LONGECITY

Could someone clarify the patent status of Targretin?

 

http://www.drugs.com...gretin-gel.html

 

If there is a generic version as noted below, why are there posts about $49,000 Bexarotene annual treatment costs?

A generic drug should be priced, theoretically,  at marginal cost which is much much closer to $0 than it is to $49,000.

 

This is of considerable relevance here as the AD patient who was on Bexarotene and stabilized for 2 years had to give up treatment due to

the 1,200 euro per month expense. If we are now talking about $20 copay prescriptions, then money limitations are now off the table.

 

Is a generic drug company typically (aside from some notable recent examples) truly allowed to charge pharmaceutical

scale prices for a drug in which they have not been exposed to any development risk? In this instance there is some mention

of generic exclusivity of Targretin for a particular company.

 

 

http://www.empr.com/...article/425463/

 

There is also mention of an October 2016 patent expiration for Targretin.

Should this be the date when large price declines should be expected?

 

I suppose there might be quite a few more prescriptions for the "cancer" indication with the $20 copay.

 

Edited by mag1, 14 February 2016 - 06:56 PM.

Inflammatory mediators leading to protein misfolding and uncompetitive/fast off-rate drug therapy for neurodegenerative disorders.

Inflammatory mediators, including free radicals such as nitric oxide (NO) and reactive oxygen species (ROS), can contribute to neurodegenerative diseases in part by triggering protein misfolding. In this chapter, we will discuss a newly discovered pathway for this phenomenon and possible novel treatments. Excitotoxicity, defined as overstimulation of glutamate receptors, has been implicated in a final common pathway contributing to neuronal injury and death in a wide range of acute and chronic neurological disorders, ranging from Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Alzheimer's disease (AD) to stroke and trauma. Excitotoxic cell death is due, at least in part, to excessive activation of N-methyl-d-aspartate (NMDA)-type glutamate receptors, leading to excessive Ca(2+) influx through the receptor's associated ion channel and subsequent free radical production, including NO and ROS. These free radicals can trigger a variety of injurious pathways, but newly discovered evidence suggests that some proteins are S-nitrosylated (transfer of NO to a critical thiol group), and this reaction can mimic the effect of rare genetic mutations. This posttranslational modification can contribute to protein misfolding, triggering neurodegenerative diseases. One such molecule affected is protein disulfide isomerase (PDI), an enzyme responsible for normal protein folding in the endoplasmic reticulum (ER). We found that when PDI is S-nitrosylation (forming SNO-PDI), the function of the enzyme is compromised, leading to misfolded proteins and contributing to neuronal cell injury and loss. Moreover, SNO-PDI occurs at pathological levels in several human diseases, including AD and PD. This discovery thus links protein misfolding to excitotoxicity and free radical formation in a number of neurodegenerative disorders. Another molecule whose S-nitrosylation can lead to abnormal protein accumulation is the E3 ubiquitin ligase, parkin, which contributes to the pathogenesis of PD. One way to ameliorate excessive NO production and hence abnormal S-nitrosylations would be to inhibit NMDA receptors. In fact, blockade of excessive NMDA receptor activity can in large measure protect neurons from this type of injury and death. However, inhibition of the NMDA receptor by high-affinity antagonists also blocks the receptor's normal function in synaptic transmission and leads to unacceptable side effects. For this reason, many NMDA receptor antagonists have disappointingly failed in advanced clinical trials. Our group was the first to demonstrate that gentle blockade of NMDA receptors by memantine, via a mechanism of uncompetitive open-channel block with a rapid "off-rate," can prevent this type of damage in a clinically efficacious manner without substantial side effects. For these Uncompetitive/Fast Off-rate therapeutics, we use the term "UFO drugs" because like Unidentified Flying Objects, they leave very quickly as soon as their job is finished. As a result, memantine blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this by preferentially entering the receptor-associated ion channel when it is excessively open, and, most importantly, when its off-rate from the channel is relatively fast so that it does not accumulate to interfere with normal synaptic transmission. Hence, memantine is clinically well tolerated, has been used in Europe for PD for many years, and recently passed multiple phase III trials for dementia, leading to its approval by the FDA and European Union for moderate-to-severe AD. Clinical studies of memantine for additional neurological disorders, including other dementias, neuropathic pain, and glaucoma, are underway. We have also developed a series of second-generation drugs that display greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites, including critical thiol groups that are S-nitrosylated. In this case, in contrast to PDI or parkin, S-nitrosylation proves to be neuroprotective by decreasing excessive NMDA receptor activity. Targeted S-nitrosylation of the NMDA receptor can be achieved by coupling NO to memantine, yielding second-generation "UFO drugs" known as NitroMemantines.

