OUR APOLOGIES: IMAGES UNAVAILABLE

The next question we asked is whether there would be local neurotoxicity of the plaques that would cause the decreased metabolic rate. For that reason we measured the size of the Golgi apparatus in all of the cells where you see a point. The next step was to point out the presence of all the plaques. Next we measured the distance between the core of the plaque and the cells in which we measured the size of the Golgi apparatus. If the plaques would be locally neurotoxic as would be assumed by the cascade hypothesis, one would presume that cells which are nearby would suffer more from toxicity than cells which are far away, and that depending on the distance the metabolic rate would change. Well this is not what we found.

If you measure the size of the Golgi apparatus against those from the core of the plaque you can see that there is no relation whatsoever. If there was local neurotoxicity, then one would expect very low levels here going up to higher levels further away from the plaque. So again the metabolic rate and the presence of plaques seem to be independent. This is another point I mentioned already: cell death is a phenomenon that is only important in a couple of areas of the brain. Question was whether there is a local induction of cell death from the plaques in CA1. As you know from the work of Mark West, there is a lot of cell death in CA1. So we measured cell density in the area around the plaques, depending on the distance from the plaque core. What we found was that there was a small decrease in cell density around the plaque. However this could account for only 2% of the cell death. This means that if there is any cell death from plaques, it was negligible.