1229 replies to this topic

[albedo]

Magnesium and in particular L-threonate for its better capability to rise brain magnesium levels has been discussed in many places here at LC. I pop recently into this 2015 paper which you might find interesting:

 

By suppressing the expression of anterior pharynx-defective-1α and -1β and inhibiting the aggregation of β-amyloid protein, magnesium ions inhibit the cognitive decline of amyloid precursor protein/presenilin 1 transgenic mice

http://www.ncbi.nlm....pubmed/26293690

 

“Alzheimer's disease (AD) is associated with a magnesium ion (Mg(2+)) deficit in the serum or brain. However, the mechanisms regulating the roles of Mg(2+) in the pathologic condition of AD remain unknown. We studied whether brain Mg(2+) can decrease β-amyloid (Aβ) deposition and ameliorate the cognitive decline in a model of AD, the APPswe/PS1DE9 transgenic (Tg) mouse. We used a recently developed compound, magnesium-L-threonate (MgT), for a treatment that resulted in enhanced clearance of Aβ in an anterior pharynx-defective (APH)-1α/-1β-dependent manner. To further explore how MgT treatment inhibits cognitive decline in APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling pathways were investigated. In neurons, ERK1/2 and PPARγ signaling pathways were activated by MgT treatment, which in turn suppressed (by >80%) the expression of APH-1α/-1β, which is responsible for the deposition of Aβ and potentially contributes to the memory deficit that occurs in AD. More important, Aβ oligomers in the cerebrospinal fluid (CSF) further promoted the expression of APH-1α/-1β (by >2.5-fold), which enhances the γ-cleavage of APP and Aβ deposition during AD progression. These findings provide new insights into the mechanisms of AD progression and are instrumental for developing better strategies to combat the disease.” (red mine)

 

[ceridwen]

APP/PSEN2 here wonder if it would be worth experimenting with as I'm not taking Nilotinib at present.

[Mian Ali Ismail]

APP/PSEN2 here wonder if it would be worth experimenting with as I'm not taking Nilotinib at present.

Wht do you think about Dnase 1 Ceridwen?In a case report it cured one patient 

[ceridwen]

I think it would be good. Group buy?

[Mian Ali Ismail]

Yes ! We can start a group buy.We can include other people in our group buy with other neurodegenerative diseases.

[Der Springende Punkt]

I would definitely join a group buy for dnase 1.

[Mian Ali Ismail]

SInce there are us three interested in group buy and other potential people as well.We should move the conversation forward by finding a supplier,getting it checked by another third party laboratory and then delivering it to the interested people.Patients should know the response/improvement they are having in about 2 days to a weak  as this was the amount of time it took to notice the improvement starting.This could very well be the cure we are looking for !

[Alex_G]

I would be interested in a group buy for DNase I as well.

[Mian Ali Ismail]

Thnks guies for showing interest.Im currently in talk with Logic to arrange a group buy for Dnase 1 who will contract the suppliers ! I will let you guies know of any recent development.

[mag1]

You all are amazing!

If someone did not grab this bull by the horns we would have had to wait years (decades?) for an update on this!

Why wait decades when we could find out in two days!

 

Really would be startling if there were actually a cure with a published patient and no one did anything.

 

Has anyone looked into going through an off-label prescription from the regulated channels?

I wonder if the pharma involved might even establish a special program to help patients gain access.

Perhaps the FDA would have rules against that.

 

Anyone on the thread have any comments on possible side-effects of DNAse1 at these doses?

A pancreatic enzyme sounds fairly innocuous, though you never know.

 

 

Edited by mag1, 16 June 2016 - 03:20 AM.

[Mian Ali Ismail]

Thnks mag 1. I read in a news paper that the reasearchers reccommended the use of the drug offlabel but I doubt that insurance would cover it until all clinical trials requirements are met.You could contact the researchers and ask them of any sideeffects but there werent any sideeffects in this trial.

 

Victor and George Tetz and the Human Microbiology Institute, please contact Max Smetannikov with MVG at 917 310 339

[docmaas]

I'm interested too but I'd really like to see a sample size > 1.  

