دانلود کتاب Human Aging: From Cellular Mechanisms to Therapeutic Strategies

فهرست مطالب :

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