http://www.ncbi.nlm....pubmed/17678953

Edited by Logic, 01 March 2016 - 01:19 PM.

A recent paper of a discovery about the similarity of laminopathies and age-related progressive neurodegenerative disorders:

Lamin Dysfunction Mediates Neurodegeneration in Tauopathies
Frost B, Bardai FH, Feany MB
Curr Biol. 2016 Jan 11
http://www.ncbi.nlm....pubmed/26725200
Abstract
The filamentous meshwork formed by the lamin nucleoskeleton provides a scaffold for the anchoring of highly condensed heterochromatic DNA to the nuclear envelope, thereby establishing the three-dimensional architecture of the genome [1]. Insight into the importance of lamins to cellular viability can be gleaned from laminopathies, severe disorders caused by mutations in genes encoding lamins. A cellular consequence of lamin dysfunction in laminopathies is relaxation of heterochromatic DNA [1]. Similarly, we have recently reported the widespread relaxation of heterochromatin in tauopathies [1]: age-related progressive neurodegenerative disorders, including Alzheimer's disease, that are pathologically characterized by aggregates of phosphorylated tau protein in the brain [2, 3]. Here we demonstrate that acquired lamin misregulation though aberrant cytoskeletal-nucleoskeletal coupling promotes relaxation of heterochromatin and neuronal death in an in vivo model of neurodegenerative tauopathy. Genetic manipulation of lamin function significantly modifies neurodegeneration in vivo, demonstrating that lamin pathology plays a causal role in tau-mediated neurotoxicity. We show that lamin dysfunction is conserved in human tauopathy, as super-resolution microscopy reveals a significantly disrupted nuclear lamina in postmortem tissue from human Alzheimer's disease brain. Our study provides strong evidence that tauopathies are neurodegenerative laminopathies and identifies a new pathway mediating neuronal death in currently untreatable human neurodegenerative disorders, including Alzheimer's disease.

 
Interesting... but do you have any clue what to do to prevent this? Would HDAC inhibitors help to keep the DNA archored to the nuclear envelope, by virtue of not unfurling so readily?

I am not sure yet, because this is rather new:

as the corresponding entry in the blog of the current university of the study's main author writes:
Skeleton That Protects Brain Cells’ Control Center Is Found To Be Damaged
http://gsbs.uthscsa....d-to-be-damaged
"... Dr. Frost and two co-authors showed - for the first time - that lamin dysfunction can cause the death of brain cells, which are called neurons. ..."

What does the thread think of the accumulating evidence supporting hemodialysis for Alzheimer prevention?

It is somewhat pricey, though. Anyone have any ideas how it might be made a little more affordable?

 

http://www.ncbi.nlm....pubmed/26923028

http://www.ncbi.nlm....pubmed/26228626

http://www.ncbi.nlm....pubmed/22699459

Edited by mag1, 09 March 2016 - 04:07 AM.

Could it also help patients?

It already seems to be.

 

Finding a cure for Alzheimer's, as with many other illnesses, is a two step process:

 

First, find an effective treatment.

Second, make sure the treatment has good patent protection.

Third, if not, go back to the first step.

 

That makes it a three step process.

Edited by mag1, 10 March 2016 - 05:03 AM.

True I hadn't looked at the links

Researchers Identify Virus and Two Types of Bacteria as Major Causes of Alzheimer’s
 
"...we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept..."
 
