پیری انسان: از مکانیزمهای سلولی تا استراتژیهای درمانی
Human Aging : From Cellular Mechanisms to Therapeutic Strategies
معرفی کتاب «پیری انسان: از مکانیزمهای سلولی تا استراتژیهای درمانی» (با عنوان لاتین Human Aging : From Cellular Mechanisms to Therapeutic Strategies) نوشتهٔ Calogero Caruso, Giuseppina Candore، منتشرشده توسط نشر Academic Press در سال 2021. این کتاب در فرمت pdf، زبان انگلیسی ارائه شده است.
Human Aging: From Cellular Mechanisms to Therapeutic Strategies offers an exhaustive picture of all the biological aspects of human aging by describing the key mechanisms associated with human aging and covering events that could disrupt the normal course of aging. Each chapter includes a summary of the salient points covered, along with futures prospects. The book provides readers with the information they need to gain or deepen the skills needed to evaluate the mechanisms of aging and age-related diseases and to monitor the effectiveness of therapies aimed at slowing aging. The book encourages PhD and Postdoc students, researchers, health professionals and others interested in the biology of aging to explore the fascinating and challenging questions about why and how we age as well as what can and cannot be done about it. Concentrates on different processes, e.g., oxidative stress, cellular senescence and Inflammaging Offers the ability to access cross-sectional knowledge more easily Written by expert researchers in biogerontology who are actively involved in various fields within aging research Front Cover Human Aging: From Cellular Mechanisms to Therapeutic Strategies Copyright Contents Contributors About the editors Preface Chapter 1: Aging and longevity: An evolutionary approach 1.1. Introduction 1.2. Why does aging occur? 1.3. Mechanisms of aging 1.4. Causality and chance in aging and longevity 1.5. Conclusions and future perspectives References Chapter 2: Demographic aspects of aging 2.1. Introduction 2.2. Understanding the process: Browsing around the demographic transition theories 2.3. Aging inequalities 2.3.1. Differences by gender, education, and cause of death 2.3.2. Does having a longer life also mean having a better life? 2.3.3. Economics of population aging 2.4. Conclusions and perspectives References Chapter 3: Pathobiology of aging: An introduction to age-related diseases 3.1. Introduction 3.2. Complexity 3.3. Hallmarks of aging 3.4. Genomic instability 3.5. Epigenetic alteration 3.6. Deregulated nutrient sensing pathways 3.6.1. FOXO3 3.6.2. Insulin/IGF-1 pathway 3.6.3. mTOR pathway 3.6.4. Sirtuin pathway 3.6.5. Autophagy 3.7. Loss of proteostasis 3.8. Mitochondrial dysfunction 3.9. Telomere attrition 3.10. Cellular senescence 3.11. Stem cell exhaustion 3.12. Altered intercellular communication 3.13. Cancer and aging 3.14. Conclusion and future perspectives References Chapter 4: Cellular senescence and senescence-associated secretory phenotype (SASP) in aging process 4.1. Introduction 4.2. Signaling pathway stimulating the appearance of SASP 4.3. SASP components 4.4. MiRNA and extracellular vesicles as new regulators and components of SASP 4.5. SASP profile in different cell types 4.6. Cellular senescence, SASP, and aging 4.7. Conclusions and future perspectives References Chapter 5: The role of inflammaging in the development of chronic diseases of older people 5.1. Introduction 5.2. Basic mechanisms: Cellular senescence, inflammaging, molecular inflammation, and senoinflammation 5.2.1. Cellular senescence 5.2.2. Inflammaging 5.2.3. Molecular inflammation 5.2.4. Senoinflammation 5.3. Is chronic inflammatory state a common denominator of ARDs? 5.3.1. T2DM 5.3.2. Chronic aging-related respiratory diseases 5.3.3. Atherosclerosis 5.3.4. Frailty 5.3.5. Alzheimer's disease (AD) 5.3.6. Parkinson's disease (PD) 5.4. The case of COVID-19 5.5. Proposed interventions to prevent ARDs 5.6. Conclusion and future perspective References Chapter 6: A new perspective on ROS in aging with an integrated view of the gut microbiota 6.1. Introduction 6.2. The reactive oxygen species 6.3. The biological function of ROS 6.4. The oxidative stress theory of aging 6.5. ROS signaling in gut barrier, inflammation, and dysbiosis of gut microbiota in aging 6.6. Conclusion and future perspective References Chapter 7: Aging of immune system 7.1. Introduction 7.2. Changes in the adaptive immunity 7.2.1. T cells 7.2.2. B cells 7.3. Changes in the innate immunity 7.3.1. Neutrophils 7.3.2. Monocytes and macrophages 7.3.3. Dendritic cells 7.3.4. Mast cells, eosinophils, and basophils 7.4. Inflammaging 7.5. Conclusions and future perspectives References Chapter 8: Vaccination in old age: Challenges and promises 8.1. Introduction 8.2. The state of the art 8.2.1. Adjuvants 8.2.2. Influenza 8.2.3. Streptococcus pneumoniae 8.2.4. Varicella zoster virus 8.3. Challenges and promises 8.3.1. TLR agonists 8.3.2. Virosomes, viral vectors, reverse vaccinology 8.3.3. Interleukin-7 8.3.4. Inhibitors of mitogen-activated protein and adenosine monophosphate-activated protein kinases as therapeutic inter ... 