Aging is associated with multiple sensory and motor impairments, including hearing loss, poor eyesight, reduced muscle strength, and increased reaction time. In many cases, sensory-motor deficits involve changes in the transduction or output systems and the knowledge concerning senescence of the processing mechanisms permits compensation through adjuncts, such as hearing aids and corrective lenses. In contrast, senescence of the central nervous system mechanisms involved in cognition is not well understood, creating a challenge for treating the impairment in short-term memory and increased forgetting associated with normal aging. In addition, overlaid upon the memory deficits and response slowing, is dementia linked to Alzheimer’s or Parkinson’s disease. In considering the mechanisms of aging-related changes in cognitive function, several questions arise:
How do the cellular properties of neurons change during normal aging?
Do the changes represent the decline in neural function per se, or compensation for senescence of a more fundamental process?
Are these properties different from age-related disease, or is Alzheimer’s disease an inevitable consequence of a long life?
Certainly there is some interaction between diseases of the elderly and normal aging, because the appearance of these diseases increases with age. Nevertheless, there are important differences between the cognitive decline due to neurodegenerative ailments, which are more prevalent in the elderly, and memory deficits that arise in healthy elderly individuals. Unlike neurodegenerative diseases, cognitive changes associated with senescence are not linked to overt brain lesions or a significant loss of neurons [1, 2], although normal aging may be accompanied by some loss of neuronal elements, including changes in the branching of axons and in the number or size of synaptic contacts [3]. More important may be the fact that aging is associated with a shift in the timing or level of transmission through neural structures. The transmission properties of neurons and the functional connectivity between neurons determine the fidelity of sensory processing, computational capability, and the reliability of motor output. In turn, changes in transmission properties or functional connectivity can provide developmental control on the emergence of behavior, and may represent a mechanism for recording and integrating experience. As such, a decrease in transmission through a brain structure or a shift in the ability to modify synaptic connections could constitute a functional lesion that may form the basis for cognitive decline during aging.
Due to the invasive nature of studies that directly record cell discharges and synaptic responses from brain structures, it currently is not feasible to measure transmission properties in humans. Surface electrodes have been used, however, to detect and characterize age-related changes that may contribute to functional lesions. As humans age, the amplitude of sensory-evoked responses wane and the response latency increases [4]. Changes in the latency of transmission through sensory systems could contribute to age-related impairments in the temporal processing of sensory information [5, 6]. Studies in aged animals indicate that conduction velocity (i.e., the speed at which that an action potential travels down the axon) decreases for neocortical, cerebellar, and peripheral sensory and motor neurons [7–15]. The cause of this reduced conduction velocity is unclear, but it may result from alterations in the myelin sheath [16, 17].
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