“...The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease –[b] particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation...”

http://neurosciencen...neurology-3826/
 
Lipopolysaccharide  and how to eliminate it and gram negative bacteria is something that should be all over this forum for a good many health and longevity reasons IMHO!

Do we already know how to do this?

Yes, this might be quite true about an infectious origin for Alzheimer`s, though please refer to steps 2 and 3 above.

That's why no one mentioned it before this. I can feel the spryrochetes moving as many Lyme patients can and yes I do have HSV1. Haven't been able to get rid of it.

It is especially disappointing that evidence exists for a dementia connection to herpes simplex 1.

If HSV-1 were causing the epidemic of this century, would not a focused global effort be capable of developing a vaccine for it?

At least then we would not have decades more debate about whether or not herpes is causing Alzheimer's!

 

In fact the infectious hypothesis crops up time and time again in the research literature.

Various diseases might or might not be related to infections.

 

Should it not be a Global Millennial goal that all such infectious agents which might cause illness should be targeted for significant

financing? The world is already spending well over $1 billion per day on dementia. Investing in vaccines would make a very

good investment.

 

A herpes vaccine would surely be a great place to start, though from wiki:

 

"... has failed to proceed to a Phase III trial in the year 2006, due to financial reasons."

or "...  Although already proven as very safe and effective in studies on animals, [a proposed herpes]  vaccine is currently not involved in any clinical trials,

mainly due to lack of funding"

 

Can we really afford not to fund these vaccines?

 

https://en.wikipedia...implex_research

 

We are quickly reaching a point where most industrialized societies are facing an Alzheimer's catastrophe and resulting sociopolitical stress from it "due to financial reasons."

When America soon confronts an Alzheimer tab of $1 trillion per year, people will likely wonder how could we have possibly not invested more effort and money into vaccines?

Edited by mag1, 11 March 2016 - 06:06 PM.

It is especially disappointing that evidence exists for a dementia connection to herpes simplex 1.

If HSV-1 were causing the epidemic of this century, would not a focused global effort be capable of developing a vaccine for it?

At least then we would not have decades more debate about whether or not herpes is causing Alzheimer's!

 

In fact the infectious hypothesis crops up time and time again in the research literature.

Various diseases might or might not be related to infections.

 

Should it not be a Global Millennial goal that all such infectious agents which might cause illness should be targeted for significant

financing? The world is already spending well over $1 billion per day on dementia. Investing in vaccines would make a very

good investment.

 

A herpes vaccine would surely be a great place to start, though from wiki:

 

"... has failed to proceed to a Phase III trial in the year 2006, due to financial reasons."

https://en.wikipedia...implex_research

 

We are quickly reaching a point where most industrialized societies are facing an Alzheimer's catastrophe and resulting sociopolitical stress from it "due to financial reasons."

When America soon confronts an Alzheimer tab of $1 trillion per year, people will likely wonder how could we have possibly not invested more effort and money into vaccines?

 

Interesting. Was there some evidence that Vitamin D was  indicated as a possible modulator or killer of Herpes infection? Was the combination of Vitamin D and Curcumin found to help Alzheimer's? Throw in Pterostilbine, and Grape Seed extract, and maybe one or more could help with Herpes virus which might be in the brain. I am just wondering.

 

Edited by heisoktoday, 11 March 2016 - 06:11 PM.

Interesting, vitamin D seems to be related to herpes zoster.

http://www.ncbi.nlm....pubmed/26163058

 

Couldn't find any direct research for curcumin/ grape seed etc. and herpes simplex, though might want to stock up on brown algal extract.

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

...
 
“...The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease –[b] particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation...”

http://neurosciencen...neurology-3826/
 
Lipopolysaccharide  and how to eliminate it and gram negative bacteria is something that should be all over this forum for a good many health and longevity reasons IMHO!

 

 

Apparently PQQ is effective in mitigating the effects of lipopolysaccharides, so it may be something worth looking into.

