"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Aluminosilicates -

General Information:

Wikipedia entry:
Dr. Ray Shahelien entry: 



If aluminosilicates are in themselves toxic to nerve cells, then the elimination of amyloid beta plaques may not be enough.  It may slow down the progression of AD, but not arrest it.  The body may in fact form Amyloid beta as a way of protecting the brain from the toxic affects of aluminosilicates.  But the band aid itself may eventually becomes a problem when iron (or other metal ions) attach to the AB.  Where do the so called "globulomers" come into play?  How are they formed?  Could the presence of the aluminosilicates cause the formation of the golbulomers? Or, could it be a chemical reaction that occurs on the surface of the AB with iron attached acting as a catalyst that not only forms toxic OH, but also toxic globulomers?  Also, what role does scyllo-inositol play, and how might ethanol consumption botch things up?  It would be informative to know if there is a relationship between ethanol consumption and AD, either promoting or inhibitting.  Apparently, there have been studies that show that red wine consumption is protective against AD.  It has been suggested that it is the red pigments or tannins.  But could it be the ethanol itself promoting the production of scyllitol in the brain?  In mice, adding scyllitol to their diet has been shown to dissolve (or cause the dissolution of) amyloid beta plaques.  But in humans, the body is capable of synthesizing scyllitol.  Ethanol consumption has been shown to cause high levels of scyllitol to accumulate in the CIS. Either ethanol disrupts the normal metabolic processes that scyllitol participates in, or it spurs the CIS to produce more scyllitol than normal.  If the latter is true, then moderate ethanol consumption should lead to the elimination of amyloid beta plaques.

Other interesting things to note:
 - Desferrioxamine, the iron (and aluminum) chelator has been proven to arrest the progression of Alzheimer's disease symptoms.  Do iron or other metal ions bound to beta amyloid plaques play an essential role in AD? Would deferasirox (Exjade) or myo-inositol hexakisphosphate (IP6 or InsP6)be as effective?
- Clioquinol, a antiobiotic and weak metal chelator, has been shown to halt AD progression and cause the eventual dissolution of AB plaues. How does this drug afftect globulomers, which appear to be separate entities from the plaques?  (Perhaps it reduces the Helicobacter pylori bacterial infection?)
-  Could AD be prevented in asymptomatic people by preventing the formation of aluminosilicates in the brain?  This could easily be accomplished by food supplements and/or dietary changes.  [What foods and/or supplements?]
- If aluminosilicate formation is the beginning of the AD process, is there a way to directly attack aluminosilicate?  Such substances as hydrochloric acid will disolve it, but in-vivo use of hydrochloric acid is impossible.  There may be other ways of attacking it.  Perhaps more complex compounds that are able to cross the blood-brain barrier are able to disolve aluminosilicates without causing the surrounding tissue damage. Another far-out thought is the use of modulated x-rays or microwave r.f. to impart enough energy to the aluminosilicate that it will disassociate, and the constituent parts will bind harmlessly with other materials (which would have to be made available before applying the energy). Aluminosilicates are essentially rocks that can not be removed from the brain by usual methods.
-  Could a mechanical pump (e.g. COGNIShunt®) be used to remove CIS fluids, and thereby provide a way to remove aluminosilicate precipitates from the CIS?]

Known sources:

Natural sources:





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Updated: July 2, 2012
Inception: July 2, 2012