Niemann Pick Type C and Alzheimer’s ?

There may be many Alzheimer’s-like diseases.  It is my opinion that the root cause of Alzheimer’s disease is the loss of glutathione recycling and the release of mercury from its glutathione-bound form.  This “loose” mercury poisons all enzymes that contain sulfhydryl (reduced sulfur) groups at their active sites, which includes several phosphatases and kinases, one of which is cited in the Niemann-Pick article you linked.

Since collapse of the glutathione system is the hallmark feature of sudden infant death syndrome and autism, I refer to these as Alzheimer’s like diseases.  But SIDS has no known brain pathology (as separate from death, which could be a brain-specific pathology).  And autism has brain pathology which is very qualitatively distinct from Alzheimer’s disease.  But I predict that we will see “set differences” (in its mathematical meaning) among inhibited sulfhydryl enzymes in these, and other, conditions.

So, for example, for Alzheimer’s disease, there is a catastrophic change in the phosphorylation cycle in the brain.  The kinase enzymes, which phosphorylate enzymes, are dynamically balanced by the phosphatase enzymes, which de-phosphorylate enzymes.  The dynamics is metastable, flipping from an overphosphorylated state to an underphosphorylated state, because kinases phosphorylate phosphatases and kinases, and phosphatases de-phosphorylate phosphatases and kinases.  Some kinases increase their activity when phosphorylated, and others decrease their activity when phosphorylated.  Same for phosphatases.  So the system is always unbalanced, swinging through the average phosphorylation level and correcting towards the other way only after hitting a phosphorylation peak or trough.  In the brain, a subset of these phosphatases and kinases are sulfhydryl enzymes.  So when mercury escapes from glutathione, critical phosphatases and kinases are inhibited which selectively damages the dephosphorylation side of the metastable cycle, pinning it in an overphosphorylated state.  No more cycling.  Overphosphorylated tau protein accumulates and precipitates into neurofibrillary tangles.  This is a mid-term manifestation of Alzheimer’s disease.  Beta-amyloid precipitation is a late stage.

Although the mercury toxicity is not limited to the brain, only the brain has this metastable phosphorylation cycle, which among other things, tightens and relaxes the cytoskeleton.  So the brain shows unique toxicity and symptomatology from this pathology.  I suspect that in autism, the dynamic of immune-mediated feedback between the gut and the brain is selectively sabotaged.  In SIDS, the babies die suddenly, so we don’t know the extent or selectivity of symptoms.  But Archie Kalokerinos, MD (author of the excellent book Every Second Child) was able to prevent 99% of vaccination-induced SIDS by post-vaccination injection of vitamin C, which stabilizes the glutathione system against overload by mercury and/or immune-mediated inflammation.  This is the basis for my recommendation of pre- and post-vaccination C for infants, children and adults facing vaccinations of any kind.

In Pick disease, only one kinase may be malfunctioning.  But this appears to be sufficient to produce Alzheimer’s like symptoms, although there may be an entirely different pathway for the pathology that results.  I suggest that this might be a sub-set of the enzyme inhibition of Alzheimer’s disease that I mentioned above.

If so, the same therapies outlined in my YouTube presentation could be helpful.

The compartmentalization of the glutathione redox crisis on one or both sides of the blood-brain barrier could also be a major confusing factor regarding symptoms.  Many people with Alzheimer’s disease do not seem to have much body pathology.  On the other side, teens with idiopathic dilated cardiomyopathy do not seem to have mental symptoms at all, at least until the acute moment of sudden death (like SIDS?).

That’s all for now.  Please feel free to circulate this email in any way you want.  —Steve