 

Pyrroloquinoline quinone (PQQ) inhibits lipopolysaccharide induced inflammation in part via downregulated NF-κB and p38/JNK activation in microglia

http://www.ncbi.nlm....pubmed/25314304

 

 

...Further a systemic LPS treatment acute inflammation murine brain model was used to study the suppressive effects of PQQ against neuroinflammation in vivo. Mice treated with PQQ demonstrated marked attenuation of neuroinflammation based on Western blotting and immunohistochemistry analysis of Iba1-against antibody in the brain tissue. Indicated that PQQ protected primary cortical neurons against microglia-mediated neurotoxicity. These results collectively suggested that PQQ might be a promising therapeutic agent for alleviating the progress of neurodegenerative diseases associated with microglia activation

If you go to the Search dropdown menu, click GoogleSiteSearch and type in HSV you will find that its eradication and the means to do so have been discussed extensively.

Off the top of my head:

• VCO
• BHT
• Emodin
• Bavituximab
• DRACO

You can do a google site search for those too.

But don't pick on HSV alone:

Eliminate Lipopolysaccharide! Kill gram negative bacteria!

This should be a great huge flashing neon sign in any Longecity member's head IMHO.

It does nasty things to you NAD+ levels and increases Inflammation and NF-kB for a start...

(Almost all telomerase activators are NF-kB inhibitors...think old immune system...)

The levels, starting in the ever more leaky gut, increase with age...

 

Edited by Logic, 11 March 2016 - 08:05 PM.

I just wanted everyone on the thread to know that things are really moving in genomics land.

 

Oxford Nanopore appears to be driving their nanopore tech forward!

Very very exciting!

 

If we could soonish have $100 full genomes it would completely change the landscape for the research into Alzheimer's genetics (and all other diseases).

Really maxed out about this!

 

http://omicsomics.bl...dy-got-one.html

Edited by mag1, 11 March 2016 - 10:26 PM.

Anyone have an opinion on the supplement Tauroursodeoxycholic acid (TUDCA) for Alzheimer's?

 

https://en.wikipedia...eoxycholic_acid

Thanks Mag1, Arisia, Logic and all others who take the time to educate us. Logic, thanks for recommending the search feature, but also giving us something to go on. Some simply say search, but new people need some direction.

• VCO
• BHT
• Emodin
• Bavituximab
• DRACO

I dug a little deeper into the D side of things, and found this:

 

"Serum vitamin D levels are positively associated with varicella zoster immunity in chronic dialysis patients"  http://www.nature.co...icles/srep07371

 

There also seems to be some indication that deficiency in D could be observed in Dementia or Alzheimer's patients.

 

"Maybe. But it's too soon to say for certain. New research suggests people with very low levels of vitamin D in their blood, known as vitamin D deficiency, are more likely to develop Alzheimer's disease and other forms of dementia.

For example, a large 2014 study published in Neurology showed people with extremely low blood levels of vitamin D were more than twice as likely to develop Alzheimer's disease or other types of dementia than those with normal vitamin D levels. But it's important to point out that the association between vitamin D deficiency and dementia risk is only observational at this point. More research is needed to show cause and effect."

 

 

http://www.mayoclini...rs/faq-20111272

 

 

Liver function and AD

 

http://www.ncbi.nlm....pubmed/26957302

 

In terms of clinical management of Alzheimer's and a range of other illnesses, the recent FDA approval of an exoskeleton has substantial implications. 

https://www.scienced...60311084406.htm

Thanks Mag1, Arisia, Logic and all others who take the time to educate us. Logic, thanks for recommending the search feature, but also giving us something to go on. Some simply say search, but new people need some direction.

• VCO
• BHT
• Emodin
• Bavituximab
• DRACO

 
Pleasure Heisoktoday.
I'll keep that in mind.
Generally, if you have an ailment, the search feature will bring you to a list like the above.
 

I dug a little deeper into the D side of things, and found this:
 
"Serum vitamin D levels are positively associated with varicella zoster immunity in chronic dialysis patients"  http://www.nature.co...icles/srep07371
 
There also seems to be some indication that deficiency in D could be observed in Dementia or Alzheimer's patients.
 
