674 replies to this topic

[theobromananda]

Look at post 187, or you might ask Empiricus how he got some from China.

 

Here, here!

I would be willing to organize a group buy for HEPPS in Europe for 1kg total. I'd just need about 7 people - price would be 25€/100g (plus/minus shipping; need to calculate).

 

Anybody interested?

 

[Meggo]

I'm in

[Thoth]

I am also interested

[ceridwen]

Yes please

[Moumou]

Count me in, with one condition, purity and source infos.

[Ducky-001]

Just a word of caution against destroying the plaques as they may actually be beneficial in protecting the brain against invading viruses. More and more research shows evidence that the true villain in Alzheimer's is herpes viruses and other similar viruses.

 

https://www.theatlan...heimers/564887/

William Eimer, a member of Moir’s team, demonstrated this protection by injecting the common herpes virus HSV–1 into the brains of two kinds of mice: normal rodents and ones that were genetically engineered to produce high levels of amyloid beta in their brains. The latter were better at resisting the viruses. Eimer then got similar results when he injected a different herpes virus, HHV–6, into human cells growing in a dish.

Amyloid beta protects against these viruses by latching onto them in large numbers, imprisoning them in self-assembling cages. That’s typically a good thing, but Moir argues that if the process goes on for too long, it builds up to the problematic plaques of Alzheimer’s. According to him, amyloid beta is still at the heart of the Alzheimer’s story, but it isn’t the villain. “In our model, Alzheimer’s is caused by amyloid beta’s reaction to something else, and most likely some kind of infection” like herpes, he says.

 

 

https://www.medicaln...cles/322463.php

Alzheimer's risk 10 times lower with herpes medication

 

 

So, my thinking is that long time dosing with anti viral medication may be a better route for protecting against alzheimer's, perhaps combined with the procedure described in this thread.

 

 

 

[Andey]

Just a word of caution against destroying the plaques as they may actually be beneficial in protecting the brain against invading viruses. More and more research shows evidence that the true villain in Alzheimer's is herpes viruses and other similar viruses.

 

 

  I stumble often on the idea that Alzheimer`s is not really one disease but a syndrome that could be a result of a few different diseases.

 Some causes are physical defects in CNS clearance pathways, the insuline resistance of the brain, infection.

[Turnbuckle]

Just a word of caution against destroying the plaques as they may actually be beneficial in protecting the brain against invading viruses. 

 

 

Ah, no. In mice, viruses may act as a glue for amyloid beta, but in humans it is hyperphosphorylated tau. So plaques aren't beneficial. Far from it.

[Ducky-001]

Ah, no. In mice, viruses may act as a glue for amyloid beta, but in humans it is hyperphosphorylated tau. So plaques aren't beneficial. Far from it.

 

 

Which begs the question, if something is not beneficial to the body (at least in small quantities), why does the body make it? The amyloid hypothesis has been spectacularly unsuccessful in treating Alzheimer's (https://www.theatlan...othesis/517185/) but I guess the prestige runs to deep for there to be a turnaround anytime soon.

 

The “amyloid hypothesis” began with a simple observation: Alzheimer’s patients have an unusual buildup of the protein amyloid in their brains. Thus, drugs that prevent or remove the amyloid should slow the onset of dementia. Yet all drugs targeting amyloid—including solanezumab from Eli Lilly and bapineuzumab from Pfizer and Johnson & Johnson, to add a few more high-profile flameouts to the fail pile—have not worked so far.After Merck’s announcement last week, one neurologist told Bloomberg that “there is mounting evidence—of which this is another piece—that removing amyloid once people have established dementia is closing the barn door after the cows have left.

[Turnbuckle]

Which begs the question, if something is not beneficial to the body (at least in small quantities), why does the body make it? The amyloid hypothesis has been spectacularly unsuccessful in treating Alzheimer's (https://www.theatlan...othesis/517185/) but I guess the prestige runs to deep for there to be a turnaround anytime soon.

 

 

AD is a two pronged disease, involving both amyloid beta and tau. Treating either alone doesn't work. This has been discussed from the first post in this thread, and I suggest you read the first reference in that first post.

