Communication Problems

Although we used to believe that age-related decline in memory was caused by a cumulative loss of neurons, more recent research has taught us that this is not the case. Experts now believe that the changes in the brain that play the most prominent role in age-related memory decline all bear on the brain's networking capability—the transmission of information from point to point via neurotransmitters, receptors, and synapses.

A structural change found in nonhuman primates is a reduction in the number of dendritic spines in a type of neuron called pyramidal cells. Spines are the filament-like branches that extend from neurons and create synapses with other neurons. It is almost certain that a reduction in spines also occurs in most aging humans 46 as well. A loss of spines would directly cause a decrease in synap-

tic density, which, in turn, would diminish the degree of connectedness among neurons and thereby downsize the brain's information processing speed and capacity.

The loss of neurons in particular brain areas may hinder communication between cells by degrading the specific functions of those areas. The aging brain is vulnerable to loss of neurons in structures that produce neurotransmitters important for memory, including acetylcholine, dopamine, and serotonin. Fewer neurons in these areas can mean lower levels of these key neurotransmit-ters, leading to the type of problems that are familiar starting in middle age, such as trouble concentrating on and remembering what you're reading.

Let's take a closer look at other changes the brain undergoes beginning in middle age that interfere with the normal flow of information from neuron to neuron, making it harder for you to process information effectively, learn, and remember.

One is a change in the number and function of receptors, the docking points on neurons where neurotransmitters attach themselves when neurons send messages to each other. In several parts of the brain, there is a decrease in receptors for dopamine. Perhaps of greater importance is a decline in the function of receptors for NMDA (N-methyl-D-aspartate), which play a major role in helping the chemicals important for learning and memory move from one neuron to the next. The changes in NMDA are especially noticeable in the frontal cortex and the hippocampus, regions of the brain involved in declarative memories.

Another change that contributes to age-related memory loss is the development, starting around age sixty, of lesions in the brain's white matter, the bundles of axons that transmit messages throughout the brain and central nervous system. Psychologists in Scotland reported a unique longitudinal study in 2003 in which they compared the cognitive test scores of people at age seventy-eight with their test performance at age eleven. This comparison was possible because Scotland had conducted a survey of hundreds of eleven-year-olds in 1932 and kept the results on file in local health department offices. The tests assessed memory and learning, non- 47

verbal reasoning, processing speed, and executive functions (the ability to plan ahead and coordinate different tasks).

MRI scanning of the brains of the seventy-eight-year-olds revealed that people with the most extensive white matter lesions exhibited the steepest decline in cognitive abilities relative to their performance as eleven-year-olds. Especially fascinating, the extent of white matter lesions was a slightly stronger predictor of test scores of people at age seventy-eight than their earlier scores were. You can see the difference in Figure 4.1, which shows a brain MRI of an elderly person with minimal white matter lesions and a brain MRI of a person of the same age with extensive white matter lesions.

We don't yet have a way to prevent white matter lesions from forming in old age, but we do know that these lesions are more common in some people than in others. People with cerebrovas-

figure 4.1 White Matter

MRI of two age-matched (eighty-one-year-old) individuals, one with minimal white matter lesions (top two panels) and the other with extensive white matter lesions (bottom two panels). Lesions are present in the deep white matter surrounding the butterfly-shaped ventricles, appearing as light gray spots (on the left) and white spots (on the right). From C. R. Guttmann, R. Benson, S. K. Warfield et al., "White Matter Abnormalities in Mobility-Impaired Older Persons," Neurology, 54, 1277-1283.

48, Reprinted by permission of Lippincott Williams & Wilkins.

cular risk factors, including hypertension, high cholesterol, heart disease, and diabetes, are especially prone to white matter disease. To the extent that you can reduce your risk of these diseases, you may also be able to minimize the accumulation of white matter lesions in the brain—and preserve your memory and related functions. (I discuss this in more detail in Chapter 5.)

The fact that some people age more successfully than others is not surprising, and there is evidence of variability in the way our brains change with age. In a 2002 study at Stanford University, fMRI was used to measure the pattern of brain activation in three subregions of the frontal cortex during a memory task in young adults and two subgroups of elderly people. The subgroup of elderly people with worse memory performance exhibited decreased levels of activation in all three brain regions compared to the group of elders who demonstrated better memory performance. When compared to their young counterparts, the high-performing elders exhibited a similar pattern of brain activation in two areas and greater activation in the third area. This finding suggests that the

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