[reverett123]

Thought I would give it its own thread-
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=p ubmed_pubmed&LinkReadableName=Related%20Articles&I dsFromResult=2502304&ordinalpos=1&itool=EntrezSyst em2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Disc overyPanel.Pubmed_Discovery_RA&log$=relatedarticle s&logdbfrom=pubmed

1: C R Acad Sci III. 1989;309(2):43-7.

[L-tyrosine: a long term treatment of Parkinson's disease]

[Article in French]

Lemoine P, Robelin N, Sebert P, Mouret J.

Unité clinique de Psychiatrie biologique, C.H.S. Le Vinatier, Lyon-Bron.

That l-dopa represents a major advance in Parkinson treatment should not hide
that a number of problems remain unanswered: on-off effects, transient
improvements... Based on the beneficial effects of l-tyrosine in dopamine
dependent depressions and narcolepsy, five naive patients diagnosed after sleep
polygraphy criteria and five l-dopa and/or dopamine agonist treated patients were
prescribed l-tyrosine as a long-term treatment. For some patients, 3 years of
L-tyrosine treatment was followed by better clinical results and many fewer side
effects than with L-DOPA or dopamine agonists. However, the theoretical long-term
sparing neurons potentiality of approach requires further studies.


PMID: 2502304 [PubMed - indexed for MEDLINE]


I was told that a typical doseage was 1.5 g and 4x daily. Verify that however, and always start low. One possible advantage of this combined with lower doses of Sinemet is that it might even out the ups and downs. Even if our bodies can only make half what we need there is a big advantage in even that.

[rosebud]

That is the (amino acid?) that our own bodies use to produce dopamine when we are healthy. It ALSO nurtures adrenaline production, with all its side lines like (epinepherine ?), noradrenaline and way out in left field...melanin, which gives is our coloring and is the patron saint of a suntanner!..

Now I'm writing this off thee cuff...so feelfree to correcct my contribution to this thread. In Canada we can buy L-tyrosine at the health food store and it comes in 500 mg capsules. My experience with it is... start slow because I did get some agitation from it and I'm not one to have problems with drugs/nutritional supplements...usually.

If your looking for it in foods, it can be found in almonds, avacado's, pumpkin seeds, bananas and a variety of other seeds and nuts. I always have trouble with avacados and bananas...never made the connection until I read about the tyrosine. I'll leave it there for now, but will be back to this thread later when I have more time.

Rick, what would we do without you?

[reverett123]

Originally Posted by rosebud

That is the (amino acid?) that our own bodies use to produce dopamine when we are healthy. It ALSO nurtures adrenaline production, with all its side lines like (epinepherine ?), noradrenaline and way out in left field...melanin, which gives is our coloring and is the patron saint of a suntanner!..

Now I'm writing this off thee cuff...so feelfree to correcct my contribution to this thread. In Canada we can buy L-tyrosine at the health food store and it comes in 500 mg capsules. My experience with it is... start slow because I did get some agitation from it and I'm not one to have problems with drugs/nutritional supplements...usually.

If your looking for it in foods, it can be found in almonds, avacado's, pumpkin seeds, bananas and a variety of other seeds and nuts. I always have trouble with avacados and bananas...never made the connection until I read about the tyrosine. I'll leave it there for now, but will be back to this thread later when I have more time.

Rick, what would we do without you?

Ah, gee, Rosebud. You guys would shuffle on along without me, but thanks.

[reverett123]

From an excellent 5-page monograph in the Alternative Medicine Review.
Free download at www.thorne.com/media/TyrosineMono12-4.pdf



Parkinson’s Disease
Although tyrosine use in Parkinson’s disease
(PD) is not well researched, studies on animals, post-
mortem Parkinson’s patients, and dopamine metabo-
lites in live Parkinson’s patients indicate it may be of
30,31
Post-mortem examination re-
therapeutic beneit.
veals hyperactivity of surviving neurostriatal neurons. It
is thought tyrosine supplementation may enhance the
synthesis and release of dopamine from these hyperac-
tive neurons. Tyrosine may actually prove superior to
L-dopa (conventional Parkinson’s treatment) because it
is normally present in the diet and side efects tend to
30
Evaluation of tyrosine’s efect in 23 PD
be minimal.
patients demonstrated 100 mg/kg tyrosine daily raised
plasma and cerebral spinal luid tyrosine and homova-
nillic acid (a major dopamine metabolite) levels, indi-
30

cating increased catecholamine synthesis and release.
In a small (n=10), long-term French study (English full
text unavailable), ive PD patients received tyrosine and
ive received L-dopa. hree years of tyrosine therapy
resulted in better clinical results and fewer side efects
than L-dopa treatment; study details and dosages were
32
not available.

[reverett123]

Paste from a PDF and see whatyou get. Download the original - you want it anyway.