 

Mike

[Mian Ali Ismail]

 Is anybody already taking Dnase 1 and can pulmozyme used in nebulizer be taken orally without any sideeffects ?

[Mian Ali Ismail]

Treatment with DNase I in the present case allowed our patient to withdraw from a terminal state and resulted in significant improvements in cognitive and behavioral function, including the ability to walk and perform everyday tasks with near independence. DNase I was used as a repurposed FDA-approved medication [14]. Significant recovery was observed in all areas of cognitive and motor function, indicating the possibility of a DNase-sensitive target involved in generating the symptoms of AD.

Cell-free DNA, including bacteria-derived DNA, may be one such target [15]. Circulating cf-DNA has been observed to play an important role in the progression and maintenance of different disease states, including cancer, stroke, and other [16, 17]. Our previous research revealed its possible role as a therapeutic target in graft-versus-host diseases [18].

Though there are various suggestions regarding the origins of serum and plasma cf-DNA, many researchers have speculated that it results from apoptosis, necrosis, or both, or that this cf-DNA is secreted by cancer cells, microorganisms, hematopoietic cells, and/or neutrophils [19]. However, the physiological role of cf-DNA in the progression of these diseases remains to be discovered. Some have theorized that this role is mechanical in nature, increasing blood viscosity and leading to ischemia, while others suggest that cellular uptake of cf-DNA is involved in the development of metastatic conditions [20]. Little research has focused on the role of cf-DNA in neurodegenerative conditions, particularly AD. Further studies are required in order to evaluate the role of cf-DNA in the incidence and progression of neurodegenerative pathologies.

[Psilociraptor1]

Sci Transl Med. 2016 May 25;8(340):340ra72.
Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease.
Kumar DK1, Choi SH1, Washicosky KJ1, Eimer WA1, Tucker S1, Ghofrani J1, Lefkowitz A1, et al.
The amyloid-β peptide (Aβ) is a key protein in Alzheimer's disease (AD) pathology. We previously reported in vitro evidence suggesting that Aβ is an antimicrobial peptide. We present in vivo data showing that Aβ expression protects against fungal and bacterial infections in mouse, nematode, and cell culture models of AD. We show that Aβ oligomerization, a behavior traditionally viewed as intrinsically pathological, may be necessary for the antimicrobial activities of the peptide. Collectively, our data are consistent with a model in which soluble Aβ oligomers first bind to microbial cell wall carbohydrates via a heparin-binding domain. Developing protofibrils inhibited pathogen adhesion to host cells. Propagating β-amyloid fibrils mediate agglutination and eventual entrapment of unatttached microbes. Consistent with our model, Salmonella Typhimurium bacterial infection of the brains of transgenic 5XFAD mice resulted in rapid seeding and accelerated β-amyloid deposition, which closely colocalized with the invading bacteria. Our findings raise the intriguing possibility that β-amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis. These data suggest a dual protective/damaging role for Aβ, as has been described for other antimicrobial peptides.

PMID: 27225182

 

PubMed Commons:

Claudiu Bandea 2016 May 28 8:06 p.m.

Remarkable results, questionable report

 

"Our findings raise the intriguing possibility that β-amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis" (1). Indeed, fascinating findings. What Kumar et al. did not articulate, though, is that their result is one of many findings, observations, and arguments supporting the theory (2,3) that:

 

(i) β-amyloid, tau, α-synuclein, huntingtin, TDP-43, prion protein and other primary proteins implicated in neurodegenerative diseases are members of the innate immune system;

(ii) The isomeric conformational changes of these proteins and their assembly into various oligomers, plaques, and tangles are not protein misfolding events as defined for decades, nor are they prion-replication activities, but part of their normal, evolutionarily selected innate immune repertoire;

(iii) The immune reactions and activities associated with the function of these proteins in innate immunity lead to Alzheimer’s, Parkinson’s, Huntington’s, ALS and Creutzfeldt-Jakob Disease, which are innate immunity disorders.

