Alzheimer's Symptom Reversed in Mice
> 8/3/2007 1:29:38 PM

Alzheimer's disease is still not fully understood, but one prominent theory posits that neural degeneration is caused by excess amyloid beta. While not harmful in small doses, amyloid beta can form a debilitating "senile plaque" around neurons if too much of it interacts with the ABAD enzyme. Dr. Frank Gunn-Moore, leading a team of researchers from Saint Andrews University, has found a way to prevent this dangerous interaction.

Dr. Gunn-Moore began by making elaborate computer models of the shapes of amyloid beta and ABAD, looking for an easy tactic for interfering with the way that they join. Moving from theory to the laboratory, he was able to synthesize an inhibitor that blocks amyloid beta from attaching correctly in mouse brains. Senile plaque is large enough to view under a microscope during routine autopsy, so it was easy to see that its production was truly being reduced. However, because the role of amyloid beta in Alzheimer�s is not entirely agreed-upon, Dr. Gunn-Moore looked for an additional indicator that his inhibitor was having a definite effect upon the course of the disease. For this purpose, he monitored peroxiredoxin II levels, which have a specific pattern correlated to Alzheimer�s progression. Use of the inhibitor returned peroxiredoxin II levels to normal.

The new inhibitor sounds promising enough that the Alzheimer's Research Trust extended their grant to allow three more years of research. It seems that rogue protein blocking medication, which we discussed hopefully a few months ago, may soon become a reality. While amyloid beta buildup may not be the only cause of Alzheimer�s, it is certainly either one cause or at least a damaging symptom of the disease. Any reduction of neuron death would be celebrated by the millions of families worldwide who are watching their relatives slip away.

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