Namenda & Amantadine: Is Alzheimer's Disease A Viral Dementia?

In a conversation with the unit director of an Alzheimer's unit 5 years ago, while I was a Long Term Care Ombudsman, I was informed that there was a new drug on the market which was having more or less dramatic effects in Alzheimer's units.

After the prescription of Namenda, it was found that patients could gradually be weaned from a number of other drugs; beginning with the anti-psychotics, then, working backwards, with the mood-stabilizers, etc. etc.

And, after a few weeks to a couple of months at this, it was found that many--but not all--"Alzheimer's" patients could be maintained on the Namenda alone.

Now, it just so happens that I have had a number of discussions with a Dr. Lee Smith, a retired opthalmologist in Mishawka, Indiana, who has done quite significant research over a period of several years on an anti-viral called amantadine...

Which, it turns out, is what Namenda is.

Thus, if treating someone diagnosed with "Alzheimer's Disease" results in a significant decrease of some of the worst symptoms, it would not be unreasonable to conclude that Alzheimer's Disease is, in fact, a virus.

Now, the relationship to the under-acid stomach becomes more clear:

One of the functions of stomach acid is to destroy bacteria, viruses and other ingested pathogens.

Thus, if a person is observed to have an under-acid stomach and has been diagnosed with "Alzheimer's Disease", there would be a greater likelihood that such a diagnosis was of a viral disease.

In fact, there are certain people for whom the use of Namenda has no appreciable effect whatsoever: those who have been diagnosed with vascular dementia, which is a hardening of the arteries of the brain.

Even more interesting, the association of accumulations of aluminum in the brains of those with "Alzheimer's Disease" may very well be the direct result of the fact that the vast majority of non-prescription antacids on the market consist of....

ALUMINUM HYDROXIDE

As do most toothpastes and some anti-perspirants.

So, maybe the differential diagnosis should be between vascular dementia, viral dementia (now called Alzheimer's Disease), and Vitamin B12 deficiency dementia.

There are a number of notes on my website at:

irisnutritioncognitionresearch.blogspot.com...

as well as external links to more information about Namenda, mementine, or amantadine.

Michael Cecil

Very interesting thanks, time for some personal behaviour modification.

I think your right to question the origines of Alzheimers, specially in light of your own experiences, background and knowledge.

A wise man once told me that the problem with science is that it has provenance. Every thought is an addition to a chain of thought which becomes a deep well of knowledge whose provenance can be traced back through the years.

New thoughts stand in stark opposition to the current well of thought and are therefore provoking to those people whose life lies in the balance of their knowledge.

I found your post enlightening.
biglove xxxxxx

Originally posted by Lagrimas
I think your right to question the origines of Alzheimers, specially in light of your own experiences, background and knowledge.

A wise man once told me that the problem with science is that it has provenance. Every thought is an addition to a chain of thought which becomes a deep well of knowledge whose provenance can be traced back through the years.

New thoughts stand in stark opposition to the current well of thought and are therefore provoking to those people whose life lies in the balance of their knowledge.

I found your post enlightening.
biglove xxxxxx

Oh, by the way, when I talked to a member of the family who is a pharmacist, I was told that the use of Namenda was, at that time, RESTRICTED to use ONLY in Alzheimer's units--the rationale for which should be OBVIOUS.

But, when I checked with a friend who is a doctor, I was told that, just so long as the drug is on the market, it can be prescribed by a doctor....

Even if the patient is NOT in an Alzheimer's unit.

Don't know if this has changed over the past 5 years.

Michael Cecil

A side effect of amantadine is the stimulation of central dopamine receptors in, among other places, the basal ganglia (the reason it is also used in Parkinsonian disorders). Mental deterioration in Alzheimer's is directly proportional to dopamine-releasing neuron destruction, so obviously, if you can stimulate the remaining dopamine-releasing neurons to release their neurotransmitter, this can (somewhat) make-up for the neuronal loss the patient has experienced.

So, yes, amantadine is an antiviral, but the side effect is the reason it is being prescribed to patients with dopamine deficiency symptoms.

