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Aging : How Aging Works, How We Reverse Aging, and Prospects for Curing Aging Diseases / Michael Fossel, editors.

Elsevier ScienceDirect eBook - Biomedical Science 2024 Available online

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Format:
Book
Contributor:
Fossel, Michael, editor.
Language:
English
Subjects (All):
Aging.
Cartilage.
Osteoarthritis.
Telomere.
Physical Description:
1 online resource (274 pages)
Edition:
First edition.
Place of Publication:
London, England : Mica Haley, [2024]
Summary:
Aging: How Aging Works, How We Reverse Aging, and Prospects for Curing Aging Diseases explains the process of aging beyond mere entropy, exposing it as a complicated and dynamic process that undercuts maintenance and permits age-related disease.
Contents:
Front Cover
AGING
AGING: HOW AGING WORKS, HOW WE REVERSE AGING, AND PROSPECTS FOR CURING AGING DISEASES
Copyright
Dedication
Contents
Contributors
About the editor
Foreword
Preface
Acknowledgments
1 - Introduction to aging and age-related disease
1. Introduction
2. How did we get here?
3. How to understand aging
4. The limited role of biomarkers
5. A unified systems model
5.1 Upstream risk factors
5.2 Downstream outcomes
6. Caveats
7. Prospects for intervention
References
2 - Age-related disease: Central nervous system
2. The dementias
3. Therapeutic status
4. Neuroanatomy
5. Cell types
6. Biochemical changes
7. Aging as a key process
8. Unified systems model: Cell aging in the central nervous system
9. Summary
3 - Age-related disease: Cardiovascular system
1. Determinants of arterial stiffness
2. How to define early vascular aging
3. Mechanisms important for modifying arterial stiffness and vascular aging
4. Factors in early life influencing arterial stiffness and early vascular aging
4.1 Vascular aging and the brain
4.2 Treatment of vascular aging and its consequences
5. Healthy and supernormal vascular aging
6. Treatment of cardiovascular risk and clinical manifestations
7. Emerging role of polypill for cardiovascular prevention
8. Summary: Aging and cardiovascular risk-mechanisms and clinical aspects
9. Role of cell aging in cardiovascular disease
10. Prospects for intervention
Acknowledgment
Further reading
4 - Age-related disease: Bones
1. Introduction: Bone anatomy and homeostasis
2. Skeletal maintenance and remodeling
2.1 Activation (phase 1)
2.2 Resorption (phase 2)
2.3 Reversal (phase 3)
2.4 Formation (phase 4).
3. Osteoporosis: An overview
4. Therapeutic options to treat osteoporosis: Current interventions
4.1 Antiresorptive and osteoclast-targeting therapeutics
4.2 Bone anabolics
4.3 Prospective therapeutics
5. Cellular components of an aging bone
5.1 Osteoblasts
5.2 Osteocytes
5.3 Osteoclasts
5.4 Adipocytes
5.5 Endothelial cells
6. Biology of an aging bone: Mechanisms and pathways
6.1 Biology of an aging bone: Cellular senescence
6.2 Biology of an aging bone: DNA damage and genomic instability
6.3 Biology of an aging bone: Telomere dysfunction and shortening
6.4 Biology of an aging bone: Mitochondrial dysfunction
6.5 Biology of an aging bone: Epigenetic regulations
6.6 Biology of an aging bone: Loss of proteostasis
7. Therapeutic options: Future potential interventions and emerging trials
8. Conclusion
5 - Age-related disease: Joints
1. Cartilage structure and function: a primer
2. Aging and osteoarthritis
3. Replicative senescence in cartilage
4. Stress-induced senescence in cartilage
5. The senescence-associated secretory profile in chondrocytes
6. Autophagy: A complex interrelationship with senescence
7. The role of sirtuins in chondrosenescence
8. The emerging role of circadian clocks in senescence
9. mTOR, nutrient sensing, and senescence in cartilage
10. Stem cell exhaustion?
11. The role of the extracellular matrix in initiating and stabilising cellular senescence
12. Chondrosenescence: Can the advancing tide be reversed?
13. Conclusion
6 - Age-related disease: Kidneys
2. Aging kidney
2.1 Structural changes of the aging kidney
2.1.1 Micro-anatomical changes
2.1.1.1 Nephrosclerosis
2.1.1.2 Nephron hypertrophy
2.1.2 Macro-anatomical changes
2.1.2.1 Kidney volume.
2.1.2.2 Kidney cysts and tumors
2.2 Functional changes of the aging kidney
2.2.1 Age-related decline in GFR
2.3 Cellular senescence in renal aging
2.3.1 Signaling pathways implicated in cellular senescence and renal aging
3. Common alterations in cellular and molecular mechanisms of renal aging and CKD
3.1 Renin-angiotensin system (RAS) activity and the kidney function
3.1.1 The connection of RAS with Klotho in the kidney
3.1.2 The role of RAS in AKI-CKD progression
3.2 Klotho and Wnt/β-catenin signaling
3.3 Peroxisome proliferator-activated receptor (PPAR)-γ
3.4 Chronic inflammation
3.5 Oxidative stress
3.6 Vascular changes
