Alzheimer's Reversal #7 of 9

Transcript

We get to the point where the Alzheimer's Cascade goes mainstream where it becomes recognizable as Alzheimer's Disease by doctors and researchers microtubules are assembled from Alpha and beta tubulin proteins using GTP as the energy source first GTP is used to assemble dimers then another GTP is used to assemble each dimer pear into multiple strands 13 of which spontaneous into each microtubule microtubules serve as a transportation that work just like a highway system where semi tractor-trailers Hall groceries from a central warehouse to local supermarkets microtubules are polarized meaning that they have Direction and always point from the nucleus of a neuron down the axons and dendrites to the nerve terminal in other words from the central warehouse to the neighborhood stores there are two kinds of semi tractor trailers the Kennison motor proteins attached to the microtubule facing forward and moves outbound material from the nucleus to the terminus the dining motor protein attaches backwards and moves other materials inward bound towards the nucleus beta tubulin contains multiple so Hydro groups two of which are immediately adjacent to the active site for GTP binding in the presence of mercury GTP binding is inhibited and microtubule assembly is prevented this Toxic effect of mercury also disassembles assemble microtubules into 2 billion pieces beta tubulin binding is known to be inhibited and Alzheimer's disease GTP binding by Beta tubulin is also known to be inhibited by root canal teeth this not well-known finding suggests that a Comprehensive Dental evaluation by a practitioner armed with a beta tubulin sensitive as he should become a high-priority part of an overall clinical evaluation for Alzheimer's disease it also suggests that people interested in prevention should either avoid root canal procedures in favor of extraction or use more sophisticated root canal procedures utilizing ozone to sterilize Dental tubules of anaerobic bacteria and calcium oxide slurries to fill Dental tubules one of the supplemental slides at the end of this presentation has additional details about one known root canal neurotoxin one last item there is test tube evidence that mercury toxicity towards microtubules is aggravated by zinc the clinical imported this finding is not clear but additional details of this finding are presented in one of the supplemental slides at the end of this presentation there are other Alzheimer's disease related phenomena that relate to Mercury toxicity that we have yet to discuss this will begin with Tau protein one of the most important of the Alzheimer's phenomena that have not yet been mentioned are neurofibrillary Tangles which are made up of microtubules Associated Tau protein these Tangles are visible under microscopes and are one of the Hallmarks signatures of a post-mortem Alzheimer's diagnosis done at autopsy the Tau protein in these Tangles has been determined to be over phosphorylated which is a midterm manifestation of Alzheimer's disease caused by earlier to stabilization of the kinase phosphatase enzyme systems that have already been mentioned one of the most well-known manifestations of Alzheimer's disease is beta amyloid plaque which is predominantly made up of beta-amyloid protein this plaque is well-known because it is highly conspicuous under microscopes a dominant feature at autopsy and was one of the first signs identified as being associated with Alzheimer's disease however beta amyloid plaque does not accumulate until later stages of Alzheimer's disease and is therefore not likely to be causal influence in the underlying pathology a far more important factor that is critically associated with Alzheimer's disease risk is inflammation however this subject will be postponed for more detailed discussion later in the presentation another risk factor that is well-known is the genetic risk from apoe although apoe genotype is probably not anywhere as important as inflammation it is hypothesized to have a direct bearing on Mercury status and is therefore intimately tied to the theme of this presentation there are three variations of the apoe gene in humans we get one apoe gene from each parent so we each carry to a Bowie jeans apoe3 is by far the most common form and roughly 90% of the population carries one copy of the apoe 3-g and roughly 60% carries to a Poe III jeans there are two less common variant a poet jeans apoe2 which is protective regarding Alzheimer's risk and apoe4 which increases risk so on the chart of all possible combinations of these jeans from your mother and father having two of the high risk jeans has the earliest onset having only one of the high-risk Gene is the next earlier onset having to medium risk jeans or one high risk in one protective Jean gives even later on set and having one protective and no high-risk Gene provides the latest age of onset having two protective jeans would presumably be even later on set but that is so rare that there is no statistical evidence to prove it yet regardless the risk is oriented diagonally across the chart the apoe genes code for a protein which is made up of a chain of amino acids when the amino acid sequences of these proteins are compared all but two of them into acids are identical the two that are different light positions 112 and 158 on the chain the protective protein has two systems at these positions the most common a poet protein has 116 and when Arginine and the high-risk protein has two argentines at these positions the amino acid cysteine contains the self Hydro group just like glutathione is it possible that these cysteine residues could bind to Mercury and decrease the brain's Mercury burden the correlation seems too perfect for this not to be the case the arrows for cysteine and the Alzheimer's risk are exactly identical now let's return to a more detailed discussion of inflammation this concludes the genetic discussion