The Ageing Process
“How Our Bodies and Minds Change”
Aging is a process that concerns us all. The increasing armamentarium provided by molecular biology and other techniques has allowed greater understanding of some of the processes involved. Numerous definitions of aging exist; an acceptable and commonly used definition is that aging is the total of all changes an organism undergoes from its conception to its death, including development, maturation and adulthood. There are many theories about how our bodies and minds change as we age, but no matter how much research or theories have been formed, one thing remains true is that our bodies and minds does, and will, change with age and one thing can be agree upon is that the end results in all these studies is that the body and minds does go through many changes during our life time. Since the life span varies between and within species and human longevity is partially hereditary, it is clear that genetic factors, the biology of the brain, and our culture effect the function of the brain and influence the aging process ( Johnson 1993, Schacter et al. 1993, Vijg et al. 1995).
Twin studies show that genetic differences account for about a quarter of the variance in adult human lifespan. While a great deal of research has focused on diseases of aging, there are only a few informative studies on the molecular biology of the aging brain. Many molecular changes are due in part to a reduction in the size of the brain, as well as loss of brain plasticity, Recent genome-wide studies demonstrate that a relatively small number of genes exhibit age-dependent gene expression changes. Studies in rodent, monkey, and human brains estimate the number of genes exhibiting age-dependent changes to represent less than 10%, and commonly less than 5%, of the entire genome. Human studies of longevity face numerous theoretical and logistical challenges, as the determinants of lifespan are extraordinarily complex. However, large-scale linkage studies of long-lived families, longitudinal candidate-gene association studies and the development of analytical methods provide the potential for future progress. The age-related changes of a large number of genes were investigated using gene microarray technology in prefrontal cortex samples from human subjects aged 13 to 79 years. The data from this study identified life-long progressive changes in expression with age in approximately 7.5% of genes tested, while expression levels for the large majority of genes were strikingly unchanged throughout adult life. ( Lee CK., Weindruch R., Prolla TA. Gene-expression profile of the ageing brain in mice. Nat Genet.2000;25:294–297.)
Linkage analysis is the traditional means of genetic mapping in humans. In longevity studies, genome-wide linkage scans are often hampered by a lack of availability of multi-generational DNA from long-lived individuals, and by the phenotypic heterogeneity of increased lifespan as a trait. In addition, traditional linkage studies require very large sample sizes to identify genetic regions that are involved in complex multifactorial phenotypes such as lifespan. Human lifespan is of vital importance, both for individuals and society. Familial recurrence patterns for longevity, has given cause for optimism that it will be possible to identify other genetic variants that affect lifespan. While there progress in determining the longevity of humans, there are still illnesses and diseases that must be addressed to determine if they plays a role in our physical and mental changes as we get older.
Loss of memory and of cognitive function affects people worldwide. Such loss may be the result of different progressive neurological disorders of the brain. It affects both men and women and is common in the elderly. While it’s true that certain brain changes are inevitable when it comes to aging, major memory problems is not one of them. That’s why it’s important to know the difference between normal age-related forgetfulness and the symptoms that may indicate a developing cognitive problem. Memory loss may be characterized as the difficulty or failure for immediate or delayed recall. As we grow older, we experience physiological changes that can cause glitches in brain functions we’ve always memory loss, the first type of memory loss relates to the failure to recall, within a few seconds, a specific object. Memory lapses can be frustrating, but most of the time they aren’t cause for concern. Age-related memory changes are not the same thing as dementia. This type of memory loss can be helped by supplementing with acetyl l-carnitine, a vitamin that will combat this initial short term memory loss. The second type relates to failure to recall a specific object, within a few minutes. Amnesia is an extreme condition in loss of memory. Amnesia, meaning "forgetfulness"; is a deficit in memory caused by brain damage. Essentially, amnesia is loss of memory. It is a disturbance which results in partial or total inability to recall, altogether, past experiences. Many forms of amnesia fix themselves without being treated. The aging process generally results in changes and lower functioning in the brain, leading to problems like memory loss and decreased intellectual function. Age is a major risk factor for most common neurodegenerative diseases, including mild cognitive impairment, Alzheimer's disease, cerebrovascular disease, Parkinson's disease, and Lou Gehrig's disease. Memory loss is not an inevitable part of the aging process, the brain is capable of producing new brain cells at any age, and so significant memory loss is not an inevitable result of aging. But just as it is with muscle strength, you have to use it or lose it. Your lifestyle, health habits, and daily activities have a huge impact on the health of your brain.
