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What this series is about ... Health and Ageing News offers a systematic approach to quality of life. Our aim is to bring to you state-of-the-art information on government policy reforms, research findings, book reviews, news, and articles that highlight the understanding of a successful ageing process. The articles will cover a range of critical topics including biology, behavioural and social sciences, epidemiology, clinical practice and health, food and nutrition, and social research, planning and practice. Organised into sections addressing innovative developments in these fields, we hope to reach a broad audience and to facilitate a continuum of self-care. Each contribution will address the applied implications of health care research and offer practical guidance to readers dealing with these issues in their own lives and in the care of their families. As a whole, major advance in information technology has transformed health communication and health literacy. This series represents the highest levels of current scholarship in health and ageing, and a strong foundation for future research. |
Ageing
Ageing is a process of gradual maturation. While the biological systems slow down over time --including the process of cell division, capacity for growth, and function -- maturation has many positive components of development (e.g. increased wisdom, experience, and expertise). The changes that occur can be described in two categories: those that result from older age, and those that result from disease, lifestyle, and environmental exposures. However, this complex is hard to define because people age differently. Some acquire disease and impairment, and others seem to escape disease altogether and are said to have died of "old age." Some animals, including certain birds and fish, do not appear to age at all.
Successful ageing is healthy ageing. It refers to a process by which deleterious effects of ageing are minimised and biological functions preserved for continued living. People who age successfully avoid experiencing the many disease-related features of ageing and remain functional, both physically and mentally. In this connection, ABS data reports that the percentage of community-dwelling people > 65 who report needing assistance with activities of daily living has decreased over the last two decades, as has the percentage of people with debilitating disease. One viable explanation for these changes is an increase in the percentage of people who are ageing successfully, although there may be other explanations.
Biology of ageing
How and why do we age? Scientists around the world are peering into our cells and seeking clues to these complex questions. Are the answers in our genes? Does it have to do with how we process certain foods, or even how we use the very air we breathe? Each day researchers are seeking new knowledge that may help us all live healthier and longer lives.
Ageing is the result of a gradual accumulation of unrepaired molecular damage, increased fractional damage of cells, impairment of organ tissues and eventual decline of body functions. In successful ageing the decline of physiologic functions is not disease-related. The distinction between normal and disease-related decline may sometimes be unclear or defined simply by statistical distribution, except in particular situations. For example, with presbyopia (decreased accommodation of the lens of the eye), the distinction is clear because it occurs in virtually all older people. Thus, no cause or explanation for presbyopia has been identified other than ageing itself. However, with glucose control and cognition, statistical distribution defines the distinction between normal and disease-related. While some degree of glucose intolerance is a normal part of the ageing process, diabetes, a common condition, is a disease. Cognitive decline is usually universal with ageing and it is a part of the normal process of ageing; however, dementia, though common in late life, is a disease.
Cells are critical building blocks of our body. How and why cells age, lose their ability to function and reproduce, and ultimately die may help us understand the causes (and perhaps the cures) for many age-related diseases and conditions.
Oxidative damage -- Can antioxidants prevent wear and tear on our cells? The answer is "Yes". In each moment, in the natural process of oxidation (converting oxygen into energy), the body produces toxins called "free radicals". These molecules can cause damage to cells and the DNA (the deoxyribonucleic acid molecule found in living cells). As people age, the "mopping up" process becomes less efficient.
Free radical or oxidative damage is implicated in several age-associated diseases from cancer and diabetes to Alzheimer's, Parkinson's and heart disease. Some research suggests that this damage may be a central cause of the ageing process itself. Scientists are now investigating how diets rich in antioxidants (Vitamins C and E, two of the most common) can limit the harm caused by oxidative damage and perhaps even slow the ageing process.
Telomeres -- Is there a biological clock for cellular ageing? DNA sequences are the blueprint of life. Telomeres are cap like structures at the tip of all DNA of human chromosomes. DNA replicates repeatedly in human cells to pass hereditary information from one generation to the next. As the cells grow and divide, their DNA is protected and copied by telomeres. These telomeres have a huge impact on the behaviour of the cells. Telomeres shorten as we age. The question of whether short telomeres cause ageing or the diseases of ageing is a topic of ongoing research.
