156 replies to this topic

[Mian Ali Ismail]

NEW YORK, June 7, 2016 /PRNewswire/ -- Researchers at the Human Microbiology Institute (HMI) have uncovered a potential new Alzheimer's treatment that significantly reversed the late-stage effects of the debilitating neurodegenerative disease.

Logo - http://photos.prnewswire.com/prnh/20160606/376069LOGO

The results, published in the Journal of Medical Case Reports, details the promising results that the research duo of Victor and George Tetz had in treating a 77-year-old Alzheimer's patient with the repurposed medication deoxyribonuclease I, an enzyme approved by the U.S. Food and Drug Administration for the treatment of mucus buildup in cystic fibrosis patients.

"Our results show potential for reversing the effects of a disease that dramatically impacts not only millions of patients around the world, but also their families," said George Tetz, scientific officer, at HMI.  "Our experimental drug has given one patient a new lease on life, and now we are continuing with our tests with the hopes of reversing the devastating effects of Alzheimer's disease and other incurable diseases like dementia and Parkinson's."

According to the published case study, the male patient had been diagnosed with dementia and behavioral disturbance secondary to late-onset Alzheimer's disease 30 months before the researchers first saw him. He had been undergoing routine treatment, but his cognitive condition continued to deteriorate and he had rapidly progressing amnesia and behavioral changes.

The patient was unable to remember his name or family members, among other things, and had been diagnosed as terminal when his family agreed to try DNase I. Just two days after treatment began, improvements were seen. And he was soon able to recognize family members, dress himself, tie his shoelaces, feed himself and walk and ride an exercise bike.

"Treatment with DNase I allowed the 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," said Victor Tetz, scientific advisor at HMI.

HMI, a non-profit research organization, is working to convert its work into a drug to help treat dementia, Alzheimer's and Parkinson's diseases.

Alzheimer's disease is the most common cause of dementia and is characterized by a progressive loss of brain tissue leading to amyloid-b accumulation and severe decline in cognitive function. 

More than 5 million Americans are living with Alzheimer's disease. The cause of Alzheimer's disease is poorly understood, and available treatments are limited in their efficacy, particularly for patients with more severe symptoms.

http://www.prnewswir...-300280725.html

[resveratrol_guy]

Thanks for making a thread about this, Ali. Here is the detailed summary.

While I find the claims rather dubious (like MMSE going from 3 to 18), the basic approach is novel and potentially productive. As I understand it, they're using DNase 1 to cleave "cell-free" DNA, meaning DNA strands that are randomly floating around the system and presumably getting in the way. To date, I've never heard of this stuff being a problem in any form of dementia; the focus has been on plaque disaggregation and vascular healing, not DNA cleaving.

However, surely DNA must comprise a significant portion of insoluble neuron mass. By "insoluble", I'm referring to the neurolysis products which cannot cross the BBB after the neuron dies, leading to the aggregration of intercellular junk. The dominant theory seems to be that phosphotau is the most harmful such junk, which eventually aggregates into neurofibrillary tangles much too large to eliminate other than by macroautophagy, which is impaired in Alzheimer's brains. But maybe this is sort of wrong. Maybe a large portion of the plaque is actually residual DNA left from dead neurons and invasive pathogens such as fungi and virusses. After all, these strands would be much too large to cross the BBB, except via a breach, which even in dementia patients, is relatively rare as compared to functional vessels.

It's also possible that researchers have been aware of this DNA mass for years, but presumed that it was just a normal part of healthy neurons, and disregarded it in their analysis. After all, one would need to sequence it in order to discover that it was, to the contrary, either postapoptotic or alien in origin. This reminds me of the discovery of neural microtubules, which according to Dr. Stuart Hameroff, was delayed for decades because the stain that was used to analyze neurons caused these internal structures to rapidly dissolve. In other words, maybe this "rogue DNA" has been staring us in the face for years, hiding likes trees in a forest.