 

Generating data and observations, although essential, represents only half of the scientific process; the other is their interpretation and integration into the existing knowledge and paradigms. That’s where the article by Kumar et al. falls short.

 

Perhaps the authors were not fully familiar with the literature and paradigms in the field of neurodegenerative diseases. Or, perhaps, Kumar et al. did not consider it relevant to discuss their results in the context of previous findings, ideas and hypotheses. For example, the authors did not address or explain their results in context of the ‘prion’ paradigm, which has dominated the thinking in the field of Alzheimer’s and other neurodegenerative diseases in the last few years (e.g. 4,5,6,7). Nor did they refer to a related study entitled "Alpha-synuclein expression restricts RNA viral infections in the brain" (8), which is highly relevant considering the fact that alpha-synuclein, a putative member of the innate immune system and the primary protein implicated in Parkinson’s, is a significant player in Alzheimer’s disease. Also, some might consider highly questionable leaving out the study by Kobayashi et al. entitled "Binding sites on tau proteins as components for antimicrobial peptides" (9).

 

Given these omissions, it's no wonder in her The New York Times article on Kumar et al. study, Gina Kolata wrote: "The Harvard researchers report a scenario seemingly out of science fiction".

 

This is interesting though I'm having some internal conflict about it. Dr Judith Milkossy and Alan McDonald have also posted numerous studies identifying spirochetal infections in alzheimers lesions. My issue is that amyloids are also fundamental components of bacterial biofilms and therefor would be expected to bind to microorganisms without necessarily conferring immunity to the host. Unfortunately I do not have access to that full article, but I'm wondering if the authors are conflating "microbial entrapment" with intentional biofilm formation. There is also the possibility that certain bacteria exploit innate immune function and cross seed with endogenous amyloids making the distinction somewhat ambiguous. My personal feelings are that the presence of accumulated amyloids is more suggestive of biofilm formation than functional immune response. Interestingly I've noticed that many herbs that are reported to reverse beta-amyloid deposits are also potent biofilm erradicators. Ie flavonoids and related compounds such as baicelain and EGCG.

 

Interestingly the use of DNaseI is also a noted biofilm disrupter. I'm surprised to hear of in vivo efficacy though. Especially for a brain disorder.
 

Edited by Psilociraptor1, 28 June 2016 - 10:54 PM.

[normalizing]

what is the meaning of "biofilm disruptor" can you explain the meaning better and how this mechanism works?

Edited by normalizing, 29 June 2016 - 04:41 AM.

[Psilociraptor1]

what is the meaning of "biofilm disruptor" can you explain the meaning better and how this mechanism works?

 

Pretty much exactly what it sounds like. Something that disrupts biofilm development and or the structural integrity of mature biofilms. There is no "one" mechanism for it. DNases have been said to destabalize them by cleaving some of DNA that's wound into the biofilm matrix. I don't know enough to say what their exact structural role is. Chelating agents can disrupt some biofilms that rely on iron for structure. Biofilm disruptors may also be proteolytic enzymes, quorum sensor inhibitors, agents which stimulate bacterial disaggregation pathways etc. This is a pretty understudied science and what works in vivo is almost completely unknown but these are the sorts of things studied in labs at the moment.

[Psilociraptor1]

So I referred to Dr Miklossy earlier. Just realized she recently published a new study discussing the role of infectious microorganisms and biofilm formation in Alzheimers http://content.iospr...sease/jad160451 So it seems that both human and bacterial amyloids may be involved though the interaction isn't totally clear.

[Mian Ali Ismail]

Hi Guies,

 

I recieved an Email from the researchers in which they replied to my question regarding Side effects that there were No Side effects in the patient taking Dnase 1.

 

Best Regards

 

[normalizing]

there are always side effects in everything we take be that food, supplement synthetic or natural etc. they must be bullshitting

[Logic]

So I referred to Dr Miklossy earlier. Just realized she recently published a new study discussing the role of infectious microorganisms and biofilm formation in Alzheimers http://content.iospr...sease/jad160451 So it seems that both human and bacterial amyloids may be involved though the interaction isn't totally clear.