Exciting investigations now underway focus on telomeres as well as telomerase. Telomerase is the enzyme that replenishes telomeres in the cell. Telomerase is evolving into a new tool in clinical medicine. For example, this enzyme holds the promise of engineering new life into old tissue. Blocking this enzyme , on the other hand, may inhibit the growth of cancer. Other studies are exploring the potential of telomerase for a variety of purposes.
DNA damage and repair -- How does ageing affect cells ability to repair themselves? As indicated earlier, as internal and external toxins damage the DNA, the intricate repair system of the body is unable to maintain the integrity of DNA code and of the cells and their function and, over time, the DNA repair system falters. Some scientists believe that the accumulation of uncorrected DNA damage over years is a major cause of ageing and age-related diseases.
Understanding the role that DNA damage and its repair, or lack of repair, play in ageing and age-related diseases is a first step. However, research is going further to investigate how we may take the next logical step--that is, to treat DNA damage and to prevent DNA damage. If our DNA repair systems are in fact the guardians of the genome, can we strengthen those guardians and live healthier and longer lives? In this connection, Roth & Gellert (2000) provide an interesting discussion in their paper New guardians of the genome, (Reference: Roth DB, Gellert M. New guardians of the genome, Nature 2000; 404: 823-5).
Mitochondrial ageing-- What is the effect of ageing on the cell's energy supply? Mitochondria are tiny cellular bodies or organelles among the most complex structures within the cell. They have both an outer and inner membrane. Most of the energy-producing reactions occur at the inner membrane, which is made of lipids (fats) studded with proteins. Anything that compromises this structure can undermine the ability of the mitochondria to produce energy. Mitochondria also contain a small loop of DNA.
The assertion that mitochondrial damage and disruption contribute to ageing, and to a number of diseases that we associate with growing older, has gained wide acceptance among researchers. While scientific knowledge of the mechanisms that contribute to age-related mitochondrial damage is by no means complete, a fair amount is known about the generation of renegade oxygen free radicals -- the compounds that indiscriminately damage components of the mitochondria. Thus, the understanding and current research of mitochondria and ageing has tended to focus on several other interrelated areas:
- Minimising the generation of compounds toxic to mitochondria;
- Neutralising and protecting mitochondria from oxidants that are formed; and
- Repairing mitochondrial damage once it has occurred.
In addition to the DNA repair mechanisms, there are varieties of substances in the body that serve to control damage to mitochondria. These include antioxidants, the enzyme SOD (superoxide dismutase), and uncoupling proteins (UCPs). Scientists are now seeking ways to improve the efficacy of these compounds or processes to reduce cellular damage associated with mitochondrial damage.
Our next issue in this series will aim to discuss cellular senescence, and the genetics of longevity and ageing.
References
- American Federation for Ageing Research (AFAR) Biology of Ageing.
- Kirkwood , TBL, 1977. Evolution of ageing. Nature, 270, 301-304.
- Harman D 1956. Ageing: a theory based on free radical and radiation chemistry. Journal of Gerontology, 11, 298-300.
- Kapahi P, Boulton ME, Kirkwood TBL, 1999. Positive correlation between mammalian life span and cellular resistance to stress. Free Radical Biology & Medicine, 26, 495-500.
- Friguet B, Bulteau A, Chondrogianni N, Conconi M, Petropoulos I, 2000. Protein degradation by the proteasome and its implications in ageing. The Annals of the New York Academy of Sciences, 908, 143-154.
- Blackburn EH, 2000. Telomere states and cell fates. Nature, 408, 53-56.
- Griffith JD, Comeau L, Rosenfield S, Stansel, RM, Bianchi A, Moss H, de Lange T, 1999. Mammalian telomeres end in a large duplex loop. Cell, 97, 503-514.
- Ramsey MJ, Moore DH, Briner JF, Lee DA, Olsen LA, Senft JR, Tucker JD, 1995. The effects of age and life-style factors on the accumulation of cytogenetic damage as measured by chromosome painting. Mutation Research-DNA-ageing Genetic Instability and Ageing, 338, 95-106.
Monika Bhatia
Editor, Health and Ageing