Even if this theory is true, it doesn't mean that phosphotau, amyloid, vascular compromise, or metal ions are irrelevant. But it might mean that we can partially reverse progression with a monotherapy, which would be rather astounding if true.

If anyone has more research on this, let's hear about it.
 

[deetown]

Thedistribution of deoxyribonuclease I (DNase I) in human and rat stomachs was examined by biochemical, molecular biological and immunohistochemical techniques. By the use of monoclonal anti-human DNase I and polyclonal anti-rat DNase I antibodies, we determined that strong immunoreactivity was present in the cytoplasm of chief cells of the human fundus and the rat pars glandularis, respectively. High DNase I enzyme activity was detected in tissue homogenates of both human fundus and rat pars glandularis. The presence of DNase I-specific mRNA was verified by reverse transcriptase-polymerase chain reaction analysis of the total RNAs extracted from human and rat stomachs. Immunoelectron microscopy revealed gold particles localized in the chief cells, with most labelling in exocrine secretory granules. These results show that the chief cells of human and rat stomach produce DNase I. This is the first report to demonstrate that secretion of DNase I is controlled by the chief cells in human and rat stomachs.

→ source (external link)

BACKGROUND:
Deoxyribonuclease I (DNase-I) plays an important role in the elimination of damaged-, aging- or cancer cells. Various authors suggest that programmed cell death (PCD) is attenuated in cancer cells due to a reduced activity of DNase-I.
MATERIAL AND METHODS:
In this work, we evaluated cell viability (violet crystal stain), cell proliferation (tritiated thymidine) and DNA degradation of tumoral cells (Calu-1, SK-MES-1, HeLa, HEp-2, L-929) incubated with different concentrations of DNase I. PBMN cells and human fetal fibroblasts served as controls.
RESULTS:
Our results showed a >90% decrease in the viability of HeLa and HEp-2 cells, and >50%<90% decline in Calu-1, SK-MES-1 and L-929 cell viability, incubated with 9 mg/ml of DNase-I in comparison with control cells (p<0.05). The incorporation of [3H]thymidine showed a 50% decrease in tumoral cells. Control cells showed no significant differences. Tumor cell DNA degradation was observed after nuclease treatment, however the typical DNA ladder, characteristic of the apoptotic cell, was not observed. The morphology of some DNAse-I treated tumor cells suggested autoschizis
CONCLUSION:
Our results suggest that the use of a DNA nuclease might have some benefits in the treatment of cancer since it inhibits cell growth, probably by inducing autoschizis.

→ source (external link)

Exerciseis a potent stimulus for enhancing circulating DNase activity

→ source (external link)

abstract: Theconcentration of circulating DNA (cirDNA) and deoxyribonuclease activity in blood plasma of healthy donors and patients with colon or stomach cancer were analyzed. The concentration of DNA was measured using Hoechst 33258 fluorescent assay after the isolation by the glass–milk protocol. A 1-kbp PCR product labeled with biotinylated forward and fluorescein-labeled reverse primers was used as a substrate for DNase. DNase activity was estimated from the data of immunochemical detection of the nonhydrolyzed amplicon. The average concentration of cirDNA in the plasma of healthy donors was low (34 ± 34 ng/mL), and was accompanied with high DNase activity (0.356 ± 0.410 U/mL). The increased concentrations of cirDNA in blood plasma of patients with colon and stomach cancer were accompanied by a decrease in DNase activity below the detection level of the assay. The data obtained demonstrate that low DNase activity in blood plasma of cancer patients can cause an increase in the concentration of cirDNA.

