How far away is a treatment that stabilises this disease?

[Graham]

Thanks for the link Johnny, absolutely fascinating!

For me Neil, I never went on to tracheotomy support but I well remember the fear/terror when my lungs went into decline. It was not a reversal as such, more of a plateauing of symptoms I would say.

Dr Bedlack is my kind of doctor. In fact the microbiome is interesting. I will continue with Coronation Chicken from time to time even though it really does not agree with me.

[neil m]

Dunno Neil. I too would like to know!

Well what happened ie did you have mnd and then you got better? Reversed symptoms?

[neil m]

Talking reversals here’s a guy in Ireland who says he’s done exactly that?!
not sure about the ems, still I bought one to try comments please

https://fb.watch/c2OydDMZOU/

[LindaB]

Johnny5 thanks for the link👍🏻

[Johnny5]

Dr Bedlack is studying ALS reversals. I think he has documented 43 that he can verify.

[Graham]

Dunno Neil. I too would like to know!

[neil m]

I agree Johnny.

I have defeated MND, with the battle scars, yet science is not the slightest bit interested how I have done it! It is as if I have patented something!!

Hi Graham
are you being serious? If so how did you do that?

[neil m]

I have been taking Tudca every day since AMX 00035 was shown to reduce the progression, AMX 00035 is 50% Tudca and 50% Sodium Phenylbutyrate which is very expensive.
you can buy Tudca on Amazon btw.
I take the same dose that showed statistically significance ie 2 grams a day.
should AMX become available then il add the other part.

[EvelynMW]

i got turned down for resaerch because my progression is too slow! I was happy to hear that at the same time as being slightly annoyed.

[Graham]

I agree Johnny.

I have defeated MND, with the battle scars, yet science is not the slightest bit interested how I have done it! It is as if I have patented something!!

[Johnny5]

It is hard to justify shooting at a target if you do not know where the target is. A long-term progressive study on longevity to identify what exactly is the difference between those who survive 10-20 years vs 2-3 years should identify what the target is.

Just shooting in the dark has done very little for decades. If what they are doing is not/has not gotten results, it is time to change the way they do it. Simple logic and common sense, nothing out of a book.

[Onein300]

John D Hi there.

re the £50m project please take a read of our update here

https://patientsunited2endmnd.org/2022/02/07/status-update/

We will updating further soon.

Subscribe to our website to get updates. We will be updating at least monthly.

https://patientsunited2endmnd.org/subscribe/

With regards to TREGs they have been implicated for years, and Coyas attempt at boosting is one attempt, but in my opinion a bit of a sledgehammer to crack a nut. Not only does it involve a rather complex and risky procedure, it involves out of body processing and re injection.

But there are many ways to boost and target TREGs, including drugs like Interlukin 2 which has just finished trials in the trial Mirocals. We are expecting results very soon. Yes it's unlikely to be a game changer, but if successful would provide a simple way to boost TREGs.

MND research has vastly progressed in the last 5 years and targets have solidified. In addition gene therapies are starting to breakthrough, and probably Tofersen is still very likely to be the breakthrough drug for sod1.

At the same time there are at least 3 other gene therapies ongoing in trial including 2 for sporadic MND.

Genetics is probably ultimately the reason why some people progress slower, for example the common variant unc13a has good evidence for a protective gene/progression speed.

Science has to take the lead, and despite our plight just simply rushing unproven drugs to market is not the best strategy.

My personal ethos is that we must do nothing that potentially slows or delays the arrival of eventual truly effective treatments. I for one would want a treatment available before my son gets older! Trials are largely an altruistic act and we must think of those to come. We will save more lives by being very analytical and using solid regulations.

Best wishes

Lee

[John D]

The easiest and probably most reliable way of keeping up with research is via the MNDA’s research pages and subscribing to their monthly Newsletter - https://www.mndassociation.org/research/

Onein300 Lee - Any progress in obtaining the £50m from the Government?