 

There is a lot of anti biofilm info on Longecity:
https://cse.google.c...0&gsc.q=biofilm

 

I am keen to hear your recommendations and find possible synergistic/powerful combinations capable of effectively treating all the different varieties Psilociraptor1.
I feel that starting with those that form in the gut would be best?

Edited by Logic, 30 June 2016 - 12:16 PM.

[Psilociraptor1]

 

So I referred to Dr Miklossy earlier. Just realized she recently published a new study discussing the role of infectious microorganisms and biofilm formation in Alzheimers http://content.iospr...sease/jad160451 So it seems that both human and bacterial amyloids may be involved though the interaction isn't totally clear.

 

There is a lot of anti biofilm info on Longecity:
https://cse.google.c...0&gsc.q=biofilm

 

I am keen to hear your recommendations and find possible synergistic/powerful combinations capable of effectively treating all the different varieties Psilociraptor1.
I feel that starting with those that form in the gut would be best?

 

 

Sorry my post limit prevented me from getting back to you XD To be honest I'm not sure about the ones in the gut. Some of them are healthy and prevent colonization by pathogens. So it's not quite as black and white as the fact that you probably shouldn't have significant biofilm formation in your brain. So I'm not sure whether there are any supplements or drugs which descriminate between healthy intestinal biofilms and unhealthy ones. It's not something I've looked into extensively. As for the types in alzheimers plaques and localized disease processes, there is very little info on this. One of the problems is that many of the agents you've linked to in the search have not been shown to be so effective against spirochetal biofilms that were demonstrated in the paper i linked. Unfortunately I don't have a source as it was unpublished work but Eva Sapi who is the leader in borrelial biofilms claims to have tested around 100 compounds at the request of others. She talks about this on some of her youtube lectures if you're interested. In contrast she said staph biofilms practically melt away with some of the agents mentioned. So there is definitely a level of heterogeneity that makes this a difficult thing to tackle. One of the only ones she found truly remarkable was stevia (note different formulations had dramatically different effects) http://www.ncbi.nlm....les/PMC4681354/ Her theory is that as a "sugar-like" molecule it sort of acts as a trojan horse, signaling biofilm communities to open nutrient channels and making them permeable to stevia (which is an antimicrobial itself) as well as other antibiotics. I'm not aware of any proof of this, but other sugar substitutes like xylitol and erythritol have also been noted for antibiofilm effects. It seems lactoferrin might have some effect as well http://www.newhaven.edu/887913.pdf Unfortunately it seems as if her students sometimes publish without undergoing peer-review. Notice how the title talks about cannabidiol yet theres no cannabidiol mentioned anywhere in the paper. She herself is a respectable scientist so I don't worry so much about the credability and assume its just part of the learning process.

 

So beyond that one of the strategies I've been using is, in the light that alzheimers plaques may be spirochetal biofilms, looking up herbs known for their neuroprotective properties and scanning the literature for their effects on beta-amyloid disaggregation. This may not be particularly relevant given that mouse alzheimer models don't account for biofilm amyloids and there is an obviously complex interplay between endogenous and bacterial amyloids. But nonetheless it may indicate some antibiofilm potential. I only started this the other day and haven't had the mental energy to rigorously analyze these studies so this is just a starting place for me but I'll share it nonetheless.

 

Salvia Miltiorrhiza (dan shen) - increases alpha-secretase, decreases amyloid fibril formation, protects against amyloid induced cytotoxicity, and dissociates preformed amyloid fibrils

 

http://www.ncbi.nlm....pubmed/19154776

http://www.ncbi.nlm....pubmed/22102154

http://www.ncbi.nlm....pubmed/23506133

 

Withania Somnifera (ashwagandha, indian ginseng) - decreases amyloid burden through peripheral transport by lipoprotein system. This is interesting. I knew that lipoproteins played a role in endotoxin detoxification but didn't know about amyloid transport.

