Bill Gates in a recent GatesNotes post talks about how expensive and time consuming clinical trials for Alzheimer’s disease are. What I have been arguing is that a lot of chronic illnesses are due to dysregulations of epigenetic mechanisms. Aconitase 1 is an iron-sulfur enzyme in the citric acid cycle which is required to produce 2-oxoglutarate and also regulates iron metabolism. Many enzymes are iron dependent and 2-oxoglutarate dependent enzymes. In terms of epigenetic dyregulations dysregulation of TET enzymes, which demethylate DNA and Jumonji domain-containing proteins, which demethylate histones, are key. TET enzymes and Jumonji domain-containing proteins are iron and 2-oxoglutarate dependent enzymes. With aconitase 1 dysregulated TET enzymes and Jumonji domain-containing proteins will be dysregulated due to lack of availability of 2-oxoglutarate and dysregulation of iron metabolism. With TET enzymes and Jumonji domain-containing proteins dysregulated there will be epigenetic dysregulations. There, however, can be many different kinds of epigenetic dysregulations whereby many different chronic illnesses can develop. A key point is that all these diseases could respond to the same treatment. One six week trial of the supplements in schizophrenia could open up a pathway for a new treatment for Alzheimer’s disease. The evidence for dysregulation of aconitase 1 and dysregulation of epigenetic mechanisms in Alzheimer’s disease is strong. I recently published a paper, A disease-modifying treatment for Alzheimer’s disease: focus on the trans-sulfuration pathway on this subject. The treatment has been modified from what is the paper. Please see the Treatment page.