Kooperativer Bibliotheksverbund

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Umfang: 1 online resource (411 pages)

ISBN: 0-323-90236-7

Inhalt: Anti-Aging Drug Discovery on the Basis of Hallmarks of Aging is a comprehensive and timely book on all aspects of anti-aging strategies. The book provides comprehensive, foundational knowledge on the mechanisms of aging and current anti-aging strategies and approaches developed. Aging research has experienced an unprecedented advance over recent years with the discovery that the rate of aging is determined, at least to some extent, mainly by our genetics and modulated by environmental factors. The hallmarks of aging describe the molecular and cellular processes that govern biological aging and their variation in individuals.

Anmerkung: Front Cover -- Anti-aging Drug Discovery on the Basis of Hallmarks of Aging -- Copyright Page -- Contents -- List of contributors -- Preface -- 1 The aging: introduction, theories, principles, and future prospective -- 1.1 Introduction -- 1.2 Modern theories of aging in biology -- 1.2.1 Three subcategories exist in programmed theory -- 1.2.1.1 Programmed longevity -- 1.2.1.2 Endocrine theory -- 1.2.1.3 Immunological theory -- 1.2.2 The error or damage theory has the following subcategories -- 1.2.2.1 Wear and tear theory -- 1.2.2.2 Rate of living theory -- 1.2.2.3 Cross-linking theory -- 1.2.2.4 Free radical theory -- 1.2.2.5 Somatic DNA damage theory -- 1.3 Principles -- 1.4 Extrinsic and intrinsic factors on aging -- 1.4.1 Circles and systems of social support on aging -- 1.4.2 Smoking on aging -- 1.4.3 Leisure activities on aging -- 1.4.4 Diet on aging -- 1.4.5 Physical health effects of exercise on aging -- 1.4.6 Cognitive health effects of exercise on aging -- 1.4.7 Aging intervention and future stem cell research -- 1.5 Future perspective (aging therapies) -- 1.5.1 Caloric restriction -- 1.5.2 Stem cell therapies -- 1.5.3 Hormonal therapies -- 1.5.4 Telomere-based therapies -- 1.5.5 Therapies to come -- 1.6 Summary -- References -- 2 Impact of aging at cellular and organ level -- 2.1 Introduction -- 2.2 Multicellular organization: human body -- 2.3 Changes associated with aging -- 2.4 Aging in cells -- 2.5 Aging in tissue and organs -- 2.6 Models to study aging -- 2.7 Antiaging therapy/treatment -- 2.8 Conclusion -- Competing interests -- Declaration of interest -- Financial support -- Authors' contributions -- References -- 3 Brief about hallmarks of aging -- 3.1 The nine hallmarks of aging -- 3.1.1 Stem cell exhaustion -- 3.1.1.1 DNA damage on stem cell survival -- 3.1.2 Genomic instability. , 3.1.2.1 Genetic deterioration and somatic mutations -- 3.1.3 Telomere attrition -- 3.1.3.1 Structure and function of telomeres -- 3.1.3.2 Telomere aging and cellular senescence -- 3.1.4 Epigenetic alterations -- 3.1.4.1 DNA methylation -- 3.1.4.2 Histone modifications -- 3.1.5 Deregulated nutrient sensing -- 3.1.5.1 Lipid sensing -- 3.1.5.2 Amino acid sensing -- 3.1.5.3 Glucose sensing -- 3.1.6 Altered intercellular communication -- 3.1.6.1 Inflammaging -- 3.1.7 Loss of proteostasis -- 3.1.7.1 Molecular chaperones -- 3.1.7.2 Proteolytic systems -- 3.1.7.3 Autophagy -- 3.1.8 Cellular senescence -- 3.1.8.1 Triggers of senescence -- 3.1.8.2 Senolytics -- 3.1.9 Mitochondrial dysfunction -- 3.1.9.1 Mitochondrial DNA -- 3.1.9.2 Mitohormesis -- 3.2 Conclusions -- References -- 4 