3.7 Telomere shortening
4. Prevalence of CKD in the elderly
4.1 Classification of CKD and staging
4.2 Etiology
4.3 Progression
4.4 Vulnerability of aged CKD patients
4.5 Vascular consequences of CKD
4.5.1 Coronary and peripheral vascular disease
4.5.2 Cerebrovascular disease and cognitive functioning
5. Risk factors for CKD in the elderly
5.1 Diabetes
5.2 Obesity
5.3 Hypertension and cardiovascular diseases
5.4 Acute kidney injury
5.5 Nephrotoxins
5.6 Smoking
5.7 Genetic components
6. CKD care and management for the elderly
6.1 Blood pressure monitoring
6.2 Erythropoiesis-stimulating agents
6.3 Acidosis
6.4 Cardiovascular risk assessment
6.5 Insulin and glucose control with oral agents
6.6 Prevention of AKI
6.7 Stabilization of CKD progression
7. Conclusion
7 - Age-related disease: Immune system
2. The aging of the immune system
2.1 The hematopoietic stem cell system
2.2 Erythrocytes and platelets
2.3 Setting the focus to the innate and adaptive immune system
2.4 Age-related changes in the innate immune system.
2.5 Age-related changes in the adaptive immune system
2.6 Inflamm-aging
2.7 Immune risk phenotype
3. Examples of conditions related to immune system aging
3.1 Infectious diseases
3.2 Autoimmunity
3.3 Cancer and other neoplasms
3.4 The role of immunosenescence in health and disease: An introduction to telomere biology
4. Biomolecular mechanisms of immunosenescence
4.1 Role of the telomere biology system
4.2 Regulation of telomerase activity
4.3 Mitochondria, telomere biology, and cellular aging
4.4 DNA damage and repair mechanisms
4.5 Crosstalk between telomere biology and epigenetic processes
5. Upstream risk factors
5.1 Genetic factors
5.2 Lifestyle and environmental factors
5.2.1 Pathogen load
5.2.2 Mental distress
5.2.3 Nutrition
5.2.4 Effects of physical activity and exercise on immune functions
5.2.5 The importance of sleep for health
6. Biomarkers/downstream factors related to aging and immunosenescence
6.1 Indirect and direct measures of free radicals
6.2 Protein glycosylation and its changes with age
6.3 Mitochondrial health index (MHI) and the Bioenergetic Health Index (BHI)
6.4 Epigenetic aging clocks
7. Future perspectives
7.1 Genetic therapy and pharmacological interventions to stimulate telomerase activity
7.2 Stem cells from umbilical cord blood as a cellular reservoir for immunological treatments/interventions
7.3 Rejuvenation effects of blood transfer and parabiosis from the young in the aged
7.4 Supplementation of nicotinamide adenine dinucleotide (NAD)
7.5 The use of senolytics
8 - Age-related disease: Skin
1. Geriatric dermatology
2. Fountain of youth and skin health
3. Chronological versus biological skin aging
4. Clinical manifestations of skin aging
5. Regenerative aesthetics.
6. Cellular senescence
7. Function of senescent cells
8. Features of senescent cells
9. Biochemical markers of cellular senescence
10. Senescence in skin aging
11. Targeting senescent cells in the skin
12. Senotherapeutic agents for skin
13. First- and second-generation senolytics
14. Translation to clinical practice
15. Targeting cellular senescence with senotherapies
16. Conclusion
9 - Age-related disease: Lungs
1. Introduction and relevant anatomy
2. The aging lung
3. Role of cell aging in age-related lung disease
4. Specific lung diseases correlated with advanced age
4.1 Emphysema and COPD
4.2 Interstitial lung diseases/interstitial pulmonary fibrosis
5. Current research, future direction, and potential interventions
10 - Age-related disease: Diabetes
1. Introduction: Type 2 diabetes is an age-related disease
2. Cellular senescence in the pathogenesis of type 2 diabetes
2.1 Cellular senescence
2.2 Adipose tissue
2.3 Pancreas
2.4 Muscle
2.5 Liver
3. The diabetic microenvironment drives senescent cell accumulation
3.1 Hyperglycemia and advanced glycation endproducts
3.2 Hyperinsulinemia
3.3 Oxidative stress and telomere attrition
3.4 Chronic inflammation and impaired immune function
4. Cellular senescence and diabetic complications
4.1 Microvascular complications
4.2 Macrovascular complications
4.3 Cognition
4.4 Cancer
4.5 Osteoporosis
4.6 Impaired wound healing
5. Current diabetes therapeutics: Impact on cellular senescence
5.1 Diet and exercise
5.2 Metformin
5.3 SGLT-2 inhibitors
5.4 GLP-1R agonists and DPP-4 inhibitors
5.5 Insulin
5.6 Sulfonylureas
5.7 Acarbose
6. Targeting cellular senescence in diabetes
6.1 Senolytic agents
6.2 SASP inhibitors ("senomorphic" drugs).
6.3 Immune strategies.
Notes:
Includes bibliographical references and index.
Description based on publisher supplied metadata and other sources.
Description based on print version record.
Other Format:
Print version: Fossel, Michael Aging
ISBN:
9780443155017
OCLC:
1425790565

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