Originally Posted by reverett123

From an excellent 5-page monograph in the Alternative Medicine Review.
Free download at www.thorne.com/media/TyrosineMono12-4.pdf



Parkinson’s Disease
Although tyrosine use in Parkinson’s disease
(PD) is not well researched, studies on animals, post-
mortem Parkinson’s patients, and dopamine metabo-
lites in live Parkinson’s patients indicate it may be of
30,31
Post-mortem examination re-
therapeutic beneit.
veals hyperactivity of surviving neurostriatal neurons. It
is thought tyrosine supplementation may enhance the
synthesis and release of dopamine from these hyperac-
tive neurons. Tyrosine may actually prove superior to
L-dopa (conventional Parkinson’s treatment) because it
is normally present in the diet and side efects tend to
30
Evaluation of tyrosine’s efect in 23 PD
be minimal.
patients demonstrated 100 mg/kg tyrosine daily raised
plasma and cerebral spinal luid tyrosine and homova-
nillic acid (a major dopamine metabolite) levels, indi-
30

cating increased catecholamine synthesis and release.
In a small (n=10), long-term French study (English full
text unavailable), ive PD patients received tyrosine and
ive received L-dopa. hree years of tyrosine therapy
resulted in better clinical results and fewer side efects
than L-dopa treatment; study details and dosages were
32
not available.

[ol'cs]

To put in words here, anything more than what I THINK i know about tyrosine from my readings as a chemist/ biochemist.
Tyrosine has, like a lot of neurotransmitters, a very simple structure (chemically), and as such, we call them "small molecules". For those of you who have studied "chemese"; it is simply 4-hydroxy phenylalanine.
We don't need to have tyrosine in our diet, because humans can biosynthesize (transform or "make") tyrosine from the very common amino acid, phenylalanine, which we get lots of from our diet, specially if our diet is rich in "protein". Protein is just a long long chain containing random amounts of the 21 "essential amino acids" (the ones that we can't make from simpler substances). When we eat protein, we just split apart this long chain of amino acids into it's simplest component amino acids.
So phenylalanine is everywhere, in protein. There is an enzyme that simply adds a "hydroxyl group" (OH of the H2O of water) at the "4"-position of the "phenyl ring" of phenylalanine, and voila, we have made tyrosine. There is another enzyme that can add another "hydroxyl group" to the 3 position of tyrosine, giving rise to L-Dopa, and so all of the other molecules that are derived in-vivo that we call "Catecholamines" are made by biotransformations of L-Dopa. Now, our bodies can do a lot with L-Dopa once it has been made. L-dopa can be "decarboxyated" (the carboxylic acid part of an amino acid gets "torn off" the molecule") to produce Dopamine, which we all know is what we lack to do the neurotransmitting that allows us to use our muscles properly.
However, making dopamine is not the only thing our bodies do with tyrosine. If tyrosine is "decarboxylated" before it gets the chance to be 3-hydroxylated; it doesn't go on to produce dopamine but instead makes a chemical called "tyramine". If it does this outside of the brain barrier (in the "periphery"), the tyramine produced is a nasty little molecule, that is responsible for something known as the "cheese effect" (it is called this because certain foods naturally have a lot of tryamine in them, and if this tyramine is not destroyed by a natural enzyme called monoamine oxidase -A, then a very bad reaction occurs that can put us in the hospital and has been known to cause death, from it's effects on heart over-stimulation.
Thus the bottom line is, tyrosine supplements can produce more dopamine and other "catecholergic" bioamines, BUT, if you have taken a "monoamine oxidase inhibitor" (these are chemicals that were created and used as antidepressants that are MEANT to not break down monoamines such as dopamine or 5-Hydroxytryptamine (a chemical that is in low concentration in certain depressed people), you won't break down any tyrosine made in the periphery and so risk death or at least a very nasty experience (do a search on "the cheese effect").
So, the only thing that i can imagine tyrosine supplements to be taken for are , if you are a vegan and KNOW that you are getting very little tyrosine and/or phenylalanine in your diet, and you are not on an MAO-A type antidepressant, you could perhaps benefit: and one more reason. If you think that you are having PD symptoms, and are NOT on an MAO-A antidepressant, and can't get hold of any L-dopa for a "self trial test" to see if you MIGHT have the beginning symptoms of PD; taking about a half a gram of pure tyrosine three times a day, for a week, just might give you a good clue as to whether your suspicions are correct and need further investigation by a trained neurologist.
That's about it. cs

[RLSmi]

from this conversation is the fact that tyrosine is a commonly occuring amino acid component of almost every protein in your body (as well as in your diet). Most (probably >99%) of the tyrosine molecules present in our metabolic mix pool do not end up as neurotransmitters such as dopa, epinephrine or norepinephrine, although some small amount normally does. Most tyrosine units are present as important structural components in your own proteins.

Tyrosine's chemical structure, with a polar, reactive hydroxy (-OH) group attached to an otherwise unreactive phenyl (-C6H4) ring group, makes it one of the star players in the massively complicated communication symphony of "signal transduction" that keeps living biological systems coordinated and running smoothly. That -OH group can chemically accept a phosphoryl (-PO3) group from ATP, the biological energy currency. That changes a tyrosine unit in a protein into a negatively charged structural component with the new capacity to electrostatically interact with positively charged structures such as amino (-NH3) groups. When the need for that interaction is past, the phosphoryl group can be easily removed to re-form the electrically neutral hydroxy.