→ source (external link)

 

[gamesguru]

i have a feeling its related to brain inflammation, and possibly HSV-1 immune response

Several lines of evidence indicate that the immune response to DNA in systemic lupus erythematosus (SLE) is antigen-driven [11–13]. For this reason, treatment of SLE with bovine DNase I was first attempted in the 1960s [14]. However, bovine DNase I was immunogenic in humans and chronic treatment was not possible. Recently, Macanovic et al. demonstrated that systemic adminstration of recombinant murine DNase I delayed the progression of SLE in NZB/W mice [15]. Therefore, systemic administration of Pulmozyme® recombinant human DNase I (rhDNase) may be an effective, non-immunogenic therapeutic for human SLE, as proposed by Lachmann [16]. rhDNase may hydrolyse the DNA component of membrane-deposited DNA/anti-DNA immune complexes, facilitating excretion of the anti-DNA antibodies into the urine and reducing glomerular inflammation. Alternatively, rhDNase may hydrolyse free and/or antibody-complexed DNA in blood, reducing the antigen load and thereby leading to a reduction in anti-DNA levels and in the deposition of immune complexes.

[Mian Ali Ismail]

I think since it helps in waste management endonuclease it might help in senesence Or probably its effect might be symptomatic.

 

Can it be taken orally and where can I get it from.Can I use the one used for nebulization and mix it in water?Will it have some side effects orally and what about its bioavailability ?

[gamesguru]

not symptomatic in the end-stage, it is definitely working to prevent or break down fibrils and plaques

[Alex_G]

I saw that on sigma aldrich's website they list human as well as bovine DNase. Is there much difference between the two? The bovine source seems as if it could be affordable.

I'm not a biologist (or anything else that would know the specifics of biochemistry) so thanks for the feedback.

[Mian Ali Ismail]

The effect of Pulmozyme overdosage has not been established. Cystic fibrosis patients have inhaled up to 20 mg Pulmozyme twice daily (16 times the recommended daily dose) for up to 6 days and 10 mg twice daily (8 times the recommended dose) intermittently (2 weeks on / 2 weeks off Pulmozyme) for 168 days. Six adult non-cystic fibrosis patients received a single intravenous dose of 125 mcg/kg of Pulmozyme, followed 7 days later by 125 mcg/kg subcutaneously for two consecutive 5-day periods, without either neutralising antibodies to DNase or any change in serum antibodies against doublestranded DNA being detected. All of these doses were well tolerated. Systemic toxicity of Pulmozyme has not been observed and is not expected due to the poor absorption and short serum half-life of dornase alfa. Systemic treatment of overdose is therefore unlikely to be necessary (see Pharmacokinetic Properties).

 

To test safety it says here that it was also given subcutaneously at125mcg/kg  for two consecutive 5-day periods.

 

Does this mean oral absorption is safe ?

[gamesguru]

Is there much difference between the two? The bovine source seems as if it could be affordable.

 

yeah, the bovine source is immunogenic in humans

[resveratrol_guy]

not symptomatic in the end-stage, it is definitely working to prevent or break down fibrils and plaques

 

Is it actually possible for DNase 1 to cleave fibrils and plaques, which are technically peptides and presumably do not contain the AGCT nucleotides? I would think not, but Wikipedia's article on it is unclear as to what it can, and cannot, cleave.

 

There might also be DNA mixed in with plaque strands, so cleaving the DNA might cause the aggregate to unwind. But I think this is unlikely because it would be hard to cleave such "knotted" DNA. So for the moment, I'm going with the theory that the mechanism of action is simply the lysis of long strands of cell-free DNA. If you cut DNA into sufficiently tiny pieces, it can do some important things: (1) migrate out of localized cfDNA aggregates and into the rest of the brain and (2) cross the BBB. Either one of these would delay the Alzheimer's process because doing so would trade concentrated pollution for diffuse pollution, the latter being less conducive to the chain reaction. And yes, I did say "cfDNA aggregate". Implicitly, I'm assuming that some of the brain plaque in AD is actually rogue DNA, probably tangled up with conventional plaque.