"Maybe. But it's too soon to say for certain. New research suggests people with very low levels of vitamin D in their blood, known as vitamin D deficiency, are more likely to develop Alzheimer's disease and other forms of dementia.
For example, a large 2014 study published in Neurology showed people with extremely low blood levels of vitamin D were more than twice as likely to develop Alzheimer's disease or other types of dementia than those with normal vitamin D levels. But it's important to point out that the association between vitamin D deficiency and dementia risk is only observational at this point. More research is needed to show cause and effect."
 
 
http://www.mayoclini...rs/faq-20111272

Resveratrol synergises with vit D to increase vitamin D receptors (VDR) and cathelicidin antimicrobial peptide (CAMP) IIRC.

Now the less pure extracts of R are from Japanese Knotweed, which is high in Emodin...

 

NB that Pterostilbene is basically a more bioavailable form of Resveratrol.

ie: Pt is likely to give the in vitro effects R, while the metabolites of R are what you should be researching if you want the learn about it's effects  in vivo.

 

Pt also disrupts biofilms like that formed by Candida.

 

One of my posts:

http://www.longecity...nd-stilbenoids/

 

resveratrol vitamin d synergy search:

https://cse.google.c...tamin d synergy

 

Edited by Logic, 12 March 2016 - 10:31 PM.

“...This drug, in very low doses, turns on the garbage disposal machinery inside neurons to clear toxic proteins from the cell. By clearing intracellular proteins, the drug prevents their accumulation in pathological inclusions called Lewy bodies and/or tangles, and also prevents amyloid secretion into the extracellular space between neurons, so proteins do not form toxic clumps or plaques in the brain,” says the study’s senior investigator, neuroscientist Charbel E-H Moussa, MB, PhD...

http://explore.georg.../news/?ID=70332

 

Here is a nice summary and info on a group buy for Nilotinib:

http://www.longecity...1-month-supply/

 

Yes, I'm pimping the buy! 
I very badly want to get Nilotinib for a dear friend of mine's mom.

She was like a 2nd mother to me and the stress we, as teens, put her through probably contributed to her condition! 

Edited by Logic, 12 March 2016 - 10:41 PM.

Metiformin and other AMPK activators are not looking too good.

 

http://www.ncbi.nlm....pubmed/26967226

 

 

The evidence of strong pathological associations between type 2 diabetes and Alzheimer's disease (AD) has increased in recent years. Contrary to suggestions that anti-diabetes drugs may have potential for treating AD, we demonstrate here that the insulin sensitizing anti-diabetes drug metformin (Glucophage®) increased the generation of amyloid-β (Aβ), one of the major pathological hallmarks of AD, by promoting β- and γ-secretase-mediated cleavage of amyloid-β protein precursor (AβPP) in SH-SY5Y cells. In addition, we show that metformin caused autophagosome accumulation in Tg6799 AD model mice. Extremely high γ-secretase activity was also detected in autophagic vacuoles, apparently a novel site of Aβ peptide generation. Together, these data suggest that metformin-induced accumulation of autophagosomes resulted in increased γ-secretase activity and Aβ generation. Additional experiments indicated that metformin increased phosphorylation of AMP-activated protein kinase, which activates autophagy by suppressing mammalian target of rapamycin (mTOR). The suppression of mTOR then induces the abnormal accumulation of autophagosomes. We conclude that metformin, an anti-diabetes drug, may exacerbate AD pathogenesis by promoting amyloidogenic AβPP processing in autophagosomes.

 

 

Note: bold-face added by me.

 

http://www.ncbi.nlm....pubmed/21623793

 

 

... However, the responses of AMPK activation are dependent on stimulation and the extent of activating stress. Evidently, AMPK signaling can repress and delay the appearance of AD pathology but later on, with increasing neuronal stress, it can trigger detrimental effects that augment AD pathogenesis. We will outline the potential role of AMPK function in respect to various aspects affecting AD pathogenesis.

 

Metiformin and other AMPK activators are not looking too good.

 

...