8.4. Conclusion and future perspectives Note added in proof References Chapter 9: Resilience signaling and hormesis in brain health and disease 9.1. Introduction 9.2. Regional specificity of brain resilience and vulnerability to stress 9.3. Hydrogen sulfide: A resilient signaling molecule in brain disorders 9.4. Plant polyphenols improve resilience and brain health via ``Vitagenes ́ ́ 9.5. Conclusions and future perspectives References Chapter 10: Different components of frailty in the aging subjects-The role of sarcopenia 10.1. Frailty definition and assessment 10.2. Physical frailty and sarcopenia: two sides of the same coin 10.3. Cellular and molecular mechanisms of Sarcopenia 10.3.1. Muscle structure and function changes 10.3.2. Mitochondrial dysfunction 10.3.3. Anabolic resistance 10.3.4. Endocrine factors 10.3.5. Inflammation 10.4. Genetic components of sarcopenia 10.5. Lifestyle risk factors for sarcopenia 10.5.1. Malnutrition 10.5.2. Physical inactivity 10.6. Management of sarcopenia 10.6.1. Nutrition and physical activity 10.6.2. Anabolic medications and pharmacological treatments 10.7. Conclusions and future perspectives References Chapter 11: Hormones in aging 11.1. Introduction 11.2. Endocrine physiology: The role of the pituitary gland and hypothalamus 11.3. Gonadal function in aging 11.3.1. Menopause 11.3.2. ``Andropause, ́ ́ male late-onset hypogonadism 11.4. Growth hormone and aging 11.5. Adrenal function in aging 11.5.1. Glucocorticoids 11.5.2. Adrenal androgens 11.5.3. Mineralocorticoids and aging 11.6. Thyroid function in aging 11.7. Conclusions and future perspective References Chapter 12: Chronobiology and chrononutrition: Relevance for aging 12.1. Introduction 12.2. Biorhythms 12.3. Central oscillator and peripheral oscillators 12.4. Clock-controlled genes 12.5. Biological clock modulation and chronodisruption 12.6. Diet, circadian rhythm, aging, and longevity 12.6.1. Distribution of macronutrients throughout the day 12.6.2. Meals frequency 12.6.3. Caloric restriction 12.7. Meals composition for successful aging 12.8. Conclusion and future perspectives References Chapter 13: Nutraceutical approach to age-related diseases-The clinical evidence on cognitive decline 13.1. Introduction 13.1.1. Chronic age-related diseases and cognitive impairment 13.2. Data selection 13.3. The state of the art 13.3.1. Ginkgo biloba 13.3.2. Vitis vinifera 13.3.3. Camelia sinensis 13.3.4. Theobroma cacao 13.3.5. Bacopa monnieri 13.3.6. Crocus sativus 13.3.7. Curcuma longa 13.4. Conclusions and future perspectives References Chapter 14: Ways to become old: Role of lifestyle in modulation of the hallmarks of aging 14.1. Introduction 14.2. Primary hallmarks and lifestyle 14.2.1. Genomic instability 14.2.2. Telomere attrition 14.2.3. Epigenetic alterations 14.2.4. Loss of proteostasis 14.3. Antagonistic hallmarks and lifestyle 14.3.1. Deregulated nutrient sensing 14.3.2. Mitochondrial dysfunction 14.3.3. Cellular senescence 14.4. Integrative hallmarks and lifestyle 14.4.1. Stem cell exhaustion 14.4.2. Altered intercellular communication 14.5. Conclusion and future perspectives References Chapter 15: Nutritional biomarkers in aging research 15.1. Introduction 15.2. Minerals (zinc and selenium) 15.2.1. Zinc 15.2.2. Selenium 15.3. Vitamins 15.3.1. Antioxidant vitamins 15.3.2. Vitamin D 15.4. Polyunsaturated fatty acids 15.4.1. The n-3 index 15.4.2. The AA/EPA ratio 15.5. Carotenoids 15.5.1. Lycopene, α- and β-carotene 15.5.2. Lutein and zeaxanthin 15.6. Polyphenols 15.6.1. Flavonoids 15.6.2. Biochemical assessment of polyphenols intake 15.7. Molecular biomarkers of aging and nutrition 15.7.1. DNA and chromosomes 15.7.2. RNA and transcriptome 15.7.3. Metabolism 15.7.4. Mitochondria 15.7.5. Cell senescence 15.8. Conclusions and future perspectives References Chapter 16: The role of cytomegalovirus in organismal and immune aging 16.1. Introduction 16.2. Host immune response to CMV 16.3. CMV, longevity, and chronic diseases 16.4. CMV and immune aging 16.5. Conclusion and future perspectives References Chapter 17: Ethics of aging 17.1. Population aging: The challenges 17.2. Moral and social attitudes to old age 17.2.1. The cultural background 17.2.2. Ageism 17.2.3. Vulnerability 17.3. Ethics of aging 17.3.1. A new subfield of bioethics 17.3.2. Age and aging 17.3.3. Field of investigation 17.4. Fair allocation of medical resources 17.4.1. Different approaches to the allocation of medical resources 17.4.2. Strategies to reduce rising healthcare costs for older people 17.4.3. Conditions of dramatically scarce medical resources 17.5. Conclusion and future perspectives References Chapter 18: Conclusions. Slowing aging and fighting age-related diseases, from bench to bedside? 18.1. Introduction 18.2. Aging and gender medicine 18.3. The role of immune-inflammatory responses in aging and age-related diseases, and therapeutic interventions 18.4. Slowing aging and fighting age-related diseases 18.5. Conclusions and future perspectives References Index Back Cover
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