 

http://www.ncbi.nlm....ubmed/22308347 

 

Sculletaria baicalein (chinese skullcap) - Shows antibiofilm affects against Borrelia. I am fairly positive I have read that it also disaggregates preformed amyloid fibrils though i can't seem to find that at the moment. Nonetheless there are numerous studies on its constituent Baicalein in regards to amyloid toxicity and deposition so I will not link them as they are quite easy to find and I haven't read enough to recommend one in particular.

 

http://www.ncbi.nlm....pubmed/26457476 (This one also suggests monolaurin is effective)

 

Curcumin and Rosmarinic Acid - multiple effects on amyloid aggregation including destabilization of preformed amyloids

 

http://www.ncbi.nlm....ubmed/14994335/

 

Fermented Ginseng - decreases amyloid burden

 

http://www.ncbi.nlm....les/PMC3659620/

 

Centella Asiatica

 

http://www.ncbi.nlm....pubmed/19048607

 

Uncaria Rhynchophylla - tested strongest on a list of herbs for anti-aggregation effects as well as showed the ability to destablize preformed fibrils.

 

http://www.ncbi.nlm....pubmed/16676329

 

As baicalein from skullcap has shown activity against borrelial biofilms and beta-amyloid deposits i find it one of the more interesting. So i looked into some other flavenoids...

 

Quercetin - anti-amyloid effects as well as anti quorum-sensing/biofilm effects in pseudomonas. Doesn't necessarily translate to spirochetes, but given the structural relation to baicalein...

 

http://www.ncbi.nlm....pubmed/27114256

http://www.ncbi.nlm....pubmed/26808465

 

EGCG (green tea catechin) - "virtually eliminates E. coli biofilm" and "remodels mature amyloid".

 

http://www.ncbi.nlm....pubmed/23611538

http://www.ncbi.nlm....pubmed/26992034

 

I haven't looked as much into others, but things like luteolin and chryoserial may be similar. I ran across something about synergy between flavanoids but forgot to save it.

 

Given the historic role of Uncaria Rhynchophylla and Chinese Skullcap in cognitive disorders I'm more intrigued by this version of uncaria and the flavenoids the most. The fact that flavenoids show some pretty strong antibiofilm effect in general is encouraging too especially given that the mouse model of alzheimers may not be reflective of the actual disease involving biofilms. On the flip side, the benefit of using alzheimer models is the good indication of bioavailability which is further supported by the historic use of skullcap and uncaria. The problem is that other flavenoids don't seem to have very good bioavailability. So this makes me wonder about baicalein. Whether it is simply unique, enhanced by other aspects of skullcap, or enhanced by herb synergy which is frequently used in traditional practices. Unfortunately herb synegy is very much a lost practice in contemporary medicine.

 

 

[ceridwen]

Have you thought about tau at all?

[Psilociraptor1]

Have you thought about tau at all?

 

To be honest I'm not that involved in reading alzheimers literature. My interest is really in microorganisms and how they promote inflammatory and metabolic diseases on a more broad level. I only dove into alzheimers because there is so little on biofilms in diseases and this was the first implication in a disease that has been studied widely. So I've heard of tau, but I'm not quite familiar with its function. Do you think it's anything that will be particularly relevant to my interest in this?

[Mian Ali Ismail]

Any news on suppliers of Dnase 1 guies ?

[mag1]

http://www.ncbi.nlm....2?dopt=Abstract

[Logic]

