It has been known for a while that the brains of people with the memory-robbing form of dementia are cluttered with a plaque made up of beta-amyloid, a sticky protein that accumulates in the neurons of the brain.
The big question, however, was whether this is a significant cause of the disease or a side effect.
Other suspects included tangles of a protein called tau; some scientists thought this was the cause.
Researchers at Harvard Medical School have begun to address these issues and look at what caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with two other forms of beta-amyloid did not cause dementia, which may explain why some people have beta-amyloid in their brains but do not show disease symptoms.
The injected rats had impaired memory function, especially for newly learned behaviors. When the mouse brains were inspected, the density brain cells was reduced by 47 percent with the beta-amyloid seeming to affect synapses, the connections between cells that are essential for communication between them.
If the results are confirmed in humans, they this discovery may lead to interesting new therapies to either remove, reduce or prevent the build-up of the particular form of beta-amylin that causes dementia.
News coverage from CNN
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