Haley’s Alzheimer’s Research
Haley took a position with the Alzheimer’s Center, a research center for Alzheimer’s disease, where he collaborated with a former graduate student of his. The NIH funded their research for five years, which used Haley’s technology to assess the differences of ATP, GDP and cyclic AMP-binding proteins in normal brains versus those with Alzheimer’s disease.”There were dramatic differences,” he says. For example, the enzyme creatine kinase, which is a fundamental enzyme, is 98 percent inhibited in Alzheimer’s patients. They also discovered that tubulin — a major brain protein that holds an axon in its extended form and controls the growth direction of axons and dendrites — is inhibited by more than 80 percent. In 1989, he published the paper2 “Aberrant guanosine triphosphate-beta-tubulin interaction in Alzheimer’s disease” in the Annals of Neurology, stating that “These results support the hypothesis that microtubule formation is abnormal in brains affected by Alzheimer’s disease.”Haley goes on to recount the story of how he got into trouble with the NIH when he decided to investigate the influence of heavy metals on Alzheimer’s susceptibility. A popular theory at the time was that Alzheimer’s was caused by aluminum toxicity. Using his technology, he was able to show that mercury was the only heavy metal capable of causing a normal brain to develop the same biochemical abnormalities — including abnormal tubulin — that you find in Alzheimer’s disease. Haley claims his research has since been replicated and confirmed. According to Haley, mercury causes the synaptic clefts to disappear and triggers the formation of neurofibrillary tangles, a major diagnostic hallmark of Alzheimer’s, by causing abnormal hyperphosphorylation of tau.