The second paper seems pointing to a time depending effect, positive first and negative later in life, and discuss AMP kinase role and mechanism of action in relation to AD. Should it indicate that, what the first paper say on metformin dosages?

• VCO
• BHT
• Emodin
• Bavituximab
• DRACO

Nope, nope, nope, maybe, probably.

 

Bavituximab and DRACO may or may not cross the BBB, and would be unlikely to work for a latent HSV infection. Getting rid of the latent reservoir is going to be a tough problem, I suspect, but maybe someone will come up with a way.

Peregrine Pharmaceuticals is currently a penny stock, can't afford to pursue the antiviral angle at the moment, and hasn't gotten Bavituximab on the market for any indication yet. DRACO doesn't yet exist as a therapy that can be delivered to a human, although that problem is in principle solvable.

Huge numbers of people have HSV infections without getting Alzheimers, so the connection between the two is not 100%.
 

 

• VCO
• BHT
• Emodin
• Bavituximab
• DRACO

Nope, nope, nope, maybe, probably.

 

Bavituximab and DRACO may or may not cross the BBB, and would be unlikely to work for a latent HSV infection. Getting rid of the latent reservoir is going to be a tough problem, I suspect, but maybe someone will come up with a way.

Peregrine Pharmaceuticals is currently a penny stock, can't afford to pursue the antiviral angle at the moment, and hasn't gotten Bavituximab on the market for any indication yet. DRACO doesn't yet exist as a therapy that can be delivered to a human, although that problem is in principle solvable.

Huge numbers of people have HSV infections without getting Alzheimers, so the connection between the two is not 100%.
 

 

 

 

Emodin has potent anti-herpes activity.

Expanding on two (1, 2) previous posts on the general antiviral actions on Emodin, it also seems to be very effective for Herpes Simplex 1. What I find interesting though, is that it's capable of actually reducing the viral load in the brain and other organs. Given the recent association of neurodegenerative diseases and Herpes infections, I think this could have some important applications. Most substances that kill the herpes virus are virucidal only against the free virus. That is, they don't affect the total viral burden inside the cell. Only the extracellular virions are affected and this makes them great topical agents. If you want to eradicate the virus completely (*cough, cure ?) you need to reduce the viral load inside the cells. I thought this was impossible but I found a few substances that can do this. Emodin is one.

There are 6 hits on Pubmed for "herpes" and "emodin". One is an in vivo study.

http://www.ncbi.nlm....m=emodin herpes

http://www.longecity...erpes-activity/

 

VCO
We have had this debate before Niner.
We know VCO crosses the blood brain barrier due to the miraculous recovery from Alz in Dr. MAry Newport's husband, who happened to be suffering from the 'diabetes type II of the brain' type of Alz.
http://www.coconutketones.com/

http://www.gainesvil...icles/130339979

http://health.usf.ed...lingstudies.htm

 

We know that VCO disrupts the lipid bilayer on virii from studies and we know that a clinically effective dosage can be obtained from a great many anecdotal reports.

BHT has similar studies anecdotal reports.

http://augmentinforc...ALTH EFFECT.htm

 

Both are mentioned, with links in the Emodin thread, as is PABA, which I forgot to mention:

 

I have personal experience with PABA, VCO and BHT:

 

I have not had a fever blister in over a year now although I am only taking VCO atm.

PABA + VCO really kicks the but of a fever blister outbreak.

I have seen 'the back of' a bad case of the flu 'broken' on more than one occasion with VCO as well as simian herpes cleared up.

BHT saved my friend from going lame like a stroke victim due to an unknown viral infection.

ie: one side of her face was drooping and her arm unusable until about an hour after a large dose of BHT:

http://www.longecity...ptoms-plz-help/

 

 

Edited by Logic, 15 March 2016 - 11:00 AM.