Alzheimer's and amantadine
Basic amantadine information
Amantadine and Parkinson's

Originally posted by VneZonyDostupa
A side effect of amantadine is the stimulation of central dopamine receptors in, among other places, the basal ganglia (the reason it is also used in Parkinsonian disorders). Mental deterioration in Alzheimer's is directly proportional to dopamine-releasing neuron destruction, so obviously, if you can stimulate the remaining dopamine-releasing neurons to release their neurotransmitter, this can (somewhat) make-up for the neuronal loss the patient has experienced.

So, yes, amantadine is an antiviral, but the side effect is the reason it is being prescribed to patients with dopamine deficiency symptoms.

Alzheimer's and amantadine
Basic amantadine information
Amantadine and Parkinson's

Well, these are things that I was certainly not aware of. My research, when I was still doing it, was merely preliminary; and always susceptible to change with the discovery of new information.

But I also am not completely clear about the precise relationship between amantadine and Namenda or mementine.

Apparently, Namenda is an "analogue" of amantadine.

Not exactly sure what that means; whether it is merely a methyl group or such being added for the purpose of applying for a patent, or whether there is, in fact, a significantly different mechanism of action as a result of such 'tweaking' because it is not precisely amantadine.

So my question would still be why Namenda works in some people with Alzheimer's disease but does not work in cases of vascular dementia which would, I suppose, result in similar destruction of neurons.

In other words, what, precisely is the cause of the destruction of the dopamine-releasing neurons (would that not also happen in instances of vascular dementia?) and does that make any difference?

Any views on that particular aspect of the issue?

Michael Cecil

Originally posted by Michael Cecil
always susceptible to change with the discovery of new information.

The sign of a great researcher

But I also am not completely clear about the precise relationship between amantadine and Namenda or mementine.

Apparently, Namenda is an "analogue" of amantadine.

Not exactly sure what that means; whether it is merely a methyl group or such being added for the purpose of applying for a patent, or whether there is, in fact, a significantly different mechanism of action as a result of such 'tweaking' because it is not precisely amantadine.

It depends on which sort of analogue we're talking about. Most drug analogue are functional analogue, meaning their chemical structure might be a tad different, but they function similarly, using the same mechanism. Often, the structural change is just to allow a smaller effective dose or to reduce toxicity.

In this case, I would say Namenda and amantadine are functional analogues, as they both work to cause faster closure of NMDA (N-methyl-D-aspartic acid) channels and stabilizing those that are already closed. NMDA acts like glutamate, that is, as an excitatory neurotransmitter. Knocking down glutamic excitation allows dopaminergic neurons to basically amplify their inhibitory role in the brain, even if you've lost some of those neurons. In some regions of the brain, this will also cause increased secretion of dopamine.

So my question would still be why Namenda works in some people with Alzheimer's disease but does not work in cases of vascular dementia which would, I suppose, result in similar destruction of neurons.

It's all about the role of glutamate and NMDA. Vascular dementia does, indeed, invlove neuronal loss, but there isn't an issue with glutamic overstimulation, so knocking this down wouldn't do much for these patients.

In other words, what, precisely is the cause of the destruction of the dopamine-releasing neurons (would that not also happen in instances of vascular dementia?) and does that make any difference?

That's the hot-button issue in Alzheimer's. What causes loss of specifically dopaminergic neurons? Some think it has to do with misfolding of certain proteins (amyloid being a front-runner). Others think it is purely a "genetic timebomb" sort of mechanism. Still others think it's an cumulative effect of various life events (infections, exposures, genetics, all rolled into one). Personally, I lean toward genetics, with the misfolded protein being the main culprit rather than the "timebomb". Several studies have shown neurons with amyloid inclusion bodies in Alzherimer's and Parkinson's patients.

Hopefully, once we have a definitive answer, we'll have a definitive therapy.

reply to post by VneZonyDostupa

Oh, yeah.

My memory is starting to come back just a little about this stuff.

