There are/were several sources reporting on these "results" from the Swedish Institute, here:

http://www.biosciencetechnology.com/...w-Brain-Cells/

http://www.seriousinjurylaw.co.uk/ne...treatments.php

http://www.investors.com/NewsAndAnal...-formation.htm

They all say the same thing although the source listed first above has the most detail. Not sure what to make of it, as Laura pointed out, what's their point? PWP have to take ldopa, there's currently not much in the way of options if you want to be able to move.

Additionally, I don't believe salamanders even have a BBB, so why they used that creature for their research is a mystery. To my knowledge, the only mammal with a brain structure like ours, meaning and including the complex BBB, is the Rhesus monkey.

They all say the same thing although the source listed first above has the most detail. Not sure what to make of it, as Laura pointed out, what's their point? PWP have to take ldopa, there's currently not much in the way of options if you want to be able to move.

Additionally, I don't believe salamanders even have a BBB, so why they used that creature for their research is a mystery. To my knowledge, the only mammal with a brain structure like ours, meaning and including the complex BBB, is the Rhesus monkey.[/QUOTE]




http://www.sciencedaily.com/releases...0408075150.htm


As in mammals, the formation of neurons in the salamander mid-brain is virtually non-existent under normal circumstances. Therefore by studying the salamander, scientists can understand how the production of new nerve cells can be resumed once it has stopped, and how it can be stopped when no more neurons are needed. It is precisely in this regulation that dopamine seems to play a vital part. Many observations also suggest that similar mechanisms are active in other animal species too. Further comparative studies can shed light on how neurotransmitters control stem cells in the brain, knowledge that is of potential use in the development of therapies for neurodegenerative diseases.

"One way of trying to repair the brain in the future is to stimulate the stem cells that exist there," says Dr Simon. "This is one of the perspectives from which our study is interesting and further work ought to be done on whether L-dopa, which is currently used in the treatment of Parkinson's, could prevent such a process in other species, including humans. Another perspective is how medicines that block dopamine signalling and that are used for other diseases, such as psychoses, affect stem cell dynamics in the brain."

Krugen,

I agree with you, but my understanding is that much of what holds us back from progress in this area is the notion that we have sinemet, so what's the rush? There are several alternatives in trial that I started to mention because I was thinking "dopa hang up" when I first read that report. I could seriously see the GABA treatment by Neurologix and Adnosine receptor antagonists taking the place of what we have now. In the article, guess I really could not understand if dopamine therapy was being discouraged or encouraged but manipulated somehow. Speaking of Adnosine antagonists, the research has been around a while, enough to constitute a book!!

Adenosine Receptors and Parkinson's Disease


The question I have is why do these treatments slog through trials or never get approved? There is a thread started here that asks a similar question:

Why don't we have parallel tracking for other conditions?

Initially designed to help AIDS patients, parallel tracking makes drugs showing promising results in phase III of the IND process available to patients whose condition prevents them from participating in controlled clinical trials. Parallel tracking is similar to the treatment IND, a program started several years earlier.


A large part of the problem IMHO is that we have no unified voice questioning the status quo, so why do anything differently? It can take on average, fourteen years for a new treatment to make it through the pipeline, we don't have that kind of time to waste. We need to start demanding more of the scientific community and advocate for alternatives to dopa replacement.

Laura

Laura
I totally agree with you. I will find out in May if I will make it onto the Cogane trial II, but the result of that trial is not due out until late 2012. Then how many more years ?

Who is to blame ?

The established Pharma companies that sell $ 3 Billion + to a captive audience with no incentive to produce a real 'cure'?
The bureaucrats that simply shuffle paper and wish to avoid any 'blame' sticking to them if drugs cause harm ?
The thousands of PWP who have no collective will or voice to embrace change ?

I suspect as with AIDS 'epidemic' and the resultant focused 'community' PR, it will only be when the costs of Alzheimers and PD become to big a drain on national budgets that the problem will be addressed.

Sighs

Good luck on the Cogane trials!

I've had a little time to look further into the salamander thing...I think we are a long way off from seeing this translate into any sort of treatment. I mentioned that salamanders regenerate their own tails. Well it turns out that dopamine is key to neuronal genesis in these processes. Those slimy little things also know when their dopamine levels are low and self-restore. Hmmm...if God or whatever designed our brains to be that intuitive then we wouldn't have this blasted disease in the first place. I'd also daresay that levodopa doesn't matter if you can't even detect you are missing a neurotransmitter until 15-20 years after the fact, so injecting it into a salamander who is also programmed to stop dopa production when the right level is reached is probably having some sort of compensatory reaction when injected with a synthetic form.

I will say that I have a new found sense of awe for the amphibian family, but mammals are way different. No mammal can do that with their dopamine, so I'd say there is a reason for that and maybe it should be left alone unless we want to start mixing species.

Also in the regenerative spirit...a neuroscientist at Cornell has just recieved a prestigious award in looking at songbirds and their capacity as adults to produce new neurons; some for very specific purposes and lasting only a short time before dying off. Interestingly hormones and social interaction also came into play. Again there is a giant leap forward in looking at implications for neurodenerative diseases, when in reality it tells us we are very similar to birds in language and speech development. The rest is all wild speculation.

I'd say that all of this does support how little we still know about the human brain and that it is way more plastic than ever thought possible. I also think we need to start seriously studying how compensatory measures mask the disease in us for so long. There might be some things we can latch onto there.

The links:

http://news.bioscholar.com/2011/04/h...ult-brain.html

http://www.medicalnewstoday.com/articles/221941.php