endocrine cells. Programmed cell death also plays a major role in development in organizing the body plan and molding intricate cellular structures such as nerve cell circuits in the brain. Rapidly progressing research into the molecular and biochemical underpinnings of the programmed cell death process are revealing novel genetic programs and molecular interactions that coordinate a process that results in death and removal of cells without an immune response and in the absence of the adverse effects on neighboring cells.

"Programmed Cell Death, Volume I," critically details the molecular, biochemical and cellular mechanisms of apoptosis. This volume covers programmed cell death in a variety of tissues and organ systems highlighting the interesting families of proteins involved in promoting or preventing apoptosis. These include the caspase and calpain families of proteases, Bcl-2 family members, and inhibitors of apoptosis proteins. Each chapter is written by an internationally recognized expert in a particular aspect of programmed cell death.

This book will provide the reader with a comprehensive understanding of the cascade of events leading from an apoptotic signal, such as trophic factor withdrawal or increased oxidative stress, to cell death. Importantly, this volume also covers signaling mechanisms designed to prevent apoptosis. Such anti-apoptotic signaling cascades involve neurotrophic factors and stress response pathways. "Programmed Cell Death, Volume I," provides the molecular and cellular foundation for http: //www.elsevier.com/locate/isbn/0444507302Programmed Cell Death, Volume II in which the roles of aberrant regulation of apoptosis in human diseases ranging from cancer to Alzheimer's disease are considered.

Collectively, the chapters in this work will provide the reader with novel insight into the inter-relationships of the function of different organelles in the sequences of events that lead to cellular dysfunction and degeneration in the aging human population. The chapters are rich in information for cell and molecular biologists pursuing studies of the different diseases covered. In addition, the clinician will find value in understanding mechanisms underlying age-related disease as such an understanding will lead to novel therapeutic approaches for an array of age-related diseases.

" Genetic Aberrancies and Neurodegenerative Disorders" presents critical reviews and emerging findings concerning the roles of genetic mutations and polymorphisms in the pathogenesis of a range of neurological disorders including Alzheimer's and Parkinson's diseases, trinucleotide repeat disorders, stroke, epilepsy and others. This volume, written by leading experts, brings together fundamental information concerning the roles of inherited traits in the pathogenesis of different neurodegenerative disorders. In addition to providing a catalogue of the known genetic alterations that are linked to specific neurodegenerative disorders, the chapters detail the current state of understanding of the cellular and biochemical mechanisms whereby the genetic aberrancies lead to neuronal dysfunction and degeneration. The emerging picture of each disorder, painted by pathological, biochemical and molecular brushes, suggests that they share key mechanisms including increased levels of oxidative stress, perturbed ion homeostasis, mitochondrial dysfunction and apoptotic proteolytic cascades. The existence of specific molecular defects provides the opportunity to design experiments that can establish the precise pathogenic mechanism of a specific mutation or genetic risk factor. The value of this approach is exemplified by recent studies of how mutations in Cu/Zn-superoxide dismutase cause amyotrophic lateral sclerosis and how presenilin mutations result in early-onset Alzheimer's disease. A theme developed among the different chapters is that events that occur during aging predispose neurons to genetic aberrancies that promote degenerative cascades, and that specific genetic defects exert their influence on particular populations of neurons in a disorder-specific manner. The chapters in this volume will stimulate readers to generate new hypotheses concerning the pathogenic mechanisms of genetic aberrancies that can be experimentally tested.