[FlexyWex101]

It is human nature to survive, we keep the faith because we want to live. Frustration of purpose is another story.

Common sense is under utilized it seems. I presented the same question to several researchers...Are there any studies on longevity comparing pALS who survive 10-20 years vs those who are gone in 2 or 3? Seems as if studies on comparison would point to whatever causes 5% of us to survive 20 years. If they find why those 5% survive so long, then they could develop treatment to change the course of this disease and provide a substantial extension of survival for the rest of the 90%. All I get are illogical answers about the necessity to test drugs on fast progressing, qualified clinical participants. There is no common sense in shooting in random directions to hit a target when you don't know where the target is. There are more living human lab rats with MND/ALS that would volunteer for this study than we have patience. Sometimes I think they spent more making genetically alterations in mice than they have in curing this disease.

I rather share your frustrations, Johnny. Smart though undoubtedly many researchers are, they also seem to be very blinkered and working to outdated paradigms. An example: in the past few years, more and more studies are rolling out which suggest that ALS is predominantly(and certainly in a good number of cases) a disease of the neuromuscular junction and the axons, that problems arise where the neurones interact with the muscles and then the motor system 'dies back'. Nerve biopsies are a low risk procedure that allow for this area to be scrutinised in intense detail, researchers could see abnormal protein aggregations, for example, or changes in gene expression (and indeed some already have, in labs) and with a decent amount of sufferers and controls they could flag abnormalities pretty quickly, yielding new targets for therapies. Yet this research isn't happening. Individual researchers and labs have made their names and earned significant amount of grants faffing around with stem cells and focusing myopically on the neurones (which animal studies have shown, even if you preserve them do not prevent symptoms and ultimately death since axon decay still occurs, so the neurones can't connect to the muscles), procedures which have so far yielded few results, and are almost certainly a dead end. But they're committed now; they've tied their research stars to that direction and it'll take a miracle to get them to shift focus. Meanwhile, ALS patients are dying, with no treatments anywhere to be seen. It's maddening.

A lot of shady stuff seems to go on at the interface of researchers, investors and bringing a product to market too. Leaving aside the issue of the difficulties of jumping through regulatory hoops and excessive red tape, a lot of biotech companies just simply do not seem to operate in good faith. I've recently been very disappointed in Coya Therapeutics, the company that is developing Dr Stanley Appel's idea of injecting ALS patients with T-Regs. Dr Appel suggested years ago that in fast progressing ALS patients there tends to be low and dysfunctional T-Regs, and that a faulty inflammatory response is implicated in progression. However, now evidence suggests that inflammation is probably a very small part of ALS and not applicable to many patients - it certainly doesn't drive decline. Coya read research, they must know this, yet they're doing interviews talking about ALS as though it is predominantly inflammation driven, and touting their treatment as a possible cure. And what is there to show so far? A 6 person study (if I recall correctly) with very ambiguous results. Probably beefing up T-Regs does something, but I can't see it buying any more than a few months, and that's in people with high inflammation. In ALSers without that they'd be better off drinking sparkling water.

[Johnny5]

It is human nature to survive, we keep the faith because we want to live. Frustration of purpose is another story.

Common sense is under utilized it seems. I presented the same question to several researchers...Are there any studies on longevity comparing pALS who survive 10-20 years vs those who are gone in 2 or 3? Seems as if studies on comparison would point to whatever causes 5% of us to survive 20 years. If they find why those 5% survive so long, then they could develop treatment to change the course of this disease and provide a substantial extension of survival for the rest of the 90%. All I get are illogical answers about the necessity to test drugs on fast progressing, qualified clinical participants. There is no common sense in shooting in random directions to hit a target when you don't know where the target is. There are more living human lab rats with MND/ALS that would volunteer for this study than we have patience. Sometimes I think they spent more making genetically alterations in mice than they have in curing this disease.