Non-Invasive 6-Minute Screening of Pre-Alzheimer’s Disease By Estimating Amount of Acetylcholine,β-Amyloid (1-42),Al,Hg & Pb of the Brain,and the Safe & Effective Treatment of Pre-Alzheimer’s Disease Using the “Selective Drug Uptake Enhancement Method”

Abstract

In pre-Alzheimer and Alzheimer’s disease it is well known that among characteristic abnormal findings in the brain, the following factors are included: 1) Marked decrease in Acetylcholine, 2) Excessive deposit of Al, 3) Excessive deposit of β-Amyloid (1-42). Using the Bi-Digital O-Ring Test Resonance Phenomena between 2 identical substances it has been possible to non-invasively study abnormal changes in Neurotransmitters such as Acetylcholine, Serotonin, Dopamine as well as β-Amyloids, Al, Hg, and Pb since 1990. According to our clinical study in the majority of normal individuals Acetylcholine in most parts of the brain including the Hippocampus area is at least 1,500 pg but most individuals develop recognizable symptoms when Acetylcholine is reduced to less than 500 μg. But in pre-Alzheimer’s patients amount of Acetylcholine often goes down below 300 pg. In all the pre-Alzheimer’s patients wherever Acetylcholine reduces in the brain, corresponding deficiencies show up as a recognizable symptoms, characterized by the dysfunction of the anatomically specific location in the brain. Metals, particularly Al and Hg, is often increased significantly anywhere between 350mg to 550mg with or without significant increase in Pb deposit, when excessive metal deposit exist Acetylcholine is almost always reduced. When β-Amyloid (1-42) increases beyond 3 or 4 ng with decreased Acetylcholine often the patient shows various degrees of short term memory deficiency. When β-Amyloid (1-42) increases over 8 ng the patient often shows a recognizable deficit of short term memory. Based on these findings the author established criteria to screen pre-Alzheimer disease quickly and non-invasively by measuring the amount of Acetylcholine, β-Amyloid (1-42), Al and Hg. As Reference Control Substances the author has been using slides of 500 μg Acetylcholine, 3ng β-Amyloid (1-42), 350mg Al and 350mg Hg for initial screening. Those who have a significantly reduced Acetylcholine can often be reversed by giving 100 mg of Cilantro tablet with the “Selective Drug Uptake Enhancement Method” (originally discovered by the author in 1990) deliver medication selectively to the brain by stimulating organ representation area of the entire brain on first segment of the middle finger of both hands, continuously stimulating at least 20 or 30 minutes to deliver Cilantro selectively to the brain. When the First segment (which represents the entire brain and face)of the middle finger of both hands is stimulated continuously and effectively more than 20-30 minutes, the amount of the Al, Hg, or Pb reduces to about 10% or even lower of the original excessive amount, which was anywhere between 350mg to 550mg. However, Selective Drug Uptake Enhancement Method becomes effective only when the ipsolatcral side of the accurate organ representation area corresponding to the pathological area is stimulated effectively, can the drug can be selectively delivered to the pathological area to be treated. When this happens Acetylcholine often increases anywhere from about 20% to 100%, but β-Amyloid (1-42) usually did not decrease significantly by removing excessive metal deposit.. Even when Acetylcholine increases over 500 μg and goes up close to 1500 μg, if β-Amyloid (1-42) remains high usually very little improvement of short term memory can be observed. In these patients often multiple bacterial and viral subclinical infection co-exist. Among the most commonly seen causes of the infection include Cytomegalo virus, Human Herpes Virus Type 6, Chlamydia Trachomatis, Mycobacterium Tuberculosis, and Pseudomonis Aeruginosa and α- Streptococcus. While we are treating these infections in the brain, after removal of excessive metal deposit is essential before treating infections effectively, as an excessive deposit of metal often inhibits effectiveness of anti-bacterial and anti-viral agents. While studying the effect of the treatment of these multiple subclinical mixed infections of the brain in 2001, the author discovered that when strong Chlamydia Trachomatis infection in the brain is significantly reduced, β-Amyloid (1-42) also markedly reduced, which resulted in significant improvement in short term memory deficiency provided that Acetylcholine has also been sufficiently increased after removing excessive metals. It is also interesting to note that those people with increased β-Amyloid (1-42) in the brain often develop so-called brownish age spots around the side of the face. The author found in this darkened pigmented area, both β-Amyloid (1-42) and Chlamydia Trachomatis are markedly increased as in the brain. In conclusion, our study indicates that the major cause of increased insoluble β-Amyloid (1-42) peptide in pre-Alzheimer’s patient is due to extensive Chlamydia Trachomatis infection of the brain, particularly in Hippocampus area. Therefore once pre-Alzheimer’s disease is detected by this method, increased β-Amyloid (1-42) peptide can be reduced significantly by treating Chlamydia Trachomatis with Doxycycline along with EPA & DHA as an effective anti-viral agent, as most of the patients have simultaneous viral infections. In order for the treatment to be effective, you first have to remove the excessive metal deposit using the Selective Drug Uptake Enhancement Method with Cilantro, and then treat with EPA & DHA and Trimox if there is additional viral and bacterial infection this treatment often increases Acetylcholine and then follow up the treatment of Chlamydia Trachomatis by Doxycycline and other compatible medications since Doxycycline is the effective antibiotics against Chlamydia Trachomatis, but it is compatible with EPA & DHA and Trimox, while other antibiotics such as Erythromycine or Azithromycine is not compatible with EPA & DHA and Trimox.