In the past, scientists looked for a single theory that explained aging. There are two main groups of aging theories. The first group states that aging is natural and programmed into the body, while the second group of aging theories says that aging is a result of damage which is accumulated over time. By understanding and describing how we age, researchers have developed several different theories of aging. The two categories are: programmed theories and error theories.
Programmed Theories assert that the human body is designed to age and there is a certain biological timeline that our bodies follow. The evidence supporting this theory is that there is not a great deal of variation in lifespan within species. Elephants die at around 70 years old, spider monkeys die at around 25 years old and humans die around the age of 80, on average. Some changes can be made based on nutrition, medical care and other demographic factors, but overall lifespan within species is fairly constant. The programmed theory is further supported by mutant variations of Drosophila and rodents that produce long-lived progeny (Martin & Loeb, 2004; Trifunovic et al, 2004), as well as by human genetic defects such as Werner's syndrome and other forms of progeria (accelerated ageing). Apoptosis—the programmed and intrinsically released death of cells—is also known as a characteristic and absolutely necessary phenomenon of normal growth and development (Höffeler, 2004; Brenner & Kroemer, 2000). These examples clearly show that death has a programmatic character in many, if not all, living organisms. The programmed theory asserts that if aging were due to wear and tear, there would be more variation in lifespan within each species, but within a species the potential lifespan is relatively constant (Prinzinger, Roland. Programmed ageing: the theory of maximal metabolic scope. EMBO Rep. 2005 July; 6(S1): S14–S19.) The Error Theories, which are, the wear and Tear, the Rates of Living, and Cross-Linking theories, assert that aging is caused by environmental damage to our body's systems, which accumulates over time. Wear and Tear Theory states that Cells and tissues simply wear out. DNA undergoes continual damage throughout life, due to various reasons. DNA damage leads to malfunctioning of genes, proteins, cells and deterioration of tissues and organs. Our ability to repair certain types of DNA damage is directly related to our life span. The rate of living theory of aging states that people (and other living organisms) have a finite number of breaths,heartbeats or other measures, and that they will die once they've used those up. the faster an organism uses oxygen, the shorter it lives, this theory is the oldest theories that attempts to describe why organisms (including humans) actually age. In ancient times, people believed that just as a machine will begin to deteriorate after a certain number of uses, the human body deteriorates in direct proportion to its use. The modern version of this theory recognizes that the number of heartbeats does not predict lifespan. The Cross-Linking Theory states that Cross-linked proteins accumulate and slow down body processes resulting in ageing. In a process called non-enzymatic glycosylation, glucose molecules attach themselves to proteins resulting in a chain of chemical reactions. This causes protein cross-linking, thus altering their biological and structural roles. Cross links (known as advanced glycosylation and products AGEs) toughens the tissues and may result in stiffening of connective tissue, hardened arteries, clouded ages, loss of nerve function and less efficient kidneys. Scientist still cannot agree on what causes our bodies and minds to change with age, but as long as humans are living there will continue to be studies to try and figure out what makes our bodies and minds change. (Aging Under the Microscope; National Institutes of Health, National Institute of Aging.) But with all being said, aging and dying are inevitable, but there are things you can do to improve your chances of living a long and healthy life.