 

The more DNA and the less conventional plaque in any given aggregate, the more likely it is that DNase 1 would be useful at disaggregation. To be clear, I think we need to imagine AD as a sort of dysfunctional garden, where the healthy plants (neurons) are interspersed with weeds (plaques and tangles). The weeds, in turn, are a mixture of several different species. And the mixture itself may vary from one location to another. cfDNA might dominate in this region, while phosphotau dominates in that one.

 

It would be nice if we could find so much as one other study which made similar observations. At least, we have the cancer studies above suggesting that cfDNA might be a universal problem rather like alpha synuclein. So, I don't think this AD theory is totally bonkers. But we definitely need more evidence.

 

[resveratrol_guy]

 

Is there much difference between the two? The bovine source seems as if it could be affordable.

 

yeah, the bovine source is immunogenic in humans

 

Too bad the human stuff is so expensive:

 

http://www.sinobiolo...ody-a-6298.html
 

[Mian Ali Ismail]

 

 

Is there much difference between the two? The bovine source seems as if it could be affordable.

 

yeah, the bovine source is immunogenic in humans

 

Too bad the human stuff is so expensive:

 

http://www.sinobiolo...ody-a-6298.html
 

It is already available in the market by the name of Pulmozyne !Cant it be used ?

 

[Der Springende Punkt]

 

i have a feeling its related to brain inflammation, and possibly HSV-1 immune response

 

 

This article also mentions the suggestion that cf-DNA could promote auto-inflammation and that this may be one reason why DNase 1 was so helpful in the patient:

 

 

In addition, it has been suggested that cf-DNA could promote auto-inflammation. In this study which was published by another group of researchers at roughly the same time auto-inflammation was observed to be a possible cause of dementia. The researchers put together strong arguments that the neurological decline common to these diseases is caused by ‘auto-inflammation’, where the body’s own immune system develops a persistent inflammatory response and causes brain cells to die.

 

[gamesguru]

one theory gaining a lot of weight is that HSV-1 is linked to dementia. the virus enters the brain from the nose or eyes, sometimes the lips. normally an equilibrium between the immune response and virus exists, but if the immune system gets overzealous (or lazy, obviously) the virus has tricky immune evasion stategies that can actually punish the whole effort. according to the theory the fibrils, tangles and waste product are the result of an immune response and overactive microglia. your immune cells are deficating in your synaptic cleft faster than your deep sleep can purge it

[Linda Gray]

Thanks for this thread. I'm very interested in the potential for MSA and Alzheimer's.

[Mian Ali Ismail]

There are 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 !

 

[deetown]

I would buy a large quantity in a group buy

[Mian Ali Ismail]

This artcle seems to describe the condition of the patient in more detail.What is interesting is the patient was able to walk who was bedridden earlier.

 

A remarkable study was published about the treatment of a 77-year-old Caucasian man with severe dementia and behavioral disturbance. The man was admitted with late onset Alzheimer’s Disease and treated with memamtine. His condition however continued to decline. 16 months after the start of memamtine treatment the patient’s condition had severely worsened. He was unable to remember his name, the calendar date, day of the week, year, or place, and could not recognize family members. Additional impairments included slurred speech, expressive aphasia, loss of bowel/bladder control, and lack of coordination marked by an inability to sit, stand, or walk unassisted.

At that point the family gave the researchers consent to start an experimental treatment with human recombinant deoxyribonuclease I (DNase I) (1500 KU/mg) given orally three times a day in conjunction with his continued memantine therapy. The DNase I was well tolerated, and no averse or unanticipated events were registered.

The reseachers reported the following results:
Our patient demonstrated considerable cognitive improvement beginning on the second day of DNase I treatment, becoming partially oriented to time and place, and once again recognizing and remembering the names of family members. He further became able to dress himself, including tying shoelaces and buttons, as well as walk independently, feed himself, and use an exercise bike. Neurologic abnormalities affecting his gait were significantly reduced. His MMSE score increased dramatically from 3 to 16, and his FAST score was reduced from 7 to 5. However, he continued to score low on the MMSE for measures of orientation to time and place, memory, and visuospatial construction.

