"Parkinson's disease is associated with depletion of tyrosine hydroxylase, dopamine, serotonin, and norepinephrine. "
From "Amino acid management of Parkinson's disease: a case study."; full text is available-


1. Int J Gen Med. 2011 Feb 28;4:165-74.

Amino acid management of Parkinson's disease: a case study.

Hinz M, Stein A, Uncini T.

Clinical Research, NeuroResearch Clinics, Inc., Cape Coral, FL, USA;

An extensive list of side effects and problems are associated with the
administration of l-dopa (l-3, 4-dihydroxyphenylalanine) during treatment of
Parkinson's disease. These problems can preclude achieving an optimal response
with l-dopa treatment.PURPOSE: To present a case study outlining a novel approach
for the treatment of Parkinson's disease that allows for management of problems
associated with l-dopa administration and discusses the scientific basis for this
treatment.
PATIENTS AND METHODS: The case study was selected from a database containing 254
Parkinson's patients treated in developing and refining this novel approach to
its current state. The spectrum of patients comprising this database range from
newly diagnosed, with no previous treatment, to those who were diagnosed more
than 20 years before and had virtually exhausted all medical treatment options.
Parkinson's disease is associated with depletion of tyrosine hydroxylase,
dopamine, serotonin, and norepinephrine. Exacerbating this is the fact that
administration of l-dopa may deplete l-tyrosine, l-tryptophan,
5-hydroxytryptophan (5-HTP), serotonin, and sulfur amino acids. The properly
balanced administration of l-dopa in conjunction with 5-HTP, l-tyrosine,
l-cysteine, and cofactors under the guidance of organic cation transporter
functional status determination (herein referred to as "OCT assay
interpretation") of urinary serotonin and dopamine, is at the heart of this novel
treatment protocol.
RESULTS: When 5-HTP and l-dopa are administered in proper balance along with
l-tyrosine, l-cysteine, and cofactors under the guidance of OCT assay
interpretation, the long list of problems that can interfere with optimum
administration of l-dopa becomes controllable and manageable or does not occur at
all. Patient treatment then becomes more effective by allowing the implementation
of the optimal dosing levels of l-dopa needed for the relief of symptoms without
the dosing value barriers imposed by side effects and adverse reactions seen in
the past.

PMCID: PMC3068871
PMID: 21475622 [PubMed]

I congratulate Conductor71 on her excellent thread. I am on SSRI drug and will ask my doctor to put me on SNRI instead. The load of research which implicit loss of norepinephrine in PD can be tested easily using established safe drugs such as SNRI class of drugs.
The other neglected neurotransmitter is Gaba.
http://neurotalk.psychcentral.com/sh...highlight=gaba

Do you know if Welbutrin XL works anything like Cymbalta or Effexor? I believe that Effexor is an SSRI, Wellbutrin isnot - and I think Cymbalta in theory is similar to an agonist in that it's a booster for dopamine replacement therapy (I.e., I am not comparing Cymbalta as an agonist in any way - just using it as a comparison in how it may work)

Back in the "old days" I would have researched all of this myself, but with limited ability to sit and work at the computer (back problems), I have over the years learned whom to trust to give reliable information. Robert, you are one smart cookie!

I have been signed up with Fox Trial Finder for some time concerning trials for dyskinesia. But I may never find one for which I won't be excluded due to having had experimental surgery for implanting RPE (dopamine producing retinal cells). But I am convinced that the experimental surgery helped, and anybody that saw me the before/after improvement ) . This is our problem; we aren't comparing apples to oranges with Parkinson's. We have no confirmation of PD via. Blood test, MRI. SPECT scan, etc.

Thanks in advance to anyone who can contribute to Robert's comment and my question about anti-depressants helping with dyskinesias.
Peg

A brief search of Welbutrin's primary effect indicates that it is primarily noradrenergic with only a minor dopaminergic component. It has no serotonergic activity. I guess if one wants to go after strong noradrenergic effects along with serotonergic ones, my Cymbalta/Welbutrin combo is one way to go.
(This was a solution recommended by my favorite psychiatrist several years ago to address diminished libido which I thought might have been due to Effexor, and i've just stayed with it.)

Robert

I am just now reading all of the comments in this thread and your reply. Are there any OTC (over the counter) products that would have he same effect that you described?

Peggy

Peg,
Not that I know of. I do know that Lilly loses the Cymbalta patent in 2013, and assume that less expensive generics are already in the works. I already take Welbutrin (buproprion) as a generic.

Robert

I am on a new rabbit trail....researching
1. Rhodiola rosea (also called artic root and aaron's rod...it is supposed to act like an MOAI and help rebuild dopamine. Just ordered this supplement from Swansons Health Products to see how it effects me.
Also
2. Chasteberry (Vitex / monk's pepper / chaste tree) ...it is supposed to help PMS, BPH, reduce sexual desire , help constipation and fibrcystic lumps and get this....INCREASE DOPAMINE ACTIVITY IN THE BRAIN...have also ordered capsules of this (will not try them at the same time of course, but take one for a few weeks and then stop it and try the other one) Herbs do not act like pharmas in that that work quietly and very gradually to make a change in your system...so 2 weeks is not enough usually to notice a change.
If any of you have time to research these also....please do. They are both thinigs that will grow in East TN, which is a major plus for me. I don't like swallowing pills and if I can tincture somethiing or drink a cup of tea from a root or leaf....that's for me (besides that...I like being my own "quality control Person" and know how it has been grown, handled, etc.... Guess I lack trust in others gathering my supplements/ or just want to do things "from the ground up"...that's what grass roots research is all about maybe??

Well, it looks like there are alot of pluses (and a minus )with Rhodiola.
Roseroot (Rhodiola/ rodiola rosea) is supposed to increase dopamine activity in the brain and inhibit prolactin secretions. Stimulate progesterone, help PMS , increase flow of urine , help constipation, and fibrocystic breast lumps, reduce sexual desire/ but may improve sexual function in men,help headaches, inflamation and swelling, acne, BPH, dementia, upset stomach and increase breast milk, has protective anti-oxidants and defends the body , it is fatique -fighting,used against colds, reduces stress induced chemicals in the body,.helps against depression, improves motor coordination and Increases mental performance and memory.
*** Small doses most effective/ large doses acts as a seditive
IT MEDIATES changes in SERATONIN and DOPAMINE LEVELS due to MOAI inhibition
It is adaptogenic. HELPS REBUILD DOPAMINE (interesting)
*CANNOT be taken with another MOAI
*May interfere with sleep...take early in day
*may restore female menses....ugh (that I don't need!)
Interesting herb....will start trying a small amount next week and report back

As far as chasteberry herb: alot of people wrote that they had bad reactions to it
rash , itching , hair loss, can make tired ,diarrhea, headache. For others it was a lfe-saver . It also has alot of good qualities....but it will have to be treated with more caution...I will try it in a couple of months after experimenting with the rhodiola first.
Will report on how Rodiola works in a few weeks. Blessings, Aunt Bean

I am posting this here because it talks of gaba. I have no idea whether it is relevent or not, but perhaps it is a bit of the puzzle.....

http://www.independent.co.uk/news/sc...g-8390165.html

'Dopamine: not about pleasure anymore':

http://today.uconn.edu/blog/2012/11/...asure-anymore/