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Anti-aging drug discovery on the basis of hallmarks of aging /
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | , , |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
London, United Kingdom ; San Diego, CA :
Academic Press,
[2022]
|
| Temas: | |
| Acceso en línea: | Texto completo |
Tabla de Contenidos:
- 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.