Late adulthood is the stage of life from the 60s onward; it constitutes the last stage of physical change. As stated earlier the average life expectancy in the United States is around 80 years; however, this varies greatly based on factors such as socioeconomic status, region, and access to medical care. In general, women tend to live longer than men by an average of five years. As we age, our body's organs and other systems make changes. These changes alter our susceptibility to various diseases. Researchers are just beginning to understand the processes that cause changes over time in our body systems. Understanding these processes is important because many of the effects of aging are first noticed in our body systems. The body changes with aging because changes occur in individual cells and in whole organs. These changes result in changes in function and in appearance. Bones tend to become less dense. Thus, bones become weaker and more likely to break. In women, loss of bone density speeds up after menopause because less estrogen is produced. Estrogen helps prevent too much bone from being broken down during the body’s normal process of forming, breaking down, and re-forming bone. Bones become less dense partly because they contain less calcium (which gives bones strength). Ligaments, which bind joints together, and tendons, which bind muscle to bone, tend to become less elastic, making joints feel tight or stiff. These tissues also weaken. Thus, most people become less flexible. Ligaments tend to tear more easily, and when they tear, they heal more slowly. These changes occur because the cells that maintain ligaments and tendons become less active. The amount of muscle tissue (muscle mass) and muscle strength tend to decrease beginning around age 30 and continuing throughout life. Some of the decrease is caused by decreasing levels of growth hormone and testosterone , which stimulate muscle development. Aging effects reduce muscle mass and strength by no more than about 10 to 15% during an adult's lifetime. More severe muscle loss (called sarcopenia, which literally means loss of flesh) results from disease or extreme inactivity, not from aging alone. Most older people retain enough muscle mass and strength for all necessary tasks. The heart muscle thickens with age as a response to the thickening of the arteries. This thicker heart has a lower maximum pumping rate. Despite these changes, a normal older heart functions well. Differences between young and old hearts become apparent only when the heart has to work hard and pump more blood—for example, during exercise or an illness. The maximum capacity of the lungs may decrease as much as 40 percent between ages 20 and 70. The muscles used in breathing, such as the diaphragm, tend to weaken. The number of air sacs (alveoli) and capillaries in the lungs decreases. Thus, slightly less oxygen is absorbed from air that is breathed in. The lungs become less elastic. In people who do not smoke or have a lung disorder, these changes do not affect ordinary daily activities. As the brain ages, some of the connections between neurons seem to be reduced or less efficient. This is not yet well understood. (University of Maryland Medical Center: Aging changes in organs - tissues - cells). Biological ageing affects everybody. It is a deleterious process, which affects the functioning of the cells, tissues, organs and finally the organism itself.
Of course genes and luck have a lot to do with how well one ages. Aging from early to late adulthood has an interconnected negative impact both mentally and physically on the human body but physical activity can help protect against cognitive decline. Physical changes as the body ages from early to late adulthood are predictable and undeniable. Physical Development depends on maturation, or the biological unfolding of growth. Every individual has a schedule built into his or her genes that controls both the timing and degree of physical growth and decline.

References
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“Many of the intricate pathways of apoptosis that instruct a cell to kill itself involve the convergence of key proteins on the membranes of mitochondria. Such proteins induce the permeabilization of mitochondrial membranes and the release of caspase enzymes and nuclease activators that set in motion the final stages of programmed cell death. Now, as Brenner and Kroemer discuss in their Perspective, a proapoptotic transcription factor called TR3 has been found to move from its normal location in the nucleus to the mitochondria and to promote release of cytochrome c, a key event in apoptosis (Li et al.)”
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Trifunovic A et al. (2004) Premature ageing in mice expressing defective mitochondrial DNA polymerase.Nature 429: 417–423 “Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in a variety of tissues during ageing in humans, monkeys and rodents. These mutations are unevenly distributed and can accumulate clonally in certain cells, causing a mosaic pattern of respiratory chain deficiency in tissues such as heart, skeletal muscle and brain. In terms of the ageing process, their possible causative effects have been intensely debated because of their low abundance and purely correlative connection with ageing. We have now addressed this question experimentally by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase. Here we show that the knock-in mice develop an mtDNA mutator phenotype with a threefold to fivefold increase in the levels of point mutations, as well as increased amounts of deleted mtDNA. This increase in somatic mtDNA mutations is associated with reduced lifespan and premature onset of ageing-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature of the spine), osteoporosis, anaemia, reduced fertility and heart enlargement. Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals.”

University of Maryland Medical Center: Aging changes in organs - tissues - cells