Two months following the initiation of DNase I treatment (19 months following initiation of memantine treatment), our patient exhibited an MMSE score 18 and a FAST score of 4. Moderate improvements in memory were observed, although visuospatial construction continued to decline. He was better able to speak and interact with others, recognize relatives, and actively attend to television programs. Our patient further became able to perform calculations, play piano, chess, and walk independently.

DNase I, is an endonuclease coded by the human gene DNASE1. DNase I is a nuclease (an enzyme that cleaves the chains of nucleotides into smaller units) that cleaves DNA. It acts on single-stranded DNA, double-stranded DNA, and chromatin. In addition to its role as a waste-management endonuclease, it has been suggested to be one of the deoxyribonucleases responsible for DNA fragmentation during apoptosis.

Cell-free DNA (cf-DNA), including bacteria-derived DNA, may be another target. The researchers noted that 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.

In addition, it has been suggested that cf-DNA could promote auto-inflammation. In this study which was published by another group of researchers at roughly the same time auto-inflammation was observed to be a possible cause of dementia. The researchers put together strong arguments that the neurological decline common to these diseases is caused by ‘auto-inflammation’, where the body’s own immune system develops a persistent inflammatory response and causes brain cells to die.

Another positive aspect is that the use of DNase I for the treatment of a disease called cystic fibrosis was approved on December 30, 1993 by the Food and Drug Administration (FDA) which means it is commonly available today. It is also a good example of strengthening the abilities of the own body to treat diseases. In this case 40 mg of human recombinant DNase I (1500 KU/mg) was given orally three times a day in conjunction with the memantine therapy (10 mg daily). The DNase I was well tolerated, and no averse or unanticipated events were registered.

Ofcourse further research is required but the results sound so spectacular that it may make sense to inquire with treating physicians of loved ones that are in a late/terminal stage of dementia about the possibilities to repeat the treatment carried out in this study.

[Alex_G]

I would definitely be interested in a group buy.

[gamesguru]

what an inspiring and remarkable story.

 

from unable to walk to playing piano and chess. perhaps the reason why spatial skills were not recovered to the same extent as cognitive measures is that the mPFC accumulates more tangles (DNAse prevents the tangles), whereas the hippocampus is afflicted mainly by lowered NTs and BNDF (afaik, DNAse has little to no activity on NTs or BDNF, its tangle mechanism is quite independent of BDNF). the one has junk/debris cause death, the other has lack of metabolism cause death. the PFC is involved in cognition, the straitum/hippocampus has a bigger role in spatial memory, not to say it wont affect cognitive functions too.

 

so to combine something simple like green tea or ginkgo or curcumin, all things that boost NTs and BDNF, might give DNAse that extra oomph, and help with persisting symptoms

We have previously shown that blueberry intervention induces both spatial memory improvements and BDNF signalling in young and old animals [23], [47]. However, despite evidence for the functional and molecular actions of blueberry and other flavonoid-rich foods, limited data exist with regards to the actions of pure flavonoids on memory [48]–[51]. For example, Maher et al (2006) [51] reported that administration of pure fisetin improves recognition memory in rodents, although the underpinning mechanisms were investigated ex-vivo in hippocampal slices. In addition, the administration of pure (−)-epicatechin has been shown to improve the retention of spatial memory in the Morris Water Maze (MWM) [50], albeit at doses above those considered to be dietary. In the present study, we have extended these studies by examining the impact of dietary quantities of pure anthocyanins and the flavanols (similar to those present in blueberry) on spatial working memory and BDNF modulation in the hippocampus of aged rats (18-month old).