 

As for your question about why does the body make it? Most of the problem comes from a variety of the APOE gene called APOE4. If you have one such gene, you have twice the likelihood of getting AD. If you have 2 copies, you are 12 times as likely. Thus the genetic basis is very strong. There is no known upside for APOE4, except possibly--and ironically--memory, though a later paper found the opposite. It is not associated with any infectious disease, and it hasn't been selected out because those who get AD are typically well past the reproductive years. Once you've had children and raised them, evolution doesn't care what happens to you.

 

Edited by Turnbuckle, 10 September 2018 - 12:35 PM.

[Ducky-001]

The paper at the beginning discusses the Amyloid and Tau, but does not speculate on why they appear. There being a gene variant that increase the chance that these problems appear does not really hold as a primary reason. The primary reason could still be virus, but the gene variant could increases the reaction to the virus infection. If the amyloid's and tau's are "virus prisons", having a more efficient prison system could be speculated as being beneficial for young individuals while killing of older ones earlier (https://www.ncbi.nlm...pubmed/17077159) , and as you say this does not affect evolution (unless the older individuals are important for the survival of the young ones).

 

If we speculate that these structures are virus prisons, does it make sense to tear down the prisons and let the inmates free too roam around doing more damage? Maybe, if the prisons themselves become the problem. But it should most certainly be combined with taking care of the inmates with a suitable method.

 

https://www.cell.com...6273(18)30526-9

 

Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection

 

Highlights

• Human Aβ protects against herpesviridae in AD mouse and 3D human neuronal cell cultures
• Fibrilization mediates Aβ antiherpetic activities, entrapping viruses in β-amyloid
• Herpesviridae infections dramatically accelerate Aβ-amyloidosis in AD models

 

 

 

(i'm not an expert on Alzheimer's, just an interested layman)

[Turnbuckle]

If we speculate that these structures are virus prisons, does it make sense to tear down the prisons and let the inmates free too roam around doing more damage? 

 

Again, read the first post. Or simply read the title of this thread--Alzheimer's protocol — dissolve & detoxify.

[Ducky-001]

Again, read the first post. Or simply read the title of this thread--Alzheimer's protocol — dissolve & detoxify.

 

Yes, but why not add something like Zovirax to it since it may remove the primary source?

[Daniel Cooper]

Which begs the question, if something is not beneficial to the body (at least in small quantities), why does the body make it? The amyloid hypothesis has been spectacularly unsuccessful in treating Alzheimer's (https://www.theatlan...othesis/517185/) but I guess the prestige runs to deep for there to be a turnaround anytime soon.

 

 

The body makes cancer, no?

[Turnbuckle]

Yes, but why not add something like Zovirax to it since it may remove the primary source?

 

There is strong genetic connection with the APOE4 allele, and once plaques gets started, it forms a vicious feedback loop with tau. Other factors may get it started in those predisposed for genetic reasons. A virus, as you mentioned, appears to act as a promoter. But once you have plaques, how is Zovirax going to get in there and remove the virus? This is shutting the barn door after the horses are gone. 

 

APOE4 is not the only AD allele. Others are involved, especially in late onset cases. These affect inflammation and the efficiency of clearance, or simply show an association. At least three more are associated with early onset, and having just one of them is bad. 

 

You can get lost in all the complications, but what I wanted to do here was to create a protocol that fixes the problem at the nexus of Aβ/tau interactions. People trying this will likely already show symptoms from that build-up--that's why they searched out this thread.

Edited by Turnbuckle, 10 September 2018 - 09:38 PM.

[William Sterog]

But APOE4 is the original mutation present in humans, according to Bredesen, it helped humans in it first stages, where trauma and infection in wounds were very common. This author also believes that Alzheimer's is not a pathological behavior of the brain, but a natural defense against pathogens and other menaces, like high sugar or homocysteine. His protocol is very interesting, he has classified Alzheimer's in three types, one of them is the one caused by chemical toxicity and viruses, this type is, apparently, both the most difficult to reverse and the one that can be almost completely resolved, if the underlying cause is cured.

