[Conductor71]

This is by the same guy who offers amino acid treatments in conjunction with levodopa therapy.

It is interesting given no one knows how DBS works and that electo convulsive therapy and magnetic resonators work for us. Here is perhaps why?

The etiology of chronic problems is not low concentrations of monoamines that need to be returned to normal as predicted by the monoamine hypothesis; it is concentrations that are normal but not high enough to compensate for postsynaptic neuronal damage. Addressing this electrical defect properly requires the system to be placed into the competitive inhibition state in order to be able to increase monoamine levels to above normal to reach the threshold level needed to establish the adequate electrical flow required.

This paper does try to sell his neurotransmitter balance based therapy...still this seems entirely plausible to me. Anyone else?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282597/

Laura

[Conductor71]

This seems to support what he is saying.


Reduced axonal transport in Parkinson's disease cybrid neurites is restored by light therapy

and also ties in nicely with the biomarker find.

Laura

[michael7733]

Originally Posted by Conductor71

This is by the same guy who offers amino acid treatments in conjunction with levodopa therapy.

It is interesting given no one knows how DBS works and that electo convulsive therapy and magnetic resonators work for us. Here is perhaps why?

The etiology of chronic problems is not low concentrations of monoamines that need to be returned to normal as predicted by the monoamine hypothesis; it is concentrations that are normal but not high enough to compensate for postsynaptic neuronal damage. Addressing this electrical defect properly requires the system to be placed into the competitive inhibition state in order to be able to increase monoamine levels to above normal to reach the threshold level needed to establish the adequate electrical flow required.

This paper does try to sell his neurotransmitter balance based therapy...still this seems entirely plausible to me. Anyone else?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282597/

Laura

voltage-gated ion channels and dopamine dispersal, Iwas seeing in my mind's eye a slow-moving, rather boring, mental movie in which several molecules of dopamine were made , somehow placed in some kind of conveyor system and dropped off at a transfer point where they waited until a sufficient electrical charge was attained to open the door to let them out. When the door opened they would, much like paratroopers, leap out into the intrastatial fluid and floa around until they came across an unfilled receptor site.

Suddenly, without warning or forethought on my part, the picture changed to an action packed adventure in which theere w er a multitude of mitchondria working furiously to make a quota of dopamine molecules that were wissked away without delay to many pressurized chambers which opened on a predetermined schedule spewing the molecules so fiercley from the opened doors that they took on the appearance of sizzler fire works. I had just had my FIRST 3-dimensional thought. I was so impressed that I did a se arch to finnd out how many mitochondria there are in a neuron. There are possibly a thousand. That model made much more sense than did the one that slowly left it all to chance.

http://https://docs.google.com/viewe...eoJjDQ_LVXsIPA

Here is a site that discusses the quantum mechanics of voltage-gated ion channels. I think we need a new brain model.

michael

[lurkingforacure]

Originally Posted by Conductor71

This is by the same guy who offers amino acid treatments in conjunction with levodopa therapy.

It is interesting given no one knows how DBS works and that electo convulsive therapy and magnetic resonators work for us. Here is perhaps why?

The etiology of chronic problems is not low concentrations of monoamines that need to be returned to normal as predicted by the monoamine hypothesis; it is concentrations that are normal but not high enough to compensate for postsynaptic neuronal damage. Addressing this electrical defect properly requires the system to be placed into the competitive inhibition state in order to be able to increase monoamine levels to above normal to reach the threshold level needed to establish the adequate electrical flow required.

This paper does try to sell his neurotransmitter balance based therapy...still this seems entirely plausible to me. Anyone else?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282597/

Laura

Maybe it's too early, but I don't get this. What I read these guys to be saying is that there is a problem with getting the dopamine to where it needs to be, because a bundle of neurons are impaired in some way, either by trauma (concussion, etc.), neurotoxin exposure (pesticides, etc.), biogenics, there are more than a few causes according to the authors. OK, I get that, they are saying PWP have enough dopamine, it's just not getting to where it needs to be...so giving levodopa does not help long-term.

I see their position that just giving one monoamine precursor will not help, as the neurotransmitters must all be in balance. So does that mean they think if we took precursors for several different monoamines, and therefore brought them into perfect balance, PD would disappear? This assumes, of course, that the perfect balance is the same for everyone, which I personally don't buy. Maybe they posit that we must all take supplements to find that perfect balance for ourselves, which I could see. Maybe I need 200mg 5-HTP but you need 750, we would just have to experiment individually to see what our own optimal balance would be.

But this is where I get confused...then at the same time they advocate giving supplements that are precursors to the monoamines? So if there is a physical problem in the transport highway, how does giving supplements help? They still can't go where they need to, even after they have been
synthsized by the body and made into the monoamines. What am I missing?

[lurkingforacure]

Originally Posted by Conductor71

This seems to support what he is saying.


Reduced axonal transport in Parkinson's disease cybrid neurites is restored by light therapy

and also ties in nicely with the biomarker find.

Laura

Could you repost perhaps? Thanks!

[pwpboy]

Concerning the dopamine theory ... why isn't there a GAD increasing med ? I thought I read somewhere not only dopamine reduces but also GAD.

[soccertese]

Originally Posted by pwpboy

Concerning the dopamine theory ... why isn't there a GAD increasing med ? I thought I read somewhere not only dopamine reduces but also GAD.

http://www.northjersey.com/news/1430...quidation.html
one approach at increasing GAB with gene therapy, great PHASE1 results, PHASE2 results not good enough to raise money for a PHASE3, had to be as good as DBS. That's why I don't get too excited by any PHASE1 trial for PD, placebo affect is huge in PD - gung ho volunteers produce more dopamine, they're unblinded and primary investigator often involved so some suspicion results might be a little skewed.

imho, problem with fooling around with amino acids is they have a positive affect in one part of the brain, negative affect in another.

[Conductor71]

Originally Posted by lurkingforacure

Could you repost perhaps? Thanks!

LFAC,

Apologies. It looks like I didn't paste the URL the right way. Here is Take Two:


Reduced axonal transport in Parkinson's disease cybrid neurites is
restored by light therapy.