Although a specific gene has not been identified as the cause of late-onset AD, one predisposing genetic risk factor does appear to increase a person’s risk of developing the disease. This increased risk is related to the apolipoprotein E (APOE) gene found on chromosome 19. APOE contains the instructions needed to make a protein that helps carry cholesterol in the bloodstream. APOE comes in several different forms, or alleles. Three forms—APOE ε2, APOE ε3, and APOE ε4—occur most frequently.
•APOE ε2 is relatively rare and may provide some protection against the disease. If AD does occur in a person with this allele, it develops later in life than it would in someone with the APOE ε4 gene.
•APOE ε3 is the most common allele. Researchers think it plays a neutral role in AD—neither decreasing nor increasing risk.
•APOE ε4 occurs in about 40 percent of all people who develop late-onset AD and is present in about 25 to 30 percent of the population. People with AD are more likely to have an APOE ε4 allele than people who do not develop AD. However, many people with AD do not have an APOE ε4 allele.
We see that the NIH will not tell the truth about the APO proteins and that they know how the APO's determine how much toxic metal a person can excrete. The article above is from 2004, while David Kirby was probably writing his book. One would think that Kirby, JB Handley and the lying scoundrels at Age of Autism would be aware of this information and would see that if 25 to 30 percent of the population can not excrete any mercury or aluminum, that it is a key factor in autism. Yet, these liars refuse to mention it.
Dishonest scientists who do Alzheimer's research abet the NIH by not admitting what is known about the function of the APO proteins. Age of Autism, Kirby and Handley also abet this twisting of important information by ignoring it.
Will this help any parents wake up to the fact that Age of Autism, Kirby and Handley are leading them astray? I can only hope.