Edited by William Sterog, 11 September 2018 - 07:08 AM.

[Ducky-001]

 But once you have plaques, how is Zovirax going to get in there and remove the virus? This is shutting the barn door after the horses are gone. 

 

 

The body might itself start to "detoxify" by removing the plaques if there is no longer a constant pressure of viruses stressing the immune system into building ever more of it. Certainly it will slow or completely cease the formation of new plaque. There is also the question that if you "open the prison" there may be temporarily at least an increased in virus concentration in the brain, possibly making the problem worse?

 

 

Found this rather old article for 2011:

 

https://journals.plo...al.pone.0025152

 

Antivirals Reduce the Formation of Key Alzheimer's Disease Molecules in Cell Cultures Acutely Infected with Herpes Simplex Virus Type 1
 

Importantly, the anti-HSV1 antiviral agents acyclovir, penciclovir and foscarnet reduced Aβ and P-tau accumulation, as well as HSV1, with foscarnet being less effective in each case. P-tau accumulation was found to depend on HSV1 DNA replication, whereas Aβ accumulation was not. The antiviral-induced decrease in Aβ is attributable to the reduced number of new viruses, and hence the reduction in viral spread. Since antiviral agents reduce greatly Aβ and P-tau accumulation in HSV1-infected cells, they would be suitable for treating AD with great advantage unlike current AD therapies, only the virus, not the host cell, would be targeted.
 

 

 

Here is one from 2014 that has done some limited trials with antivirals: (ACV = acyclovir = Zovirax)

https://www.ncbi.nlm...les/PMC4128394/

 

Herpes simplex virus type 1 and Alzheimer’s disease: increasing evidence for a major role of the virus

 

P-tau accumulation was reducible to near zero whereas that of Aβ was reducible only to a near-normal value. In fact the lesser Aβ reduction seems desirable in view of the possibility that Aβ might function at least initially as part of the innate immune system—and there are preliminary data suggesting that it does indeed have antiviral activity (Klapper et al., in preparation)—although eventually becoming toxic when over-produced. In other words, treatment should perhaps aim not to eliminate Aβ but instead to reduce it to near-normal levels—an aim achieved by ACV.
 

 

 

 

 

There is currently a trial going on it seems - https://clinicaltria...how/NCT03282916

[Turnbuckle]

In the absence of a cure or even a useful treatment, all sorts of speculative theories have arisen. It is not the purpose of this thread to address them. If anyone is looking for a treatment that will reverse AD deriving from Aβ/tau, it can be found in post 179 of this thread. If you want to add Zovirax or anything else to it, that is fine by me, but other theories should be addressed in new threads.

[sumguy90]

There is strong genetic connection with the APOE4 allele, and once plaques gets started, it forms a vicious feedback loop with tau. Other factors may get it started in those predisposed for genetic reasons. A virus, as you mentioned, appears to act as a promoter. But once you have plaques, how is Zovirax going to get in there and remove the virus? This is shutting the barn door after the horses are gone.

I think the concern here is that it'd be terrible to cure one's Alzheimer's with this protocol only to develop herpes simplex encephalitis from the freed virus particles. Perhaps adding lysine or some herbal antivirals might be a good idea.

[Turnbuckle]

I think the concern here is that it'd be terrible to cure one's Alzheimer's with this protocol only to develop herpes simplex encephalitis from the freed virus particles. Perhaps adding lysine or some herbal antivirals might be a good idea.

 

 

This is one speculation on top of another. The following is from a paper published a few years ago, and as they say, "much of this, of course, is highly speculative"--

 

To summarize, AD is a disease process, not a natural result of the aging process; HSV-1 is present in 70%–90% of the brains of older adults; HSV-1 has been identified in the tissue of patients with AD at autopsy; acute HSV-1 encephalitis affects many of the same regions of the brain that are affected by AD, and leads to long term memory loss; HSV-1 is known to reside in a latent form in the trigeminal nucleus, which projects to areas of the brain known to be affected by AD; there are indicators of an inflammatory process associated with AD, suggesting the possibility of an infectious etiology, possibly as a result of immunosenescence; activated HSV-1 virus is associated with formation of plaques and tangles, which are histologic hallmarks of AD; it is also associated with elevated cholesterol levels, also considered a risk factor for AD. Finally, there are indications that diets high in lysine and low in arginine may be associated with lower prevalences of AD.

