Answer by Steven Fowkes:

This question has been asked and answered here on Quora.
And my answer is that the cure is already here.
The key research identifying the specific mechanism of Alzheimer’s disease, as distinctly different from other dementias, was conducted in 2001 by two groups of dental researchers, one at the University of Kentucky and the other at the University of Calgary. They identified the critical influence of mercury 2+ ion in the depolarization of marine snail neurons, which are big enough to easily see with a light microscope (you can find the video on YouTube).  The depolarization of the neural growth cone is caused by the inhibition of GTP binding by beta-tubulin, which is a sulfhydryl (SH-containing) enzyme. All enzymes have disulfide groups (RS-SR), but some (a small minority) have sulfhydryl groups (RSH) at their active sites. The beta-tubulin monomer for making neuronal microtubules is just one. This is the specific metabolic lesion that causes the disintegration of the neuronal transport system that is seen in Alzheimer’s disease. This neural highway system is necessary and essential to moving material from the nucleus of the neuron down the incredibly long axons and dendrites of the neurons to the nerve termini.
This is specifically important because all of the enzymes that are seriously inhibited in Alzheimer’s disease also contain a sulfhydryl group at their active sites. While it is possible that this is a fluke chance, so far it’s ten of ten that I have investigated. And zero exceptions. Ten enzymes that are seriously inhibited (50% or above), ten have sulfhydryl groups at their active sites.
The accumulation of tau protein is cause by the selective inhibition of a small handful of sulfhydryl-containing phosphatases and kinases, which freezes the 90 second phosphorylation cycle in an over-phosphorylated state. Over-phosphorylated tau protein results, which is the primary material of neurofibrillary tangles.
The control system for mercury ion is glutathione (GSH). Both glutathione and these AD-inhibited enzymes (RSH) have sulfhydryl groups (SH), but glutathione is plentiful. So the glutathione ends up operating like a mercury ion vacuum cleaner, protecting the tiny population of sulfhydryl enzymes from decimation. The loss of glutathione recycling is the pivotal metabolic lesion that transforms a pre-dementia or dementia-like condition into genuine Alzheimer’s disease.
This is straightforwardly reversible.
It’s complicated by the large numbers of clinical facets to glutathione recycling. If only one cause is treated in a study, only a small percentage of people with Alzheimer’s disease respond.
But clinically, it is a simple matter of triage to classify 1) those with hypothyroidism, 2) those with anaerobically infected root-canal teeth, 3) those with hypo-adrenalism, 4) those with heavy metal poisoning, 5) those with infections, 6) those with food allergies (IgM, IgG and IgA sensitivities), 7) those with coagulopathies, 8) those with COPD and respiratory conditions, 9) those with chronic inflammation, 10) those on statins, etc. And let’s not forget polypharmy.
I’ll come back and finish this later. Meanwhile, feel free to look into this, here on Quora, there on YouTube, or in the primary literature.
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Let me add that this answer is assuming that the reversal of Alzheimer’s disease involves a recent diagnosis or recent onset of symptoms. Unlike the neurological damage in Parkinson’s disease, which takes place for years or even decades before symptoms develop, the neurological damage in Alzheimer’s disease appears to take place after onset and over extended periods of time. The reversals that I have seen suggest that there is truly minimal damage at onset.
But for long-term Alzheimer’s disease, there can easily be serious accumulated damage that may require significant brain reconstruction and of stem-cell therapies to be properly considered a cure. I also think that, as Aubrey writes, extensive amyloid plaque accumulation may require more than restoration of the dysfunctional enzyme systems. There is early evidence in animal studies that plaque can be quickly reversed under special conditions, but rodents are hardly a good neurological model for humans.
Let me also point out that this “cure” is generic and unpatentable. So it fails the test of being a cure by pharmaceutical standards. Even with government-sponsored research, much of the strategic goals involve the possibility of new chemical entities that can be patented. Admittedly, this is a travesty, but it is the way the system works. Hillary Clinton‘s suggestion of “better funding and leadership” is political posturing of excellent quality but also adds even more to the travesty.
The fact that dental researchers cracked the Alzheimer’s puzzle and that Alzheimer’s researchers haven’t even noticed after 13 years is not a good sign for a solution coming from industry or government.
This could be resolved to statistician gold standards in two years with 15 million dollars for a three-center study, one at a prestigious US school (Columbia University?), a second in a poor, rural care facility (a southern US state?) and the third in a foreign country (Costa Rica? Venezuela? Cuba?). But I suspect that it’s more likely that more billions will be spent than already have without worthwhile result.
I hope more people see this post as good news than bad.

How close are we to a cure for Alzheimer’s?

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