It's been several years now.

Glutamate, NMDA, "excitatory inhibition" and the meaning of the term "anti-viral blocking agent".

But, when I got to the point of misfolded protein and amyloid, I went in the direction of free-radical oxidation as a major culprit because that was the only thing that I could address in the clinical situation by means of change of nutrition, the addition of anti-oxidants, and reversion to some of the basic rules of food combining.

That is, the mixture of proteins and starches in the same meal, each with their own, and contradictory, chemistry of digestion--not to mention the inclusion of fruits at the same time, which have an almost completely different path for digestion--seemed to be the only way that I had of addressing those kinds of things.

Sometimes clinical presentations take precedence over the development of theory.

Thanks so much for the information.

Oh, by the way, I would suggest that the loss of neurons in vascular dementia would be a very specific result of , almost exclusively, free-radical oxidation; which, of course, leads directly to the consideration of homocysteine levels rather than the whole "cholesterol hypothesis" as the causative factor for arteriosclerosis. That is, the inclusion of betaine HCl in one's diet--even for those without an under-acid stomach--typically results in a decrease in homocysteine levels, if my memory serves me correctly.

Michael Cecil

Originally posted by Michael Cecil


But, when I got to the point of misfolded protein and amyloid, I went in the direction of free-radical oxidation as a major culprit because that was the only thing that I could address in the clinical situation by means of change of nutrition, the addition of anti-oxidants, and reversion to some of the basic rules of food combining.

That is, the mixture of proteins and starches in the same meal, each with their own, and contradictory, chemistry of digestion--not to mention the inclusion of fruits at the same time, which have an almost completely different path for digestion--seemed to be the only way that I had of addressing those kinds of things.

Well, all these different foods are broken down and absorbed in different parts of the GI tract specifically geared toward those sorts of compounts (lipids versus proterins versus sugars/carbs), so I don't think mixing of nutrient types really has any effect, medically.

Of course, free radical damage could always play a role. A singular role, not likely, but certainly some role.

Thanks so much for the information.

Not a problem, thank you for bringing up an interesting topic!

Oh, by the way, I would suggest that the loss of neurons in vascular dementia would be a very specific result of , almost exclusively, free-radical oxidation; which, of course, leads directly to the consideration of homocysteine levels rather than the whole "cholesterol hypothesis" as the causative factor for arteriosclerosis. That is, the inclusion of betaine HCl in one's diet--even for those without an under-acid stomach--typically results in a decrease in homocysteine levels, if my memory serves me correctly.

Hmm...I would be reluctant to discount cholesterol's role in athersclerosis. The important thing to keep in mind is that cholesterol itself is not suggested as the causative agent, it's the collection of cholesterol esters in fibrotic lesions in vessel walls. Obviously, if you have higher levels of circulating LDL, you're more likely to have cholesterol esters build up in the lesions, which leads to further fibrotic change, platelet activation/accumulation, and occlusion.

Of course, an elevated serum homocysteine should always be considered a risk for atherosclerosis. The studies I've seen link homocysteine to the initial lesions of the vessel wall, which then predisposes the patient to atherosclerotic build-up of cholesterol esters and platelets. So, really, it one link in a long chain of events.

Originally posted by VneZonyDostupa
Well, all these different foods are broken down and absorbed in different parts of the GI tract specifically geared toward those sorts of compounts (lipids versus proterins versus sugars/carbs), so I don't think mixing of nutrient types really has any effect, medically.

(Smile)

Well, that is certainly the conventional wisdom.

You might want to read just a simple book on food combining first, however.

Also, as I understand it, the homocysteine level is a measure of free-radical destruction of protein; in response to which the atherosclerotic plaques are a 'repair mechanism'.

I once had a client that was on Lipitor for 24 years--the picture is on my website--no atherosclerotic sign in his iris, who then had to have a Coronary Artery By-pass Graft (CABGX4).

I have to wonder whether, ultimately, the Lipitor prevented an atherosclerotic plaque from at least supporting his abdominal aorta inasmuch as he also was found to have a 4.5 cm. abdominal aortic aneurysm at the time of his open heart surgery..