 

Antidepressant-like effect of low molecular proanthocyanidin in mice: involvement of monoaminergic system.
Xu Y1, Li S, Chen R, Li G, Barish PA, You W, Chen L, Lin M, Ku B, Pan J, Ogle WO. (2010)

Proanthocyanidin is a phenolic product present in plants which has antioxidant, antinociceptive and neuroprotective properties, without inducing significant toxicological effects. The present study tested the hypothesis that low molecular proanthocyanidin from grapes that has optimized bioavailability, would exert antidepressant-like activities in behavioral despair tests. The results suggested that oral administration proanthocyanidin at doses of 25 and 50mg/kg for 7days significantly reduced the duration of immobility in both the tail suspension and forced swimming tests. The doses that affected the immobile response did not affect locomotor activity. In addition, the neurochemical and neuropharmacological assays showed that proanthocyanidin produced a marked increase of 5-HT levels at 25 and 50mg/kg in three brain regions, the frontal cortex, hippocampus and hypothalamus [and BDNF goes with 5-HT]. Noradrenaline and dopamine levels were also increased when higher dose of proanthocyanidin (50mg/kg) administration both in the frontal cortex and hippocampus. These effects were similar to those observed for the classical antidepressant imipramine (10mg/kg, i.p.). Moreover, Our study suggested that proanthocyanidin (12.5, 25 and 50mg/kg) dose dependently inhibited monoamine oxidase-A (MAO-A) activity, while MAO-B inhibitory activity was also found at higher doses (25 and 50mg/kg) after 7days administration. MAO-A selective inhibitor, moclobemide (20mg/kg, i.g.) produced MAO-A inhibition of 70.5% in the mouse brain. These findings suggest that the antidepressant-like effects of proanthocyanidin may involve the central monoaminergic neurotransmitter systems.

Plant-derived flavanol (−)epicatechin mitigates anxiety in association with elevated hippocampal monoamine and BDNF levels, but does not influence pattern separation in mice
T P Stringer,1 D Guerrieri,1 C Vivar,1 and H van Praag1 (2015)

Flavanols found in natural products such as cocoa and green tea elicit structural and biochemical changes in the hippocampus, a brain area important for mood and cognition. Here, we evaluated the outcome of daily consumption of the flavanol (−)epicatechin (4 mg per day in water) by adult male C57BL/6 mice on measures of anxiety in the elevated plus maze (EPM) and open field (OF). Furthermore, pattern separation, the ability to distinguish between closely spaced identical stimuli, considered to be mediated by the hippocampal dentate gyrus (DG), was tested using the touchscreen. To investigate mechanisms through which (−)epicatechin may exert its effects, mice were injected with bromodeoxyuridine (50 mg kg−1) to evaluate adult hippocampal neurogenesis. In addition, monoaminergic and neurotrophin signaling pathway proteins were measured in tissue derived from subject cortices and hippocampi. Flavanol consumption reduced anxiety in the OF and EPM. Elevated hippocampal and cortical tyrosine hydroxylase, downregulated cortical monoamine oxidase-A levels, as well as increased hippocampal brain-derived neurotrophic factor (BDNF) and pro-BDNF support the flavanol's anxiolytic effects. In addition, elevated pAkt in hippocampus and cortex was observed. (−)Epicatechin ingestion did not facilitate touchscreen performance or DG neurogenesis, suggesting a non-neurogenic mechanism. The concurrent modulation of complementary neurotrophic and monoaminergic signaling pathways may contribute to beneficial mood-modulating effects of this flavanol.

 

Plant-Derived Flavanol (−)Epicatechin Enhances Angiogenesis and Retention of Spatial Memory in Mice
Henriette van Praag1, Melanie J. Lucero1, Gene W. Yeo (2007)

Diet and exercise have a profound impact on brain function. In particular, natural nutrients found in plants may influence neuronal survival and plasticity. Here, we tested whether consumption of a plant-derived flavanol, (−)epicatechin, enhances cognition in sedentary or wheel-running female C57BL/6 mice. Retention of spatial memory in the water maze was enhanced by ingestion of (−)epicatechin, especially in combination with exercise. Improved spatial memory was associated with increased angiogenesis and neuronal spine density, but not newborn cell survival, in the dentate gyrus of the hippocampus. Moreover, microarray analysis showed upregulation of genes associated with learning and downregulation of markers of neurodegeneration in the hippocampus. Together, our data show that ingestion of a single flavanol improves spatial memory retention in adult mammals.