Sorry my post limit prevented me from getting back to you XD To be honest I'm not sure about the ones in the gut. Some of them are healthy and prevent colonization by pathogens. So it's not quite as black and white as the fact that you probably shouldn't have significant biofilm formation in your brain. So I'm not sure whether there are any supplements or drugs which descriminate between healthy intestinal biofilms and unhealthy ones. It's not something I've looked into extensively. As for the types in alzheimers plaques and localized disease processes, there is very little info on this. One of the problems is that many of the agents you've linked to in the search have not been shown to be so effective against spirochetal biofilms that were demonstrated in the paper i linked. Unfortunately I don't have a source as it was unpublished work but Eva Sapi who is the leader in borrelial biofilms claims to have tested around 100 compounds at the request of others. She talks about this on some of her youtube lectures if you're interested. In contrast she said staph biofilms practically melt away with some of the agents mentioned. So there is definitely a level of heterogeneity that makes this a difficult thing to tackle. One of the only ones she found truly remarkable was stevia (note different formulations had dramatically different effects) http://www.ncbi.nlm....les/PMC4681354/ Her theory is that as a "sugar-like" molecule it sort of acts as a trojan horse, signaling biofilm communities to open nutrient channels and making them permeable to stevia (which is an antimicrobial itself) as well as other antibiotics. I'm not aware of any proof of this, but other sugar substitutes like xylitol and erythritol have also been noted for antibiofilm effects. It seems lactoferrin might have some effect as well http://www.newhaven.edu/887913.pdf Unfortunately it seems as if her students sometimes publish without undergoing peer-review. Notice how the title talks about cannabidiol yet theres no cannabidiol mentioned anywhere in the paper. She herself is a respectable scientist so I don't worry so much about the credability and assume its just part of the learning process.

 

So beyond that one of the strategies I've been using is, in the light that alzheimers plaques may be spirochetal biofilms, looking up herbs known for their neuroprotective properties and scanning the literature for their effects on beta-amyloid disaggregation. This may not be particularly relevant given that mouse alzheimer models don't account for biofilm amyloids and there is an obviously complex interplay between endogenous and bacterial amyloids. But nonetheless it may indicate some antibiofilm potential. I only started this the other day and haven't had the mental energy to rigorously analyze these studies so this is just a starting place for me but I'll share it nonetheless.

 

Salvia Miltiorrhiza (dan shen) - increases alpha-secretase, decreases amyloid fibril formation, protects against amyloid induced cytotoxicity, and dissociates preformed amyloid fibrils

 

http://www.ncbi.nlm....pubmed/19154776

http://www.ncbi.nlm....pubmed/22102154

http://www.ncbi.nlm....pubmed/23506133

 

Withania Somnifera (ashwagandha, indian ginseng) - decreases amyloid burden through peripheral transport by lipoprotein system. This is interesting. I knew that lipoproteins played a role in endotoxin detoxification but didn't know about amyloid transport.

 

http://www.ncbi.nlm....ubmed/22308347 

 

Sculletaria baicalein (chinese skullcap) - Shows antibiofilm affects against Borrelia. I am fairly positive I have read that it also disaggregates preformed amyloid fibrils though i can't seem to find that at the moment. Nonetheless there are numerous studies on its constituent Baicalein in regards to amyloid toxicity and deposition so I will not link them as they are quite easy to find and I haven't read enough to recommend one in particular.

 

http://www.ncbi.nlm....pubmed/26457476 (This one also suggests monolaurin is effective)

 

Curcumin and Rosmarinic Acid - multiple effects on amyloid aggregation including destabilization of preformed amyloids

 

http://www.ncbi.nlm....ubmed/14994335/

 

Fermented Ginseng - decreases amyloid burden

 

http://www.ncbi.nlm....les/PMC3659620/

 

Centella Asiatica

 

http://www.ncbi.nlm....pubmed/19048607

 

Uncaria Rhynchophylla - tested strongest on a list of herbs for anti-aggregation effects as well as showed the ability to destablize preformed fibrils.

 

http://www.ncbi.nlm....pubmed/16676329

 

As baicalein from skullcap has shown activity against borrelial biofilms and beta-amyloid deposits i find it one of the more interesting. So i looked into some other flavenoids...

 

Quercetin - anti-amyloid effects as well as anti quorum-sensing/biofilm effects in pseudomonas. Doesn't necessarily translate to spirochetes, but given the structural relation to baicalein...

 

http://www.ncbi.nlm....pubmed/27114256

http://www.ncbi.nlm....pubmed/26808465

 

EGCG (green tea catechin) - "virtually eliminates E. coli biofilm" and "remodels mature amyloid".

