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SCIDIR_on1336953715 |
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OCoLC |
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20231120010655.0 |
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220723s2022 enk o 000 0 eng d |
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|a 9780323902366
|q electronic book
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|a 0323902367
|q electronic book
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|z 9780323902359
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|z 0323902359
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|a (OCoLC)1336953715
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|a RA776.75
|b .A58 2022
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|a 613.2
|2 23
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|a Anti-aging drug discovery on the basis of hallmarks of aging /
|c edited by Sandeep Kumar Singh, Chih-Li Lin and Shailendra Kumar Mishra.
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|a London, United Kingdom ;
|a San Diego, CA :
|b Academic Press,
|c [2022]
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|a 1 online resource
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|a text
|b txt
|2 rdacontent
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|a computer
|b c
|2 rdamedia
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|a online resource
|b cr
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|a 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.
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|a 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.
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|a 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.
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|a 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.
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|a 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.
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|a Description based on online resource; title from digital title page (viewed on September 13, 2022).
|
| 650 |
|
0 |
|a Aging
|x Prevention.
|
| 650 |
|
0 |
|a Drug development.
|
| 650 |
|
0 |
|a Aging.
|
| 650 |
|
0 |
|a Chemotherapy.
|
| 650 |
1 |
2 |
|a Aging
|x drug effects
|0 (DNLM)D000375Q000187
|
| 650 |
2 |
2 |
|a Aging
|0 (DNLM)D000375
|
| 650 |
2 |
2 |
|a Drug Therapy
|0 (DNLM)D004358
|
| 650 |
|
6 |
|a Vieillissement
|x Pr�evention.
|0 (CaQQLa)201-0313335
|
| 650 |
|
6 |
|a M�edicaments
|x D�eveloppement.
|0 (CaQQLa)201-0306620
|
| 650 |
|
6 |
|a Vieillissement.
|0 (CaQQLa)201-0020292
|
| 650 |
|
6 |
|a Chimioth�erapie.
|0 (CaQQLa)201-0034750
|
| 650 |
|
7 |
|a Aging
|x Prevention
|2 fast
|0 (OCoLC)fst00800326
|
| 650 |
|
7 |
|a Drug development
|2 fast
|0 (OCoLC)fst00898670
|
| 700 |
1 |
|
|a Singh, Sandeep Kumar.
|
| 700 |
1 |
|
|a Lin, Chih-Li.
|
| 700 |
1 |
|
|a Mishra, Shailendra Kumar.
|
| 776 |
0 |
8 |
|i ebook version :
|z 9780323902366
|
| 776 |
0 |
8 |
|c Original
|z 0323902359
|z 9780323902359
|w (OCoLC)1274199903
|
| 776 |
0 |
8 |
|i Print version:
|t ANTI-AGING DRUG DISCOVERY ON THE BASIS OF HALLMARKS OF AGING.
|d [S.l.] : ELSEVIER ACADEMIC PRESS, 2022
|z 0323902359
|w (OCoLC)1274199903
|
| 856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/book/9780323902359
|z Texto completo
|