Some good BHT info here:

http://www.longecity...opic/42592-bht/

Well, let's look at the record.  Emodin does have some moderate anti-herpes activity, but only at huge doses that would cause massive diarrhea in humans, and this was only shown in mice which show much better response to polyphenols than humans.  So there's no evidence that it would work in humans.  The authors of this paper made the odd claim that "the antiviral activity of emodin was found to be equivalent to that of acyclovir in vivo", although the typical dose of acyclovir is much lower than the doses of emodin they used, even adjusting for interspecies scaling.  Maybe acyclovir doesn't work well in mice? 
 
BHT looks a little scary as an oral drug:
 
http://www.ncbi.nlm....les/PMC1010948/
http://www.ncbi.nlm..../pubmed/4045049
http://www.ncbi.nlm....les/PMC1306899/
.
As a topical drug dissolved in oil, it showed some improvement in healing of genital herpes sores. This is a reasonable use of BHT, but it's not clear that it's any better than existing treatments, and isn't a cure, but does sound like it would make you feel better a little sooner.

 

VCO seems to be considered antimicrobial because monolaurin is derived from it, and monolaurin has been shown to have antimicrobial properties.  However, you don't get enough monolaurin from VCO in vivo to have an antimicrobial effect.  Here is a paper that looked at both monolaurin and VCO in vivo against S. Aureus; the monolaurin worked, VCO had no effect.

 

VCO may be helpful for Alzheimers patients, possibly through the formation of ketone bodies, but I seriously doubt that the mechanism is antimicrobial.
 

So I stand by my "nopes" on these three substances as herpes eradication tools.  At present, I don't think there is anything that can truly eradicate herpes because it is so good at hiding out in neurons.  The possible anti-herpetic action of emodin is likely not enough to compensate for its bad PK and toxicity.  BHT might be useful topically.  VCO tastes great.  I have it on oatmeal all the time.

 

Since this is an AD thread, I'll mention that the connection between HSV and AD is not entirely clear; it might be a risk factor, but isn't "the" cause.

“...This drug, in very low doses, turns on the garbage disposal machinery inside neurons to clear toxic proteins from the cell. By clearing intracellular proteins, the drug prevents their accumulation in pathological inclusions called Lewy bodies and/or tangles, and also prevents amyloid secretion into the extracellular space between neurons, so proteins do not form toxic clumps or plaques in the brain,” says the study’s senior investigator, neuroscientist Charbel E-H Moussa, MB, PhD...
http://explore.georg.../news/?ID=70332
 
Here is a nice summary and info on a group buy for Nilotinib:
http://www.longecity...1-month-supply/
 
Yes, I'm pimping the buy! 
I very badly want to get Nilotinib for a dear friend of mine's mom.
She was like a 2nd mother to me and the stress we, as teens, put her through probably contributed to her condition! 

 
Nilotinib group buy target reached.
 
People who have paid:

• resveratrol_guy 100g
• LongLife 100g
• Der Springende Punkt 20g
• noot_in_the_sky 58g
• Logic 30g
• rikelme 10g
• ceridwen 77g
• Alex_G 30 g
• 'other buyer' 200g (wants to remain anonymous)

Total: 625 grams
That means that we have reached our target.  Thx everyone!  
I will be ordering the Nilotinib on Mon, Mar 21 at 0H00 GMT.
(That's at 8pm Sunday night in New York)
Any funds received after this time will have to wait for the next Nilotinib group buy.

Nanoscopic insights into seeding mechanisms and toxicity of α-synuclein species in neurons

The self-assembly of normally soluble proteins into fibrillar amyloid structures is associated with a range of neurodegenerative disorders. Here, we monitor the fate of different forms of α-synuclein (AS), a protein implicated in Parkinson’s disease, via optical nanoscopy directly in neuronal cells. We show that exogenously added preformed AS fibrils elongate by the addition of endogenous AS, naturally present in neurons. In contrast, exogenously added monomeric AS induces aggregate formation within the cells and leads to apoptosis. The latter is significantly reduced by the addition of preformed fibrils, suggesting a neuroprotective role of fibrillar species. The visualization of these effects at the nanoscale shown here opens up new avenues for understanding the links between AS aggregation and neuronal toxicity.

http://www.pnas.org/...41-2726c8f58625