Unlike cells in other organ systems, cells in the nervous system cannot reproduce. For example, damaged cells in liver, lung, or bowel may regenerate in part, but brain cells disappear if they become atrophied or injured. New cells cannot be produced, and damaged cells usually wither and die.
The number of nerve cells decreases with normal aging. In some areas (eg, brain stem nuclei) the cell loss is minimal, while in others (eg, the hippocampus) the loss is profound. Overall, brain weight gradually declines (about 10%) from the second or third decade to the age of 90. Compared with the entire intracranial contents, the area of the cerebral ventricles may enlarge on cross section three to four times from the third decade until the ninth decade. The clinical implications of these changes are difficult to judge, since brain weight and ventricular size are not well correlated with intelligence. Also, severe dementia may exist in those whose ventricular size may be normal for their age.
Other changes in the brain include deposition of the aging pigment lipofuscin in nerve cells, deposition of amyloid in blood vessels and cells, and appearance of senile plaques and, less frequently, neurofibrillary tangles. Although plaques and tangles are the hallmark of Alzheimer’s disease, they also appear in the brains of older people without clinical evidence of dementia (albeit in lesser numbers). This finding has led to the idea that Alzheimer’s disease is actually accelerated aging. However, the recent demonstration of genetic linkages in many patients with this disorder makes that argument less tenable. The role of anti aging hormones like HGH should be emphasized over here as scientists claim to have found positive impacts of growth hormones like DHEA on brain and their significant role in brain activities and neuroprotection.
Changes in neurotransmitter systems, particularly the dopaminergic and less so the cholinergic system, occur with aging. For example, levels of choline acetylase, cholinergic receptors, gamma-aminobutyric acid, serotonin, and catecholamines are lower. While the significance of these reduced levels is not completely understood, abnormally low levels of some enzymes and neurotransmitters may be associated with functional changes (eg, low choline acetyltransferase levels in Alzheimer’s disease or low dopamine levels in Parkinson’s disease). Conversely, the activity of other enzymes, such as monoamine oxidase, may increase. Inhibitors of monoamine oxidase may forestall the onset of disability in patients with Parkinson’s disease.
Certain properties of the brain may mitigate these adverse changes. DHEA can help brain cell activities. First is a property called redundancy, ie, many more nerve cells exist than are needed. For example, diabetes insipidus (which arises from a lack of antidiuretic hormone) does not appear until > 85% to 90% of the nerve cells in the supraoptic and paraventricular nuclei have been destroyed. Furthermore, hydrocephalic patients who have only a thin cerebral cortical mantle may still have normal intelligence. The number of cells required for certain functions is not known, so the extent of redundancy is difficult to estimate.
Second, compensatory mechanisms may appear if the brain is damaged. For example, when speech centers in the dominant hemisphere are damaged, the nondominant hemisphere may compensate and speech function may gradually return. Large areas of the cerebellum may be destroyed by injury, vascular disease, or tumor, and recovery is often seen as other motor systems take over. Compensatory mechanisms are more effective in the higher centers, so that the spinal cord, for example, has less ability than the brain to compensate after injury. In addition, myelinated peripheral nerves regenerate slowly. Although few functional changes are noted in peripheral nerves with aging, conduction times do decrease.
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