 

http://www.ncbi.nlm....pubmed/23611538

http://www.ncbi.nlm....pubmed/26992034

 

I haven't looked as much into others, but things like luteolin and chryoserial may be similar. I ran across something about synergy between flavanoids but forgot to save it.

 

Given the historic role of Uncaria Rhynchophylla and Chinese Skullcap in cognitive disorders I'm more intrigued by this version of uncaria and the flavenoids the most. The fact that flavenoids show some pretty strong antibiofilm effect in general is encouraging too especially given that the mouse model of alzheimers may not be reflective of the actual disease involving biofilms. On the flip side, the benefit of using alzheimer models is the good indication of bioavailability which is further supported by the historic use of skullcap and uncaria. The problem is that other flavenoids don't seem to have very good bioavailability. So this makes me wonder about baicalein. Whether it is simply unique, enhanced by other aspects of skullcap, or enhanced by herb synergy which is frequently used in traditional practices. Unfortunately herb synegy is very much a lost practice in contemporary medicine.

 

 

Thx.
I agree that herbal synergies is becoming something of a lost 'art' and think we would do well to look more closely at oriental, ayurvedic etc combinations.

 

One certainly does not want to take out beneficial bacteria and biofilms!  Hence bacteriophages:

These are virii that live on bacteria and are very fussy/specific to the bacteria they 'consume'.

A case in point is M13 which not only kills E. Coli but serendipitously also 'dissolves' amyloid-beta plaques!

http://www.pbs.org/w...lzheimers-cure/

 

 

 

 

[Psilociraptor1]

The only problem i see with phages is that they are supposedly very specific. Most hosts are infected with many microorganisms each of which may exhibit extraordinary genetic variability within a given species alone. I'm not saying it shouldn't be used but i don't know how easy it would be to identify a particular organismal cause for a particular condition and treat it with such a narrow spectrum therapy. This is another reason herbs interest me. They tend to have complex ecological functions that are hard to produce synthetically. Ie I do wonder whether some herbs may promote healthy biofilms while dissolving others. More research into that would be certainly interesting

[Logic]

The only problem i see with phages is that they are supposedly very specific. Most hosts are infected with many microorganisms each of which may exhibit extraordinary genetic variability within a given species alone. I'm not saying it shouldn't be used but i don't know how easy it would be to identify a particular organismal cause for a particular condition and treat it with such a narrow spectrum therapy. This is another reason herbs interest me. They tend to have complex ecological functions that are hard to produce synthetically. Ie I do wonder whether some herbs may promote healthy biofilms while dissolving others. More research into that would be certainly interesting

 

Yes herbs or a herbal mixture capable of promoting healthy biofilms while dissolving others would be a boon.
I don't mean to detract from your quest and research by bringing up phages but rather add to it.
After all; biofilms consist of many 'components' and one still has to kill the biofilm forming bacteria once the biofilm is removed.

 

Yes phages are very specific.
That's both a blessing and a curse in that one does not have to worry about them killing off the wrong, beneficial bacteria in, say, the gut, or infecting healthy cells, but what works for one person's Candida infection, for example, may not work in another person's.

(Keep the gut-brain connecting in mind)

As I understand it; a visit to a phage therapy center will entail the isolation/purification of the bacteria bugging you, and then they add a vast array of phages, see which one multiplies, isolate/purify it and culture it.
You then end up with a phage specific to you particular infection/s.

 

This has hindered the commercialization of phages, but there do seem to be phage mixtures for the most common bacterial infections available.

A mixture that took out all the bad players in the gut would be something I would definitely want to get:

One can only imagine the effects of not having any toxins (LPS etc.), infections and unwanted 'nutrients' getting into one's system!

[Psilociraptor1]

That's interesting. I'll definitely have to look into that more. I didn't realize they could do a quick screening of many phages like that. Do they flat out kill an entire species? Or is it concentration dependent so you can just dial it back to a healthy balance? I don't tend to think there are bad players so much as simple imbalances in the ecology