Brain

Only a few examples of how aging affects the seven functions of the nervous system are presented, but they show the types of age effects that have been observed.

Obtaining information with the sensory systems. The neural means by which sensory stimuli are experienced involve multistage processes requiring high-quality representation of stimuli by the peripheral sensory apparatus, undistorted neural messages carried by action potentials into the brain, and accurate processing of the information by the central sensory systems. Disruption of any of these processes with age would have the potential to cause problems in the sensory domain. The sad truth is that our sensory abilities almost inevitably decline with age. The rate and severity of the decline may vary considerably among individuals and across sensory modalities within individuals, but few, if any, octogenarians possess the same sensory capacities they started out with. All the sensory modalities suffer with age, including hearing and the auditory system.

The term "presbycusis" or "presbyacusis" is typically used to describe the changes in hearing associated with aging. Whereas the most commonly mentioned manifestation of presbycusis is a loss of sensitivity for high frequency sounds, the types of hearing problems confronting older listeners extend to speech perception, hearing in noisy backgrounds, distorted loudness of sounds, and tinnitus ("ringing in the ears"). Presbycusis typically involves progressive damage to the inner ear: the cochlea (where acoustic events are ultimately translated to neural events) and the cochlear neurons (where sounds are coded as trains of action potentials and sent, via the auditory nerve, to the brain for processing). Damage to any part of the cochlea diminishes the amount and quality of auditory input to the brain, with deleterious effects on hearing.

It is in the CNS where the action potential–coded sensory information originating in the inner ear is somehow transformed into auditory perception and experience. The central components of the auditory system are threatened by two adverse correlates of aging. First, changes in the structure or function of the brain's neurons occur in the context of biological aging discussed above. Second, an otherwise "healthy" central auditory system may be secondarily affected by damage to the cochlea. It has been shown that, when certain central neurons are deprived of their normal synaptic input, physiological and anatomical changes are induced. The effects can produce additional hearing deficits. Because the altered neurons provide input to other neurons, the effects could spread. Because the central sensory systems of older individuals might be affected in two rather different ways, it is useful to differentiate two types of age-related central changes. The term central effects of biological aging (CEBA) refers to sensory changes stemming from age-related changes in neurons, metabolism, support systems, and so on. The term central effects of peripheral pathology (CEPP) also refers to sensory changes associated with modifications of neurons and neural circuits in the brain. However, these are secondary to the removal or alteration of peripheral sensory input. It would be expected that CEBA and CEPP often occur in combination, since many older people have some loss of receptor function as well as various CNS deficits.

Whether CEBA, CEPP, or both are at work, the changes that occur in the auditory CNS are multifaceted. Some neurons die off or come to perform less efficiently, becoming "sluggish" in their responses to sound. By contrast, other neurons come to respond more vigorously, probably because aging is accompanied by deficits in inhibitory neurotransmitters, which normally dampen the responses of neurons and prevent hyperactivity. A combination of these and other types of central changes are likely to contribute to difficulties that many older people have in understanding speech, even when it is loud enough for them to hear.

The storage of information (learning and memory).Research indicates that, to varying extents (according to individual differences, genotype, species, etc.), circuits and neurotransmitter systems relevant for learning and memory often exhibit deleterious changes with age; deficiencies in any of these can cause some sort of learning/memory deficit. Learning and memory involve modifications (plasticity) of synapses in neural circuits. For example, one type of synaptic change associated with learning is long-term potentiation (LTP): lasting changes in neural responses induced by situations similar to those involved with learning. Experiments have shown changes in LTP in hippocampus neurons of old rats that have learning deficits. Thus, in addition to the general types of changes that occur in aging nervous systems, processes specific to learning may be affected as well.

Production of behavior (movement, etc.). Whereas some of the age-related declines in motor skill are associated with a decrease in muscle mass and a loss of strength, the most important and interesting stories are found in the workings of the nervous system. A large portion of the nervous system is devoted to movement—deciding what to do, planning how to do it, and carrying it out. Each has been demonstrated to exhibit some degree of age-related change that might result in less effective movement. For example, the primary motor cortex is the major source of descending axons to the motor neurons of the spinal cord that control the muscles. Several studies have described abnormalities in the large neurons of the primary motor cortex of older brains, including a loss of dendrites and dendritic spines. In addition to the motor cortex, the basal ganglia (the next lower set of structures controlling movement) are involved in self-initiated, complex movements, the control of postural adjustments, and other aspects of motor behavior. The effects of damage to the basal ganglia are evident in the motor symptoms of Parkinson's and Huntington's diseases, disorders affecting these structures. Some of the mild motor disturbances that occur in healthy older people could be a consequence of less severe basal ganglia damage that has been observed during normal aging.

Modulation of behavior (emotion, arousal, stress).Our behavior varies constantly—up and down, this way and that way—in accordance with emotions, arousal, and biological clocks. One powerful modulator of behavior is stress: Various stimuli, events, or situations that are actually or potentially threatening (stressors) elicit activation of the sympathetic nervous system and a sequence of hormonal reactions, including the release of glucocorticoid hormones from the adrenal gland. Whereas the stress response is adaptive (e.g., it increases the probability of surviving dangerous situations), too much stress is generally considered to be a bad thing. Indeed, high blood pressure, suppression of the immune system, and exacerbation of diseases are known concomitants of stress. Thus, the relationship between stress and aging is potentially important. Moreover, there is evidence that, over time, glucocorticoids can actually damage the hippocampus, contributing to negative changes in the aging brain.