Jul 15 2008
Piece of Alzheimer’s puzzle recently solved by Harvard Researchers !!!
Harvard Medical School researchers claim to have solved part of the puzzle of what causes Alzheimer’s’ disease. They conducted research on the plaque build-up that consists of a sticky protein called beta-amyloid. Also, studied are tangles of a protein called tau. Some experts suspect that tau is also involved in causing dementia. The research concludes that tau may not be involved.
Scientists have long debated whether this plaque build-up is the cause or just a side effect of Alzheimer’s. The Harvard researchers, led by the team of Dr. Shankar and Dr. Selkoe, were able to induce Alzheimer’s in rats by injecting them with one particular form of beta-amyloid. It turns out that there are three forms of beta-amyloid and just one of them causes disease symptoms. The rats injected with the other two forms of beta-amyloid did not go on to develop the disease. Their results may help explain why some individuals with beta-amyloid plaque in their brains do not show disease symptoms.
The researchers used brains of individuals with Alzheimer’s who had donated their bodies to science. Using extracts from their brains; they injected the brain
s of rats with the one, two or three-molecule beta-amyloid protein. The rats were also injected with tau (plaque). The researchers found that the rats injected with the two-molecule beta-amyloid went on to develop symptoms that are characteristic of Alzheimer’s patients.
The researchers reported that the rats injected with the two-molecule beta-amyloid protein had impaired memory function (especially for newly learned behaviors). The researchers also studied two-molecule beta-amyloid protein injections in mice and found that the density of their brain cells was reduced by 47 percent. The injection in the mice seemed to affect their brain synapses that connect between cells to communicate between them.
The Harvard researchers have solved the mystery as to why some people with severe beta-amyloid plaques never show symptoms of Alzheimer’s. Those who have the two-molecule beta-amyloid proteins go on to develop Alzheimer’s while those with the one and three-molecule beta-amyloid proteins are spared. It is hoped that their experiment will give focus to new research that will lead to a cure or a means to prevent Alzheimer’s in the near future.
The research was published in the online edition of the journal Nature Medicine.
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