[resveratrol_guy]

 

 

 

 

It is already available in the market by the name of Pulmozyne !Cant it be used ?

 

 

Probably so, if you can actually acquire it. We see a hundred headlines every year saying "drug X cures Y", but then even if it works, it takes decades to make it to market and costs a fortune even when it does. These are the reasons that we had to invent group buys. And yes, I would seriously consider participating.
 

[deetown]

Pulmozyne is a tiny dose compared to the 120mg oral dose.  Also you don't know if the benefits were due to digestive issues or internal issues.  Being that the body natural produces it in the stomach I think that is a consideration.  

Edited by deetown, 15 June 2016 - 03:15 AM.

[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.

[Der Springende Punkt]

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.

 

That's great! Thanks, Mian.

[Logic]

Hi all.

 

NB that Pulmozyne/Dornase alfa is what you are interested in:

PULMOZYME is a recombinant human deoxyribonuclease I (rhDNase)
http://www.rxlist.co...mozyme-drug.htm

DNase I is a purified solution of recombinant human deoxyribonuclease I approved by the Food and Drug Administration
http://jmedicalcaser...3256-016-0931-6

 

I have contacted some of the usual suppliers without any luck:  

It seems that chem suppliers and biologic suppliers are rarely the same place.

I have a large list of other suppliers I am Emailing atm.

Once I find a supplier/s and get quote/s I will do some due diligence on the companies and post here.

 

I assume everyone wants the Pulmozyne tested by a 3rd party lab and the cost added to the price?

 

NB that Dornase alfa/Pulmozyne is an Orphan Drug:

https://en.wikipedia...ki/Dornase_alfa

So may still be covered by a patent in relevant countries. 

I dont have the time atm to look into this...  (Moving and my car died)

[Logic]

Pulmozyne is a tiny dose compared to the 120mg oral dose.  Also you don't know if the benefits were due to digestive issues or internal issues.  Being that the body natural produces it in the stomach I think that is a consideration.  

 

I agree that its altogether possible that ALZ etc sufferers have gut issues that prevent the proper breakdown of ingested DNA and that possibly the case study that this is all based on, has stumbled on the solution so to speak.

 

I think it would be worth researching how Dnase is normally produced in the gut.

Its probably some strain of gut bacteria that is lacking, but may also be due to a lack of stomach acid/PH and thus improper breakdown in the stomach before reaching the gut...?

 

(There are a large list of probiotics/superbugs (+ prebiotics) that have the potential of turning one's gut into a 24/7 supp factory!  

See LKM-512 for example, as it will also boost the autophagy of the rogue proteins implicated in dementias, IIRC.  

(If only I could afford to do more than just window shop..!))

[Mian Ali Ismail]

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

[Logic]

I have received a reply from only one 'biologics' supplier after Emailing around 15.  :(

 

I sent your inquiry to our labs, and although we didn’t have it in our catalogue, they’re interested in producing it. It will take 8 weeks for pilot experiment.
By then, we can generate a quote for scaled up production, but we need to see the logistics on a smaller scale first.

I will keep in touch with you as long as you are interested, and keep you informed as to the status and details of the product.
Please let me know if you have any further questions, I’ll be happy to work with you.

 

If anyone knows of possible suppliers please contact me.
I will also keep looking and re-Email those I have already contacted.  This is reminiscent of Nilotinib at 1st, so I am not discouraged, but short on time atm.

Edited by Logic, 22 June 2016 - 10:34 AM.

[deetown]

Thank you for doing that Logic.  Fingers crossed something works out.  Perhaps the lab Redan is using for the NRX-1074 group buy may be able to do it?

[plumper76]

I'd be interested in a group buy thanks