Several conclusions can be drawn from our review of selective changes in neural structural and function with aging. First, as we have stressed, compared to the types of brain-related changes observed in neurological and psychiatric disorders, the alterations seen in the brain with advancing age are modest. Almost all the measures of cognition, brain structure, and brain function that we examined showed essentially the same behavior: If change was found, it became worse after approximately 60-70 years of age. However, the variability in the old increased significantly, and often there were old subjects whose values on these measures were well within the range of those of young subjects.

Although much controversy exists in the research literature, some findings seem fairly consistent. The two areas of cognition that show clear declines with advancing age are some types of memory and measures of mental flexibility (i.e., fluid intelligence). Speed of cognitive and sensorimotor processing also seems to decline with age. Areas of the brain that demonstrate structural alterations include medial temporal lobe regions such as the hippocampus, the frontal lobes, regions within the basal ganglia, and a number of subcortical nuclei, such as the nucleus basalis of Meynert and the locus coeruleus, which are the sources of neuromodulatory neurotransmitters in the cortex. These transmitters play a key role in numerous cognitive processes, including memory and attention. There also seems to be an increase in the presence of white matter abnormalities with advancing age, although how this relates to alterations in cognitive performance is unclear.

Although we did not discuss in detail brain abnormalities associated with age-related neurode-generative disorders, the distinction between aging changes and disease-associated alterations was difficult for us to maintain. Long ago, it was thought that senescence was part of a continuum with dementia and perhaps also with movement disorder of the Parkin-sonian type. About two decades ago, the view changed to the notion that healthy brain aging could be distinguished from brain diseases, particularly those that lead to dementia. That is, there are changes that occur in the brain that are part of the aging process, but these are distinct from the changes due to specific brain disorders such as Parkinson's disease, cerebrovascular disease, and especially Alzheimer's disease. In our view, this distinction has become blurred. There are interactions between genetic risk factors for various brain disorders and environmental factors, such as diet, exercise, and education, that can modulate the neural changes associated with aging and brain disease. The estrogen example we presented earlier illustrates this point. Successful aging seems to be based on a sufficiently robust neuroplasticity that can keep dysfunction due to the aging and subclinical disease-related processes in check.

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