Modelling Perspectives on Aging: Can Mathematics Help us Stay Young?

Edelstein‐Keshet, Leah; Israel, Aliza; Lansdorp, Peter M.

doi:10.1006/jtbi.2001.2429

Cited by 25 publications

(15 citation statements)

References 38 publications

(32 reference statements)

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“…It appears now that the primary mechanism of general maintenance of all tissues in an organism is through a specific set of stem cells specific for each tissue type. [40][41][42][43][44] However, these stem cells gradually lose their special state of differentiation, largely through epigenetic drift rather than mutational mechanisms, and as a result the tissues that had depended on their renewal become increasingly defective through an impaired chromatin and tissue remodeling process. [45][46][47][48] It was suggested (by R.G.C.)…”

Section: How Does Ros/rns Cause Aging?mentioning

confidence: 99%

Oxidative Stress Profiling:

Cutler

2005

Annals of the New York Academy of Sciences

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Many of the most serious human diseases have a strong association with the steady-state level of oxidative damage in tissues. On an individual level this damage is defined as the patient's oxidative stress status (OSS). OSS is associated with many of the major age-related diseases such as cancer, heart disease, diabetes, and Alzheimer's disease, as well as with the aging process itself. In general, the greater the OSS of the individual, the higher the risk for disease development. To further understand the role that OSS has as a causative or an associated factor for these diseases, and to develop more effective personalized therapy to minimize OSS, requires a reliable means to measure the many different components contributing to an individual's OSS. This procedure is called oxidative stress profiling (OSP) and represents a new strategy to simultaneously assess an individual's OSS as well as to identify key physiological parameters, such as the hormone, lipid, antioxidant, or iron profile, that may be responsible for that individual's OSS. The OSP strategy provides physicians with information that enable them to make a more accurate diagnosis of the patient's condition and to recommend specific types of therapy based on better scientific data. Follow-up studies of the patient would then be conducted using these same tests until the OSS of the patient has been minimized. The OSP strategy is particularly well suited for a personalized health optimization program. The procedure is based on measuring both the steady-state levels of oxidative damage in nucleic acids, proteins, and lipids and the protective and defense processes of these components using blood, urine, and breath samples. Testing individuals before and after a controlled amount of exercise (70% VO2) may also help to obtain greater sensitivity and reproducibility. Evaluation of test results to obtain an integrated calculated OSS result for a patient represents a major challenge. One approach is to present the test results on a percentile bases, allowing results of different tests to be integrated into one or a few parameters, such as an oxidative stress and an antioxidant index. This article presents a general overview and rationale of the concept of the oxidative stress profile, tests to be used, and examples of how it may be applied.

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Section: How Does Ros/rns Cause Aging?mentioning

confidence: 99%

Oxidative Stress Profiling:

Cutler

2005

Annals of the New York Academy of Sciences

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“…Telomerase is induced in hematopoietic stem cells by cytokine stimulation and is down‐regulated again with proliferation and differentiation [49]. The presence of stem cells capable of expressing telomerase upon stimulation results in a slower overall rate of ageing in the immune system [50].The telomerase activity can be reactivated not only in stem cells. Some cells of the immune system and even fibroblasts and endothelial cells in the course of regeneration reactivate telomerase [51]. …”

Section: Dependence Of Proliferative Life Span In Vitro On Organism Lmentioning

confidence: 99%

Section: Dependence Of Proliferative Life Span In Vitro On Organism Lmentioning

confidence: 99%

Duration of senescent cell survival in vitro as a characteristic of organism longevity, an additional to the proliferative potential of fibroblasts

Yegorov

Zelenin

2003

FEBS Letters

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More than 40 years have passed since the original publication by Hay£ick and Moorhead led to the concept of the 'Hay£ick limit' of the maximum number of divisions which somatic cells undergo in vitro. This concept is still regarded as a fundamental characteristic of species longevity. Here we want to emphasize another characteristic of somatic cells, namely, the duration of their survival in vitro in the non-dividing state after cessation of proliferation. This is suggested on the basis of results of recent experiments with so-called Japanese accelerated senescent mice. Results of these experiments reveal a good correlation between the longevity of the mice, the number of duplications of their ¢broblasts in vitro, and the survival time of these cells in the non-dividing state. In routine culture conditions, cell survival time may be very long, as much as a few years. However, when the cells are grown under conditions of oxidative stress, cellular longevity is markedly shortened. This new test may serve as an additional marker of organismic longevity. The comparative value of both tests, the classical 'Hay£ick limit' and the new test, is discussed.

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“…The literature of theoretical models that have addressed the biology of ageing per se is fairly extensive but explanation of the process in the context of human physiology remains elusive (Edelstein‐Kechet et al . ; Steinsaltz et al . ).…”

Section: Introductionmentioning

confidence: 99%

Declining performance of master athletes: silhouettes of the trajectory of healthy human ageing?

Lazarus

Harridge

2017

The Journal of Physiology

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Analysis of world record performances by master athletes suggests an essentially linear decline with age until around the eighth decade after which performance decline accelerates. Because these records are obtained from highly trained individuals they can be viewed as being reflective of the diminution of integrative physiological prowess that occurs solely as a result of ageing, unaffected by the confounding effects of inactivity. It can also be argued that these performance profiles mirror and provide an insight into the trajectory of the physiology of the human ageing process. Here we propose a set point theory that hypothesises that a given threshold of physical activity is needed to age optimally and to maximise the 'healthspan'. Exercising at levels below the set point will result in ageing being contaminated by the unpredictable and pathological effects of inactivity. Exercise above this threshold stimulates adaptations towards maximising athletic performance, but is unlikely to have further beneficial effects on health. Thus the decades-long, controlled diminution in athletic performance, should not be seen as a disease process. The ageing process is separate from, and independent of, exercise-mediated processes that maintain or adapt physiological function. Whether an understanding of these mechanisms will also help uncover mechanisms underpinning the ageing process itself is open to question. However, any model which does not take into account the effects of activity will not adequately describe the inherent ageing process.

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Modelling Perspectives on Aging: Can Mathematics Help us Stay Young?

Cited by 25 publications

References 38 publications

Oxidative Stress Profiling:

Oxidative Stress Profiling:

Duration of senescent cell survival in vitro as a characteristic of organism longevity, an additional to the proliferative potential of fibroblasts

Declining performance of master athletes: silhouettes of the trajectory of healthy human ageing?

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