factor in the deficits of memory and new learning that characterize Alzheimer's, if not the primary factor. The question that would remain, of course, is what gives rise to the vascular disease that causes these disabilities.

Genetic factors currently offer an exciting line of research into Alzheimer's disease. Recent success in locating the genetic region for another degenerative neurological disease, Huntington's chorea, has fostered the hope of a similar discovery for Alzheimer's. It appears that some families may have a gene on chromosome 21 that is associated with Alzheimer's disease. Another group of families among whom the disease develops later in life may have an affected gene on chromosome 19. Still other families in which Alzheimer's disease appears to be genetically based, however, show no evidence of an association with either chromosome. It seems likely that more than one gene can cause Alzheimer's disease, and the number of cases that are mainly genetic in origin remains uncertain.

A different sort of genetic lead comes from the observation that Down's syndrome, which is known to be caused by a mutation of chromosome 21, takes the form of mental retardation followed by dementia. The specific mutation is the existence of three chromosomes (or three copies of part of the chromosome) instead of the usual two, but the molecular biological mechanisms by which this surplus affects mental functioning are not yet understood.

An added reason to look at chromosome 21 is that the gene that codes for amyloid—the protein contained in senile plaques— is located there. Affected patients in a few families with Alzheimer's disease have shown a consistent defect in their amyloid gene. The normal aging human brain also contains amyloid, and the walls of blood vessels bear a similar material; some researchers have suggested therefore that the amyloid found in plaques is transported there from other, “healthy” sites. The mechanism for this process, which would involve a defect in the breakdown of amyloid from a larger precursor molecule, is under investigation by Dennis Selkoe, of the Harvard Medical School, and others.

Another explanation proposes that the low levels of acetylcholine observed in Alzheimer's disease could be an analogue to the low levels of another neurotransmitter, dopamine, ob-

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