Alzheimers

In 1995-1996 Dr. Marsh viewed pictures of brain tissue and thought of two possible explanations for the “holes” observed in the tissues.  Mechanism 1, the commonly accepted explanation, suggests the re-absorption of cells.   Mechanism 2, a new  hypothesis, is that the protein modifications from a primarily alpha-helical structure to a more beta-pleated sheet component, results in reduced solubility (as known from the foods sciences) and protein precipitation.  This thought led to a conclusion that Alzheimer’s disease could be a PRION disease, which was a novel thought in 1995-1996.

Dr. Marsh contacted the Alzheimer’s Foundation in St. Louis seeking collaboration to test brain tissue of deceased Alheimer patients for nitrogen content.  Mechanism 1 would yield a normal nitrogen balance.  Mechanism 2, however, should exhibit increased nitrogen content.  Information concerning the mechanism of the disease could yield valuable information in developing drugs to slow, stop, or reverse those mechanisms. 

This experiment was not funded.

Additional work was considered on PRIONs.  Considering the spheres of influence for vicinal water (link) of 50 to 100 molecular diameters improves the probability of molecular interactions which allow one Scrapie-form PRION to influence the structure of a native-form PRION by three orders of magnitude.  The article describing these calculations is in process.