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6.11: Aging Changes in the CNS

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    Correlations between the alterations in reflexes, conscious sensation, and voluntary movements and age changes in the structure and functioning of the CNS are not well understood. The reasons for this ambiguity include (1) the necessity of studying brains obtained from autopsies, which have undergone variable degrees of postmortem changes, (2) the difficulty in determining how much, if any, disease was present in the brain or in other organs, and (3) the paucity of psychological or behavioral information about the people whose brains are studied. However, as these correlations become clear, it may become possible to influence the decreases in nervous system functioning caused by aging.

    Spinal Cord

    In the white matter, there is an age-related decrease in the motor neurons, especially of motor neurons that control somatic motor functions. These neurons carry anticipatory impulses and main impulses from the brain to lower somatic motor neurons in spinal cord gray matter. Within the gray matter, the average loss of motor neurons is approximately 25 percent during adulthood and into very old age. The rate is highly variable, and may be two to three times higher in some individuals. There seems to be a preferential loss of somatic motor neurons. This corresponds with the loss of motor units in muscles (see Chapter 8).

    Brain

    Dimensions

    Many studies report that there is a decrease in the size and weight of the brain as age increases. The fluid‑filled cavities inside the brain enlarge, the raised ridges (gyri) on the surface shrink, and the grooves (sulci) between the gyri become wider (Figure 6.7). (Suggestion 131.02.Figure 6.7)

    clipboard_e147dc45481b79b37653857d9d1e452f3.png
    Figure 6.7 Structure of aging (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

    How much of the age‑related shrinkage of the brain is due to aging and how much is due to diseases such as atherosclerosis has not been determined. One reason for the overall shrinkage may be a decrease in the number of neurons in several areas of the brain. The cause of this neuron death is not known, and there is no indication that what is considered to be a normal amount of overall shrinkage has any effect on brain functioning.

    Numbers of Neurons

    Some parts of the brain show a substantial decline in the number of neurons, and this may affect specific functions. In the cerebrum, these parts include areas that control voluntary movements, areas for vision and hearing, and possibly areas involved in other conscious sensations. Other parts of the cerebral cortex seem to lose few if any neurons. The cerebellar cortex, which coordinates muscle movements and controls many complicated muscle reflexes, and the basal ganglia, which are also involved in modifying muscle actions, lose many neurons (Figure 6.5, Figure 6.6).

    The regions of the brain other than the cerebral hemispheres and the cerebellum are referred to as the brain stem. The only regions of the brainstem that seem to lose neurons because of aging are the nucleus of Meynert, which produces acetylcholine for short‑term memory, and the locus coeruleus, which produces norepinephrine and helps regulate sleep (Figure 6.8).

    clipboard_e415c63952900a7aacf0de3db92b8bee7.png
    Figure 6.8 Regions of the brain – three views (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

    It has been suggested that neuron losses in these areas contribute to age‑related detrimental changes in the functions to which they contribute: voluntary movements, conscious sensation, muscle reflexes, memory, and sleep. However, there is no conclusive evidence that localized loss of brain neurons caused by aging has any effect on the functions performed by the areas that incur neuron loss.

    One reason why neuron loss may have no effect is that the remaining brain neurons can branch and produce many new synapses. The new neuron pathways created by the new synapses may compensate for the decrease in neurons. Second, there may initially be many more neurons in the brain than are needed, and these additional neurons may constitute a reserve capacity. Third, the loss of neurons may actually improve the brain by eliminating neurons that are not used or have made errors. The brain may be able to recognize and eliminate unused or undesirable neuron pathways and thus improve its efficiency. This process may constitute part of the development of wisdom.

    Neuron Structure and Functioning

    Many neurons remaining in the aging brain undergo several age changes. For example, the cell membranes of brain neurons become less fluid and stiffer. These changes may contribute to age‑related alterations in brain functioning by altering reception, conduction, and transmission. Second, internal membranes (e.g., endoplasmic reticulum) become irregular in structure, and many neurons have an accumulation of lipofuscin. The effects of abnormal amounts of lipofuscin are not known.

    A third change in brain neurons is the formation of neurofibrillar tangles. Normally, neurons contain long thin structures called neurofibrils. These structures are present in the cell bodies and extend down the axons. Neurofibrils seem to be important in the movement of neurotransmitters from their sites of production to the ends of the axon. The formation of tangled neurofibrils may mean that not enough neurotransmitter is reaching the end of the axon; this could result in a decrease in or an elimination of transmission by neurons with neurofibrillar tangles. The result would be a decrease in the functioning of synapses.

    Synapses

    Because most research on changes in brain synapses has been directed toward alterations caused by disease, the effects of aging are not well understood. For example, there may be dozens or even hundreds of different neurotransmitters in the brain, and much confusion and contradictory information exist about age changes in these. All that can be said at this point is that aging seems to cause decreases in some neurotransmitters in some areas of the brain. There are few or no cases where the amount of a neurotransmitter increases with aging.

    Information about age changes in the number of synapses in various brain areas is also incomplete. It is known that the number of synapses in an area may increase or decrease depending on how much use is made of that area. Neurons that are heavily used increase their number of synapses by growing new axon branches or new dendrites and dendrite branches (dendritic spines). The ability of neurons to do this decreases with age. There is also evidence that at least in some areas, neurons that get little use reduce their number of dendrites or dendritic spines and thus decrease the number of synapses in those areas of the brain.

    The interpretation of information about changes in the number of synapses is complicated because the effectiveness of synapses depends not only on their numbers but also on changes in their neurotransmitters and in the exact neuron pathways that are gained or lost. For example, many inefficient synapses may be replaced by a few efficient ones, resulting in an improvement rather than a decline in functional capacity.

    Adding to the confusion is the fact that synapses undergo age changes in structure as well as number. For example, though there is a decrease in the number of synapses in the precentral gyrus, the remaining synapses become broader. This may mean that these synapses work better and therefore compensate for those which are lost.

    Perhaps the best-known age change in synaptic structure is the buildup of the protein called amyloid. A mass of amyloid in a synapse is called a plaque. As with other age changes, different amounts of plaques develop in different areas of the brain. It is believed that plaques decrease the functioning of synapses. Normally, however, a person does not form enough plaques to alter brain functioning to a detectable degree.


    This page titled 6.11: Aging Changes in the CNS is shared under a CC BY-NC-SA 4.0 license and was authored, remixed, and/or curated by Augustine G. DiGiovanna via source content that was edited to the style and standards of the LibreTexts platform; a detailed edit history is available upon request.