 

This leads to the following hypothesis: HSV-1, latent in brain, becomes activated when in older age the ratio of lysine to arginine in the CSF favors arginine, providing a medium conducive to viral reactivation, and the process of immunosenescence releases the virus from immune system surveillance. Active HSV-1 then in turn causes AD. This process may be prevented or attenuated by increasing lysine, either in the diet, or as a supplement, or both. Studies of lysine treatment of herpes labialis suggest that supplements of 1,500 mg twice a day or more are effective for this purpose.

 

(PDF) Could lysine supplementation prevent Alzheimer’s dementia? A novel hypothesis. Available from: https://www.research...vel_hypothesis 

 

 

 

So one could certainly add lysine to this protocol. (I wouldn't add it to fruit juice, however, as the taste is lousy.)

[Empiricus]

There's a case for including fucoidan in this protocol.

 

Fucoidan inhibits amyloid-β-induced toxicity in transgenic Caenorhabditis elegans by reducing the accumulation of amyloid-β and decreasing the production of reactive oxygen species.

https://www.ncbi.nlm...pubmed/29260173

These results suggested that fucoidan might exert its protective effects against Abeta-induced toxicity in transgenic AD C. elegans by reducing the accumulation of toxic Abeta and decreasing Abeta-induced production of ROS, thus ameliorating the progression of the AD phenotype.  It was found that fucoidan treatment elevated the activity of proteosomes; therefore, fucoidan might decrease Abeta accumulation by promoting proteolysis.

 

Fucoidan inhibits cellular and neurotoxic effects of beta-amyloid (A beta) in rat cholinergic basal forebrain neurons.

https://www.ncbi.nlm...pubmed/15926913

 

Protective Effects of Fucoidan on Aβ25-35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice.

https://www.ncbi.nlm...pubmed/28300775

 

It's interesting that fucoidan also shows activity against at least one implicated virus. 

 

Therapies from Fucoidan; Multifunctional Marine Polymers

https://www.ncbi.nlm...les/PMC3210604/

6.8. Viruses: Influenza, Herpes and Dengue

Inhibitory effects of fucoidan on coated viruses are well known and were well reviewed a decade ago by Schaeffer [100]. Fucoidans have no direct pathogen killing activity but rather, they inhibit infection via receptor entry blocking and interference with replicative processes. Other sulfated polysaccharides in addition to fucoidans have been known to possess inhibitory activity against coated viruses such as Herpes and HIV [100–102]. In the case of viruses, receptor blocking activity prevents viral cell entry and there may also be inhibition of viral replication and syncytia (giant cell) formation. Drawbacks to using fucoidan as an orally delivered agent remain those of bioavailability. However, pathogens targetable from the lumen of the gut, such as viruses harbored in gut immune structures, may be particularly well targeted by oral fucoidan. As the following examples illustrate, oral dosing does have protective effects against viral infection.

 

Anti-HSV1 activity of brown algal polysaccharides and possible relevance to the treatment of Alzheimer's disease.

https://www.ncbi.nlm...pubmed/25583021

Herpes simplex virus type 1 (HSV1) induces the formation of the characteristic abnormal molecules of Alzheimer's disease (AD) brains, beta-amyloid, and abnormally phosphorylated, AD-like tau (P-tau). Formation of these molecules is inhibited by treatment with the antiviral agent acyclovir (ACV), which prevents viral DNA replication...   Four sulfated fucan extracts each prevented the accumulation of HSV1-induced beta-amyloid and AD-like tau in HSV1-infected Vero cells.

 

Fucoidan seems to protect against Aβ toxicity and target the virus.  

Note: Since fucoidan also has an impact on stem cells, I left some other fucoidan references at Turnbuckle's Stem Cell Protocol.

