RIGHT: The Alzheimer's brain, seen from the front, shows considerable shrinkage. The grooves, called sulci (plural of sulcus), are wider and the gyri (plural of gyrus), are smaller. The ventricles, chambers containing cerebrospinal fluid, are larger. In early stages, short-term memory begins to deteriorate when the cells in the hippocampus degenerate. As Alzheimer's spreads through the cerebral cortex (the outer layer), judgement and language decline, and emotional outbursts may occur.
Courtesy Alzheimer’s Disease Research, a program of BrightFocus Foundation
For the first time, there's progress on this front. In July, 1999, Elan Corporation scientists reported that they had immunized mice against a fragment of the beta amyloid protein. Beta amyloid is the insoluble gook in the plaques which clog the brain in Alzheimer's. Despite some debate, many scientists think that amyloid plaques kill neurons.
In the Elan experiment, immunization prevented Alzheimer's from getting started in mice that were genetically programmed to get it. Intriguingly, the vaccination also seemed to reverse the brain pathology in older mice whose disease had already begun.
The researchers concluded that the vaccine caused mice to mount an immune response against beta amyloid. Elan has started recruiting 48 Alzheimer's patients for a study of the safety with the vaccine.
After numerous efforts to isolate the enzyme, scientists at Amgen, a California biotech firm, have apparently succeeded in finding the gene that makes the enzyme (see "Enzymes Point Way... " in the bibliography).
Rather than searching directly for a protein that would boost beta amyloid production, the researchers added several genes to a cell culture while monitoring beta amyloid production. After eliminating genes that simply boosted the raw material for beta amyloid, they found one that seems to make the long-sought enzyme.
With at least one enzyme identified -- more may be involved -- the next step is to search for chemicals that will inhibit it, reducing the level of destructive beta amyloid. That work is ongoing in university and industry labs.
Last October, Elizabeth Gould and Charles Gross reported that new neurons occurs in several parts of the cerebral cortex that are crucial for cognitive and perceptual functions (see "Neurogenesis in the Neocortex... " in the bibliography).
The results strongly imply that the same process occurs in humans, because monkeys and humans have fundamentally similar brain structures. If the all-important cerebral cortex can accept new neurons, then the idea of using stem cells to replace neurons becomes that much more plausible -- but still as much as a decade away from the clinic.
Can't wait decades? How 'bout some simple solutions for preventing this miserable disease?
|There are 1
2 3 4 5
pages in this feature.
Bibliography | Credits | Feedback | Search <! includeFile("/home/httpd/html/whyfiles/misc/copy2000.txt"); >