But to the extent that they work, they work only in the early stages of the disease. And they are temporary solutions at best. Thus far, no treatment has been found to cure the disease or to slow its progression. In the last two decades criteria for diagnosing AD have become stricter, and ways of imaging the brain hold out the promise of even more accurate diagnoses. Between 1991 and 1995, new molecular cloning techniques made it possible to identify defects called mutations associated with AD in four genes.
Genes exist to make proteins, which direct all of the workings of the body.
The first finding in AD genetics was the discovery that a mutation in the gene that makes the so-called amyloid precursor protein results in overproduction of the protein. Research in the 1980s on families in which AD struck at an early age helped to locate this gene on chromosome 21 in 1991. Genes to account for the remaining cases of early-onset AD remain to be identified. One form of a fourth gene, called ApoE, does not always cause AD but can increase a person's chance of getting the common version of the disease that occurs in people over 65. All people with Down's syndrome develop plaques and tangles by their 40s, which puts them at increased risk of developing dementia as their life expectancy increases.