So, maybe he will not die from a heart attack; but maybe he will die from either a stroke or an AAA because no attempt was made to address the initial insult: free-radical damage to his arteries.

Michael Cecil

reply to post by Michael Cecil


Hm, well, I don't think a lack of atherosclerotic plaque would cause someone to be more prone to abdominal (or any other sort) of aneurysm. If anything, it makes them less prone.

Any time you have fibrotic lesions, fibrinoid necrosis, or fibrotic organization of a thrombus, you're going to have a decrease in vessel elasticity at that point, as well as a weakening of the wall.

Increased serum homocysteine could certainly have negative effects on the vessels, but I'm still not completely convinced it is due to any sort of "food mixing". Nearly every case of homocysteinuria/emia I'veseen was rooted in folic acid deficiency. So, while nutrition is key in preventing this condition, it's not about preventing food mixing, but rather getting proper nutrition. Folic acid is relatively a common deficiency, especially in women, so it's not surprising that elevated homocysteine would be a relatively common finding.

So, basically, yes, I agree that nutrition is key in this case. I disagree, however, that food mixing is the culprit and fall instead on the side of nutrient deficiency.

Regardless, wonderful to see someone on here actually doing the research and bringing up interesting, valid points for a change! So much better than the snake-oil posts that are all too common here.

Originally posted by VneZonyDostupa

Of course, free radical damage could always play a role. A singular role, not likely, but certainly some role.

Well, of course; but this is the point at which I lose interest in the research because it cannot really help me in what I am trying to do: diminish the incidence of these kinds of biological insults.

It is at this point that it becomes much more important to me that cayenne pepper is good for circulation and that not only is turmeric a strong anti-oxidant and anti-inflammatory; it is also an important ingredient in the diets of the people of India, who have a low incidence of Alzheimer's Disease. So I recommend to my clients that they replace cayenne pepper for black pepper and include more turmeric in their diet in addition to ginger tea; turmeric being of the ginger family.

Michael Cecil

reply to post by Michael Cecil


It certainly can't hurt to use cayenne and tumuric. When patients ask me about these sorts of alternative or complementary treatments, I always tell them to use whatever they are comfortable with and won't interfere with their current allopathic therapies. Even if the only effect they get is placebo, symptom relief is symptom relief.

Thank you for posting this thread... I'll be keeping an eye on it.

I'm afraid I won't be able to offer worthwhile contributions to it, but it caught my eye as I am the caregiver for my 88 year old aunt, who takes 20mg of Namenda daily for her dementia. She also takes 10mg of Aricept along with it.

Interestingly and frustratingly, no one's ever told me what form of the disease she has in the 5 years she's had it. I knew there were different types and thank you also for listing them. I suspect she has the B12 type, as when I initially had her go in for evaluations her doctor put her on B12 shots for 6 weeks... they were very concerned.

I will say, though, that neither of these drugs seem to do a heck of a lot, as she gets gradually worse every day, but then again I have no reference to what would have happened if she had not taken them. It's just a feeling I get.

It's an exceptionally frightening disease. To just see decades of her life vanish as if they'd never happened, including 10 years of marriage to a world famous actor, to not recognizing her home, or sometimes me and so many other things... it is, like I said, frightening. It's taken much out of my life too, but it's worth it for her to be here in her house rather than in a nursing home. My town's excellent day care allows me to try to get stuff done on weekdays.

So again, thanks for this. As an artist/web guy a lot of the techno/medical stuff is interesting to me as I can sort of get the jist, but most of it does sail right over as it were.

Peace.

And thanks for the tips on cayenne and turmeric... I'll try it out... but I doubt she'll go for it... hard to get her to eat anything.

Originally posted by PixelDuster
I'm afraid I won't be able to offer worthwhile contributions to it, but it caught my eye as I am the caregiver for my 88 year old aunt, who takes 20mg of Namenda daily for her dementia. She also takes 10mg of Aricept along with it.