Edited by Empiricus, 12 September 2018 - 04:52 PM.

[theobromananda]

Sorry for the off-topic digression, but I can only start two PMs a day. If you are interested in HEPPS in Europe, my source would be this

 

Please send me a message if you are interested.

[Thoth]

@Turnbuckle

 

My apologies if this is a silly question.

But, is it possible to substitute carnosine with beta-alanine in your protocol?

[Thoth]

@Turnbuckle

 

What are your views on The Bredeson Protocol?

 

https://www.drbredes...redesenprotocol

https://www.ncbi.nlm...les/PMC4221920/

Edited by Thoth, 13 September 2018 - 04:03 PM.

[Thoth]

@Turnbuckle

 

Also, your views on adding Melatonin to your protocol:

 

https://www.ncbi.nlm...ubmed/16364209 

Edited by Thoth, 13 September 2018 - 04:03 PM.

[Advocatus Diaboli]

Thoth, here is a working link to the melatonin article (in your post #235). 

[Thoth]

@Advocatus

 

Thanks!

[Empiricus]

The dropper of methylene blue I ordered from BlueBrainBoost comes with a note that warns not to combine with MAO inhibitors.  Curcumin is regarded as something of a natural MAOI, and since it's been incorporated into the amyloid-β part of the protocol, the question arises whether its advisable to take them at separate times.  

 

Methylene blue is a potent monoamine oxidase inhibitor

https://link.springe.../BF03017212.pdf

 

Antidepressant activity of curcumin: involvement of serotonin and dopamine system.

https://www.ncbi.nlm...pubmed/18766332

 

Comparative absorption of curcumin formulations

https://www.ncbi.nlm...les/PMC3918227/

One limitation in the study design was the sampling time frame. Our data indicated that the curcumin half-life was estimated to be 6-7 hours and that the plasma levels of the conjugated curcuminoids were not in their elimination phase. Thus, while we sampled from 0-12 hours, we propose future research to assess a 24 hour sampling period.

Edited by Empiricus, 14 September 2018 - 10:02 AM.

[Turnbuckle]

This protocol based on the one in post 179 works very well, in my opinion. Ingredient doses and and measures have been tweaked. If anyone wants to vary it or make substitutions and report back on the results, please do. 

 

 

Updated Alzheimer's protocol — experimental

(a link to the latest update can always be found on my profile page by clicking on my avatar)

 

The following in powder form can be used in fruit juice (measured doses are approximate as powders vary)--

 

HEPPS --  1 g (1/4 teaspoon)

Taurine -- 10-15 g (2-3 teaspoons)

Carnosine -- 3 g (1.5 teaspoon)

Vitamin C -- 1.5 g (1/4 teaspoon)

 

The following are best in capsules (based on commonly available doses)--

 

Olive Leaf extract 20% oleuropein (one 500 mg cap)

Olive Leaf extract 25% hydroxtyrosol (one 100 mg cap)

Dihydromyricetin (one 350 mg cap)

Nicotinamide (one 250 mg cap or up to 2 grams. Lower amounts can also be used in fruit juice)

Magnesium theonate (one 667 mg cap, also available in flavored and unflavored powder; can be used in fruit juice) 

 

 

Optional, for chelation of metals--Meriva curcumin (one 500 mg cap)

Optional, for those with herpes--Lysine, 1-2 grams

 

Dosing--

 

Take together every day or every other day for three months or as needed. Then once a week.

One might start with a lower level of HEPPS and ramp it up to 1g to avoid the initial rapid clearance of Aβ.

 

Edited by Turnbuckle, 14 September 2018 - 01:24 PM.

[Fafner55]

In cerebrospinal fluid the concentration of amyloid-β protein Aβ42 is not correlated with age, while tau protein appears to increase exponentially at a rate similar to mortality. This finding suggests that emphasis needs to be placed on clearing tau protein and addressing the underlying cause of its increase.

 

“Tau and Aβ42 in Cerebrospinal Fluid from Healthy Adults 21–93 Years of Age: Establishment of Reference Values” (2001) http://clinchem.aacc...ent/47/10/1776