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Mechanisms of Ageing and Development Apr 2002Explaining why ageing occurs is a solution to the longstanding enigma of the role of senescence in nature. Even after half a century of progress, this solution continues... (Review)
Review
Explaining why ageing occurs is a solution to the longstanding enigma of the role of senescence in nature. Even after half a century of progress, this solution continues to unfold. Evolution theory argues strongly against programmed ageing, suggesting instead that organisms are programmed for survival, not death. In the current view, ageing results from the twin principles that (i) the force of natural selection declines with age, and (ii) longevity requires investments in somatic maintenance and repair that must compete against investments in growth, reproduction and activities that might enhance fitness. In addition to explaining why ageing occurs, the evolutionary theory also provides insight into the mechanisms underlying the complex cellular and molecular changes that contribute to senescence, as well as an array of testable predictions. Some of the most interesting current problems are to understand how the genetic factors influencing ageing and longevity are predicted to respond to fluctuating environments, such as temporary periods of famine, as well as to other kinds of spatial and/or temporal heterogeneity. Rapid progress in human genomics raises the prospect of greatly increasing our knowledge of the determinants of human longevity. To make progress in understanding the role and evolution of genetic and non-genetic factors in human longevity, we need more detailed theoretical studies of how intra-population variables, such as socio-economic status, influence the selection forces that shape the life history.
Topics: Aged; Aging; Animals; Biological Evolution; Genome, Human; Humans; Longevity; Menopause; Selection, Genetic
PubMed: 11869731
DOI: 10.1016/s0047-6374(01)00419-5 -
Gerontology 1994Fishes show three types of senescence. Lampreys, eels and pacific salmon exhibit rapid senescence and sudden death at first spawning. The guppy, red panchax, medaka,... (Comparative Study)
Comparative Study Review
Fishes show three types of senescence. Lampreys, eels and pacific salmon exhibit rapid senescence and sudden death at first spawning. The guppy, red panchax, medaka, platyfish, Indian murrel and many other teleosts undergo gradual senescence, as observed in most of the vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female plaice, flatfish, rockfish) show indeterminate growth, the occurrence of senescence in them is supposed to be very slow or negligible. Neuroendocrine mechanisms are involved in rapid senescence. Most of the evidences in favour of the occurrence of senescence in fishes have been derived from studies in species showing gradual senescence. Age-related increases in mortality rate, accumulation of lipofuscin, lipid peroxidation, collagen cross-linking and decreases in growth rate, reproductive capacity and protein utilisation are clearly marked in such species. Anatomical changes in various organs during ageing also confirm increases in degenerative changes and pathological symptoms. Dietary restriction and lower environmental temperature retard the ageing processes in a few species showing gradual senescence. These results tentatively support the contention of commonality in mechanism of ageing processes in vertebrates. At present, anatomical, cellular, biochemical and genetic evidences in support or against the occurrence of slow senescence or negligible senescence in long-lived fish species are almost nonexistent. Extensive studies on ageing in fishes are needed to explain the multiple mechanisms which are not unexpected considering the number and variety of the existing species.
Topics: Aging; Animals; Environment; Female; Fishes; Longevity; Male; Models, Biological; Species Specificity
PubMed: 7926851
DOI: 10.1159/000213582 -
Ageing Research Reviews Nov 2010Ageing, which all creatures must encounter, is a challenge to every living organism. In the human body, it is estimated that cell division and metabolism occurs... (Review)
Review
Ageing, which all creatures must encounter, is a challenge to every living organism. In the human body, it is estimated that cell division and metabolism occurs exuberantly until about 25 years of age. Beyond this age, subsidiary products of metabolism and cell damage accumulate, and the phenotypes of ageing appear, causing disease formation. Among these age-related diseases, neurodegenerative diseases have drawn a lot of attention due to their irreversibility, lack of effective treatment, and accompanied social and economical burdens. In seeking to ameliorate ageing and age-related diseases, the search for anti-ageing drugs has been of much interest. Numerous studies have shown that the plant polyphenol, resveratrol (3,5,4'-trihydroxystilbene), extends the lifespan of several species, prevents age-related diseases, and possesses anti-inflammatory, and anti-cancer properties. The beneficial effects of resveratrol are believed to be associated with the activation of a longevity gene, SirT1. In this review, we discuss the pathogenesis of age-related neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and cerebrovascular disease. The therapeutic potential of resveratrol, diet and the roles of stem cell therapy are discussed to provide a better understanding of the ageing mystery.
