THE mental decline of Alzheimer鈥檚 disease may have a physical rather than a
chemical cause, say researchers at the University of Tasmania.
Most researchers are pursuing the idea that the plaques of amyloid protein
that form in the brains of Alzheimer鈥檚 patients are toxic. This poisoning
supposedly leads to the formation of abnormal tangles of other proteins in the
cytoskeleton, which gives nerve cells their shape. These tangles are thought
eventually to kill the cells.
But James Vickers and his colleagues suspected that the physical presence of
the plaques might be just as important. They used a needle to damage a small
part of rats鈥� brains and discovered that the changes this triggered bore a
marked resemblance to those in the brains of 20 patients in the earliest stages
of Alzheimer鈥檚 disease. Viewed under an electron microscope, it was found that a
cyto-skeletal protein called neurofilament had lost its normal string-like
structure and instead formed clumps and rings.
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The rats鈥� damaged neurons also started to sprout new extensions, in much the
same fashion as the cells surrounding plaques in the brains of Alzheimer鈥檚
patients. However, the rats鈥� brains did not have plaques.
Vickers speculates that plaques of amyloid protein set in train a cycle of
futile attempts at nerve cell regeneration, causing tangles of neurofilament
protein to form. 鈥淚t鈥檚 an elegant study,鈥� says Peter Schofield of the Garvan
Institute of Medical Research in Sydney. If Vickers鈥檚 theory is correct, it
might be possible to treat Alzheimer鈥檚 using drugs that stabilise cytoskeleton
proteins, such as the anticancer drug taxol.