Overview of various antiaging strategies -- 4.1 Introduction -- 4.2 Modulation of autophagy for successful aging -- 4.3 Elimination of senescent cells for successful aging -- 4.4 Plasma transfusion for successful aging -- 4.5 Intermittent fasting as a means for successful aging -- 4.6 Regular exercise for successful aging -- 4.7 Role of antioxidants for successful aging -- 4.8 Stem cell therapy for successful aging -- 4.9 Summary -- References -- 5 Elimination of damaged cells-dependent antiaging strategy -- 5.1 Introduction -- 5.2 Aging-associated disease and physiological changes -- 5.2.1 Changes in nervous system -- 5.2.1.1 Cognition -- 5.2.1.2 Memory, learning, and intelligence -- 5.2.2 Special senses -- 5.2.2.1 Vision -- 5.2.2.2 Hearing -- 5.2.2.3 Taste acuity -- 5.2.2.4 Smell -- 5.2.2.5 Touch -- 5.2.3 Changes in musculoskeletal system -- 5.3 Antiaging strategies -- 5.3.1 Senescent cell elimination as an antiaging therapy -- 5.3.2 Transfusion of plasma from young individuals to promote successful aging -- 5.3.3 Intermittent fasting as a means to combat aging. , 5.3.4 Promise of neurogenesis enhancement for successful aging and preventing AD -- 5.3.5 Physical exercise for modulating aging and preventing dementia -- 5.3.6 Promising antioxidants and herbals for promoting successful aging -- 5.3.7 Stem-cell therapy for promoting healthy brain aging and reversing AD -- 5.4 Hallmarks of aging -- 5.4.1 Genomic instability -- 5.4.2 Telomere attrition -- 5.4.3 Epigenetic alterations -- 5.4.4 Loss of proteostasis -- 5.4.5 Deregulated nutrient-sensing -- 5.4.6 Mitochondrial dysfunction -- 5.4.6.1 Reactive oxygen species -- 5.4.6.2 Mitochondrial integrity and biogenesis -- 5.4.6.3 Mitohormesis -- 5.4.7 Cellular senescence -- 5.4.8 Stem-cell exhaustion -- 5.4.9 Altered intercellular communication -- 5.4.9.1 Inflammation -- 5.5 Cellular reprogramming -- 5.6 Models of premature aging based on cellular reprogramming -- 5.6.1 Progeroid syndromes -- 5.7 Cellular rejuvenation by partial reprogramming -- 5.8 Implications for regenerative medicine: successes and limitations of in vivo reprogramming -- 5.9 Conclusion -- Acknowledgments -- References -- 6 Telomerase reactivation for anti-aging -- 6.1 Introduction -- 6.2 Aging -- 6.3 Aging-a telomere-mitochondria relation -- 6.4 Telomerase and its possible role in antiaging therapies -- 6.5 Tapping the potential of telomerase -- 6.6 Stem cells and aging -- 6.7 Future aspects in antiaging -- Acknowledgments -- Competing interests -- Funding -- Authors' contribution -- References -- 7 Epigenetic drugs based on antiaging approach: an overview -- 7.1 Introduction -- 7.2 The first wave of epigenetic drugs -- 7.2.1 DNA methyltransferase inhibitors -- 7.2.2 Histone deacetylase inhibitors -- 7.3 The second wave of epigenetic drugs -- 7.3.1 DNA methyltransferase inhibitors -- 7.3.2 Histone deacetylase inhibitors -- 7.4 The third wave of epigenetic drugs. , 7.4.1 Histone methyltransferase inhibitors -- 7.4.2 Histone demethylase inhibitors -- 7.4.3 Bromodomains -- 7.5 The fourth wave of epigenetic drugs -- 7.5.1 Revolution in biomedical sciences -- 7.5.2 Target selection -- 7.5.3 Enzyme isoform selectivity and drug designing -- 7.6 Conclusion -- References -- 8 Exploring the role of protein quality control in aging and age-associated neurodegenerative diseases -- 8.1 Proteins misfolding in aging and diseases -- 8.2 Protein quality control -- 8.2.1 Components of the protein quality control -- 8.2.1.1 Molecular chaperones -- 8.2.1.2 Ubiquitin-proteasome system -- 8.2.1.3 Autophagy-lysosomal pathway -- 8.3 Altered protein quality control in aging and diseases: lessons learned from in vitro and in vivo models -- 8.3.1 Aging -- 8.3.2 Alzheimer's disease -- 8.3.3 Parkinson's disease -- 8.3.4 Amyotrophic lateral sclerosis -- 8.3.5 Polyglutamine diseases -- 8.4 Therapeutic perspectives -- 8.4.1 Small molecules -- 8.4.2 Natural products serve as modifiers of an altered protein quality control system -- 8.4.2.1 Natural products as chaperone modifiers -- 8.4.2.2 Natural products targeting the UPS -- 8.4.2.3 Natural products targeting the autophagy-lysosomal pathway -- 8.5 Emerging techniques -- 8.6 Conclusion -- Acknowledgments -- Conflict of interest -- Author's contributions -- References -- 9 Dietary restriction and mTOR and IIS inhibition: the potential to antiaging drug approach -- 9.1 Introduction -- 9.2 The antiaging drug discovery -- 9.2.1 The nutrient-signaling mechanism of the antiaging process -- 9.2.1.1 Dietary restriction -- 9.2.2 The insulin/insulin-like growth factor signaling (IIS) pathway -- 9.3 The mechanism of pharmacological strategies in antiaging process -- 9.3.1 The mechanistic target of rapamycin -- 9.4 Conclusion -- References. , 10 Antiaging drugs, candidates, and food supplements: the journey so far -- 10.1 Introduction -- 10.1.1 Some of the factors that contribute to aging process but not limited to this -- 10.2 Antiaging drugs -- 10.2.1 FDA approved -- 10.2.1.1 Metformin -- 10.2.1.2 Rapamycin -- 10.2.1.3 L. Carnosine -- 10.2.1.4 Isotretinoin -- 10.2.1.5 Cycloastragenol -- 10.2.1.6 Urolithin-A -- 10.2.1.7 Quercetin caprylate -- 10.2.1.8 Acarbose -- 10.2.1.9 Crocin -- 10.2.1.10 Hyaluronic acid -- 10.2.2 Food supplements -- 10.2.3 Astaxanthin -- 10.2.4 Vitamin C/L-ascorbic acid -- 10.2.5 Vitamin E-concoction of tocopherols and tocotrienols -- 10.2.6 Vitamin A -- 10.2.7 Poly-phenols -- 10.2.8 Flavonoids -- 10.2.9 Resveratrol (Stilbenes) -- 10.2.10 Curcumin -- 10.2.11 Pathways targeted and their cross talks -- 10.3 Aging-molecular and biochemical significance -- 10.4 Summary -- References -- 11 Role of AMP-activated protein kinase and sirtuins as antiaging proteins -- 11.1 Introduction -- 11.2 AMP-activated protein kinase and its functions -- 11.3 Sirtuins: role of SIRT1 -- 11.4 Correlation between AMP-activated protein kinase and sirtuins -- 11.5 Effect of AMP-activated protein kinase and sirtuins on calorie restriction and longevity -- 11.6 Role of AMP-activated protein kinase and sirtuins in mitochondrial homeostasis -- 11.6.1 AMP-activated protein kinase in mitochondrial biogenesis -- 11.6.2 AMP-activated protein kinase in mitochondrial fission and mitophagy -- 11.6.3 Sirtuins in mitochondrial biogenesis -- 11.6.4 Sirtuins in mitophagy -- 11.7 AMP-activated protein kinase and sirtuins in age-associated neurodegenerative diseases -- 11.7.1 Alzheimer's disease -- 11.7.2 Parkinson's disease -- 11.7.3 Huntington's disease -- 11.7.4 Amyotrophic lateral sclerosis -- 11.8 Modulation of AMP-activated protein kinase and sirtuins. , 11.8.1 AMP-activated protein kinase activating compounds.

Weitere Ausg.: Print version: Singh, Sandeep Kumar Anti-Aging Drug Discovery on the Basis of Hallmarks of Aging San Diego : Elsevier Science & Technology,c2022 ISBN 9780323902359

Sprache: Englisch