Topics: Aging; Antioxidants; Humans; Longevity; Neurodegenerative Diseases; Resveratrol; Stilbenes
PubMed: 20732460
DOI: 10.1016/j.arr.2010.08.006 -
Ageing Research Reviews May 2021Aging is characterized by a progressive loss of tissue integrity and functionality due to disrupted homeostasis. Molecular oxygen is pivotal to maintain tissue... (Review)
Review
Aging is characterized by a progressive loss of tissue integrity and functionality due to disrupted homeostasis. Molecular oxygen is pivotal to maintain tissue functions, and aerobic species have evolved a sophisticated sensing system to ensure proper oxygen supply and demand. It is not surprising that aberrations in oxygen and oxygen-associated pathways subvert health and promote different aspects of aging. In this review, we discuss emerging findings on how oxygen-sensing mechanisms regulate different cellular and molecular processes during normal physiology, and how dysregulation of oxygen availability lead to disease and aging. We describe various clinical manifestations associated with deregulation of oxygen balance, and how oxygen-modulating therapies and natural oxygen oscillations influence longevity. We conclude by discussing how a better understanding of oxygen-related mechanisms that orchestrate aging processes may lead to the development of new therapeutic strategies to extend healthy aging.
Topics: Cellular Senescence; Longevity; Oxygen; Phenotype; Reactive Oxygen Species
PubMed: 33556549
DOI: 10.1016/j.arr.2021.101267 -
Nature Nov 2000The evolutionary theory of ageing explains why ageing occurs, giving valuable insight into the mechanisms underlying the complex cellular and molecular changes that... (Review)
Review
The evolutionary theory of ageing explains why ageing occurs, giving valuable insight into the mechanisms underlying the complex cellular and molecular changes that contribute to senescence. Such understanding also helps to clarify how the genome shapes the ageing process, thereby aiding the study of the genetic factors that influence longevity and age-associated diseases.
Topics: Aging; Animals; Biological Evolution; Energy Intake; Humans; Models, Biological; Reproduction; Selection, Genetic
PubMed: 11089980
DOI: 10.1038/35041682 -
Nature Reviews. Molecular Cell Biology Feb 2017
Topics: Aging; Longevity
PubMed: 28053345
DOI: 10.1038/nrm.2016.176 -
The European Respiratory Journal Mar 2015In ageing populations many patients have multiple diseases characterised by acceleration of the normal ageing process. Better understanding of the signalling pathways... (Review)
Review
In ageing populations many patients have multiple diseases characterised by acceleration of the normal ageing process. Better understanding of the signalling pathways and cellular events involved in ageing shows that these are characteristic of many chronic degenerative diseases, such as chronic obstructive pulmonary disease (COPD), chronic cardiovascular and metabolic diseases, and neurodegeneration. Common mechanisms have now been identified in these diseases, which show evidence of cellular senescence with telomere shortening, activation of PI3K-AKT-mTOR signalling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profiles, immunosenescence and low grade chronic inflammation ("inflammaging"). Many of these pathways are driven by chronic oxidative stress. There is also a reduction in anti-ageing molecules, such as sirtuins and Klotho, which further accelerates the ageing process. Understanding these molecular mechanisms has identified several novel therapeutic targets and several drugs have already been developed that may slow the ageing process, as well as lifestyle interventions, such as diet and physical activity. This indicates that in the future new treatment approaches may target the common pathways involved in multimorbidity and this area of research should be given high priority. Thus, COPD should be considered as a component of multimorbidity and common disease pathways, particularly accelerated ageing, should be targeted.
Topics: Aged; Aging; Cardiovascular Diseases; Cellular Senescence; Epigenomics; Humans; Metabolic Diseases; Neoplasms; Oxidative Stress; Preventive Medicine; Pulmonary Disease, Chronic Obstructive; Signal Transduction
PubMed: 25614163
DOI: 10.1183/09031936.00229714 -
Biogerontology Dec 2013
Topics: Age Factors; Aging; Animals; Health Status; Humans; Regenerative Medicine
PubMed: 24292550
DOI: 10.1007/s10522-013-9476-x -
Nature Jan 2022
Topics: Aging; Humans; Longevity
PubMed: 35046588
DOI: 10.1038/d41586-022-00070-1 -
The Lancet. Diabetes & Endocrinology Aug 2018
Topics: Aging; Humans; Protective Agents
PubMed: 30053981
DOI: 10.1016/S2213-8587(18)30214-6