I did a little investigation into Aricept and am somewhat concerned about the dosage level; that is, miligrams.

You might want to Google "huperzine", which is found in Brain Elevate by Now foods...

But at the microgram level.

Huperzine may, in fact, be a natural Aricept.

But I'm not certain. I have investigated a lot of those drugs and no longer remember which is which or the differences between them.

Michael Cecil

Originally posted by Michael Cecil

Originally posted by PixelDuster
[...] I am the caregiver for my 88 year old aunt, who takes 20mg of Namenda daily for her dementia. She also takes 10mg of Aricept along with it.

I did a little investigation into Aricept and am somewhat concerned about the dosage level; that is, miligrams.

You might want to Google "huperzine", which is found in Brain Elevate by Now foods...

But at the microgram level.

Huperzine may, in fact, be a natural Aricept.

But I'm not certain. I have investigated a lot of those drugs and no longer remember which is which or the differences between them.

Michael Cecil

Michael, thank you very much for your reply.

I will check out huperzine and that product and also run it past the doc who prescribes these things for her. He's a geriatric psychiatrist at Greenwich Hospital in Connecticut, who we see about every 3 months. Seems to know what's what, and I have on occasion given him some good ATS type questions which he seems to have answers for...

The order of magnitude in dosage you speak of is pretty up there on the concern scale! But, then again Aricept pills only come in 5 or 10mg sizes, so I don't think he's in error... seems "standard." Maybe the huperzine is something "similar yet different?"

I do find it weird and most disconcerting that these drugs are only effective in half of those that take them... what's up with that? But if they're all we've got, which they seem to be for whatever reason, (without getting all ATSy on it) I guess they're worthwhile. She's pretty "out there," and I just can't imagine what it'd be like without these drugs. It's quite awful enough!

I think I will email him a link to this thread, too... don't know if he'd have the time. He's been good at responding, so it's worth a shot.

I'll keep you posted, and thanks again!

Peace,

Pixel

reply to post by PixelDuster

My concern with these drugs, especially in the elderly, is their clearance from the system.

This involves both the de-toxification paths of the liver as well as the effectiveness of the kidneys.

So, if the liver is capable of detoxifying this unnatural substance, which is probably questionable, is that complex even being excreted by the kidneys?

This is the problem with many unnatural drugs. They all put additional de-toxification stress on the liver. The statin drugs, especially, interfere with the cytochrome p450 or some other pathway(s?).

But another question is compliance: would people even take a drug which is only 1 miligram? They might consider the dosage so small that it could not possibly be effective, or that they were being charged too much money. It seems I recall one drug--maybe Lipitor--in which the cost for 100 60 (?) mg. tablets is no more than the cost of 100 30 (?)mg. tablets. Something is fishy here.

So, if they work for awhile and then no longer work, is that because they are being accumulated in the system to a toxic level?

Huperzine is a natural substance; suggesting not only that it will not place additional stress on the liver; but, also, that it may very well be nutrition for these people. In other words, maybe 3 or six micrograms is the amount of this substance that is needed each day for normal neurological activity. But the concept of 'specific hunger' is also involved here. In other words, if the body does not need the substance in the first place, it will not accumulate it.

Another discovery of Iridology is that pharmaceutical drugs and other toxins, if they cannot be successfully de-toxified and excreted, are shunted into areas of the body with low biological energy or activity as a 'protective mechanism', I suppose. This is why aluminum accumulates in the brains of people with Alzheimer's Disease. It is already an area of low biological activity because of a previous insult of one kind or another.

But, finally, there is another issue here:

One has to know when to stop trying to prevent the process of deterioration resulting in death.

'The enemy here is not death but suffering'--as was stated by one person who got out of his hospital bed and unplugged the ventilator that was keeping him alive.

There is a whole question of ethics involved here in keeping people alive for no other reason than to pay their pharmaceutical bills.

In any case, people will be 'raised from the dead' to live additional lives anyway.

So there should not be so much angst about and resistance against a natural process.

Michael