ally microscopic lesions in the brain that contain a starchlike protein known as amyloid.

But McKhann is no longer satisfied with the conclusions of the report, which he now considers “rather myopic”—that is, too closely focused on the visible pathology of plaques and tangles. He believes instead that what is called Alzheimer's disease may not be a single entity at all and that using this simple name may in fact limit the thinking of some researchers, implying as it does that what is sought is the identity of a single disease-causing mechanism. An alternative explanation of the same clinical observations may be that several regions of the nervous system are involved, each one vulnerable to different factors. Combinations of these factors at work could give a clinical picture that is sufficiently similar, enough of the time, to hold together under the heading of Alzheimer's disease.

In the end stage of Alzheimer's, perhaps 5 to 10 years after the onset of disease, the brain shows some degeneration of the frontal and temporal lobes, particularly in the hippocampus, an area involved in short-term memory. Medical imaging reveals a significant loss of neurons, and an even greater loss of synapses—which may provide a better explanation for dementia than the tangles and plaques do. For that matter, the question of what causes dementia has any number of possible answers, most of them exceedingly difficult to disprove. There is even the possibility that such features as loss of short-term memory and reduced ability to learn are just a variant of normal aging. After all, the affected portion of the population forms a steady upward curve on epidemiological graphs. Perhaps everyone would eventually suffer dementia if they lived long enough. Since this theory is not provable, however, it is well to consider other possible causes of dementia. Among those suggested recently have been excitatory amino acids that exert a harmful effect, some form of infectious slow virus, the presence of toxic metals in the brain, vascular disease, timedelayed genetic programming, or some combination of these factors.

Excitatory amino acids can indeed cause severe deficits in the brain, including loss of memory. A dramatic illustration came recently from eastern Canada, where a number of people

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