BIOLOGY Volume 2 - A Guide to General Biology - 2004

15. HEALTH AND DISEASE

15.7. Ageing

Having reached sexual maturity, humans enter a phase of gradual physiological degradation. The changes occurring within the body lead to a decrease in Life expectancy and are referred to as ageing. Despite significant advancements in biology, The Nature of ageing remains not fully understood to this day. New and newer theories continue to be proposed to explain this phenomenon.

Ultimately, is death really so inevitable? People have long comforted themselves with the thought that sooner or later science will discover a way to slow down or completely halt age-related degradation. According to one theory, ageing is a sort of disease, a disruption of bodily Functions. Once humanity learns how to "cure" it, people will be able to live for a very long time—several hundred years. However, such a prospect raises numerous serious ethical issues.

Figs. 15.21 and 15.22 summarize some of the changes characteristic of the ageing process.

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Fig. 15.21. Changes occurring in the body during the ageing process. (After fig. 8.1, Philip Gadd (1983) Individuals and populations, Cambridge Social Biology Topics, CUP.)

Fig. 15.22. Changes in human physiological parameters during the ageing process. (From R. Passmore, J. S. Robson, A Companion to Medical Studies, vol. 2, Blackwell Sci, 2nd ed., 1980.)

15.7.1. Changes in the Brain

Unlike most Cells in our body, Neurons are incapable of division. As a result, the number of neurons in the Brain steadily declines with age. Its average mass at age 90 is approximately 10% less than at age 30. As a rule, this is accompanied by a decline in function, although the extent and nature of such age-related degradation in the absence of specific pathologies like Alzheimer's disease (see below) remain controversial. Overall, in most people, intelligence and memory weaken over the years, yet The ability to solve certain tasks requiring experience or creative thinking may actually increase. Memory deterioration manifests primarily in forgetting or poor recall of individual facts, whereas the connections between events—such as when carrying out daily routines or reading literature—older people are usually quite capable of reproducing. The main problem appears to be not the loss of accumulated information, but the acquisition of new information, although wide individual Variability is observed here as well.

Senile Dementia

Dementia is a form of mental degradation associated with physiological Changes in the brain. Certain intellectual functions, particularly memory, are gradually lost. Senile dementia is linked to the degradation of Nerve Cells during the ageing process and typically onset occurs after the age of 65. If similar changes occur earlier, it is referred to as presenile dementia.

In addition to the inability of Nervous Tissue to regenerate, other age-related factors can lead to senile dementia, such as arteriosclerosis or atherosclerosis, which impair Blood supply to the brain. Dementia can also result from brain trauma or stroke. Certain symptoms characteristic of it are observed in clinical depression, hypoglycemia, hypothermia, alcohol abuse, and hypothyroidism (reduced thyroid activity). However, nearly 80% of senile dementia cases are caused by Alzheimer's disease (see below). Another, though rarer, cause is the viral Creutzfeldt-Jakob disease ("mad cow disease").

Typically, senile dementia develops gradually: memory deteriorates first (especially for recent events), followed by a progressive decline in comprehension due to difficulties in following logical connections, and ultimately resulting in mental confusion. Irritability, emotional lability, and loss of behavioral control (aggressiveness, neglect of personal hygiene, antisocial behavior) are quite frequently noted. In advanced pathology, motor coordination becomes impaired—movements become slow, rigid, and clumsy. Towards the end of life, some individuals cease to move, speak, and apparently think altogether.

The risk of senile dementia increases with age. The probability of this condition after age 65 is about 10%, and after age 85, approximately 20%.

Alzheimer's Disease

This type of dementia was first described by the German physician Alois Alzheimer in 1907. He studied the brains of individuals who had suffered from dementia in old age. It turned out that under a Microscope, the brain tissues of such patients looked identical: their neurons were coated externally with protein plaques, while inside the neurons, protein deposits appeared as tangled neurofibrillary tangles. The patient's brain essentially shrivels due to neuron loss (Fig. 15.23), affecting two of its most vital regions—the Cerebral Cortex, responsible for consciousness, and the hippocampus, associated with memory and learning. Plaques and tangles, termed senile plaques, form as a result of the accumulation of unusual Proteins—amyloid-beta protein in the former case and abnormal tau protein overloaded with phosphate groups in the latter. Normal tau protein is a component of microtubules that form the neuronal Cytoskeleton. The Gene encoding the amyloid protein is located on chromosome 21. The presence of an extra 21st chromosome in individuals with Down syndrome leads to brain alterations similar to those seen in Alzheimer's disease.

Alzheimer's disease is difficult to diagnose because its symptoms resemble Other forms of dementia. The Diagnosis is usually confirmed only after autopsy and examination of brain tissue. Some individuals exhibit a hereditary predisposition to this disease. Furthermore, according to some data, high aluminum content in the diet contributes to its development.

Fig. 15.23. Computed tomography scans of the brain: left – affected by Alzheimer's disease, right – normal.

Nerve Conduction Velocity

Fig. 15.22 shows that with age, There is a slight but steady decrease in the conduction velocity of nerve impulses. One of the reasons for this may be impaired neurotransmitter synthesis.