The metabolic relationship of the amino acid phenylalanine, which is chemically tyrosine without its hydoxy group, is that phenylalanine, which our bodies can not make, must be supplied in our diet, but it can be converted in our body to tyrosine. However, that reaction goes only one way. This why phenylalanine is one of the 10 amino acids we must provide in our diet. These are the so-called essential (in the diet) amino acids.

Anyone still awake?

Robert

[reverett123]

This is assuming normal metabolism, uptake, and supply of not only tyrosine, but the various co-factors as well. If there is a problem anywhere in the chain...

As best I can tell, there has been little research done on this.

[reverett123]

Norepinephrine is usually overlooked but has a big role in PD. Not only does it's synthesis deplete dopamine reserves, it is also in the center of stress response. If stress hits us harder than most, then norepinephrine is involved.


1: Physiol Behav. 2005 Jan 31;84(1):33-8. Epub 2004 Dec 8.

Tyrosine prevents effects of hyperthermia on behavior and increases
norepinephrine.

Lieberman HR, Georgelis JH, Maher TJ, Yeghiayan SK.

Military Nutrition Division, United States Army Research Institute of
Environmental Medicine, Building 42, Kansas Street, Natick, MA 01760-5007, USA.
harris.lieberman@na.amedd.army.mil

Tyrosine (TYR) is the precursor of the catecholamine (CA) neurotransmitters,
dopamine (DA) and norepinephrine (NE). Catecholamines, especially NE, participate
in the response of the brain to acute stress. When animals are acutely stressed,
NE neurons become more active and tyrosine availability may be rate-limiting.
Tyrosine administration, before exposure to physical and/or environmental
stressors including cold, reduces the adverse behavioral, physiological and
neurochemical consequences of the exposure. In this study, the effects of
tyrosine (400 mg/kg) were examined on rats exposed to heat stress, for which its
effects have not been examined. Coping behavior and memory were assessed using
the Porsolt swim test and the Morris water maze. Release of hippocampal NE and DA
was assessed with in vivo microdialysis. In vehicle-treated animals, heat
impaired coping and memory, and increased release of NE, but not DA. In heated
animals receiving tyrosine, coping was not impaired and NE release was sustained,
thus demonstrating tyrosine protects against the adverse effects of heat, and
suggesting these effects result from increased central NE release. This study
indicates the effects of tyrosine generalize across dissimilar stressors and that
tyrosine administration may mitigate the adverse behavioral effects of heat and
other stressors on humans. In addition, it demonstrates that moderate heat stress
impairs coping behavior, as well as working and reference memory.


PMID: 15642604 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum




1: Physiol Behav. 2001 Feb;72(3):311-6.

Tyrosine improves behavioral and neurochemical deficits caused by cold exposure.

Yeghiayan SK, Luo S, Shukitt-Hale B, Lieberman HR.

Military Nutrition and Biochemistry Division, United States Army Research
Institute of Environmental Medicine, Kansas Street, Natick, MA 01760-5007, USA.
sylva.yeghiayan@na.amedd.army.mil

The effects of acute cold stress were assessed behaviorally and neurochemically.
The norepinephrine (NE) precursor, tyrosine (TYR), the catecholamine-releasing
compound, amphetamine (AMPH), and the adrenoceptor agonist, phenylpropanolamine
(PPA), were administered systemically either alone or in conjunction with TYR 30
min prior to cold exposure. All three sympathomimetic treatments dose-dependently
improved performance in a forced swim test following hypothermia (T(c)=30 degrees
C). AMPH/TYR or PPA/TYR combinations further improved performance vs. either
agent given alone. Microdialysis showed elevated hippocampal NE concentrations in
response to hypothermia. TYR further elevated NE concentration in cold/restrained
rats vs. saline (SAL)-treated controls. These results suggest that
sympathomimetic agents, including the nutrient TYR, which enhance noradrenergic
function, improve performance in animals acutely stressed by hypothermia.


PMID: 11274672 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/11274672?ordinalpos=1&itool=EntrezSystem2.PEntrez. Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.P ubmed_Discovery_RA&linkpos=1&log$=relatedarticles& logdbfrom=pubmed

[RLSmi]

I have read a recent review in the journal Biochemical Pharmacology by people at Emory University entitled "Norepinephrine: The redheaded stepchild of Parkinson's disease." Following is the abstract -

Parkinson's disease (PD) affects approximately 1% of the world's aging population. Despite its prevalence and rigorous research in both humans and animal models, the etiology remains unknown. PD is most often characterized by the degeneration of dopamine (DA) neurons in the substantia nigra pars compacta (SNc), and models of PD generally attempt to mimic this deficit. However, PD is a true multisystem disorder marked by a profound but less appreciated loss of cells in the locus coeruleus (LC), which contains a major group of noradrenergic neurons in the brain. Historic and more recent experiments exploring the role of norepinephrine (NE) in PD will be analyzed in this review. First, we examine the evidence that NE is neuroprotective and that LC degeneration sensitizes DA neurons to damage. The second part of this review focuses on the potential contribution of NE loss to the behavioral symptoms associated with PD. We propose that LC loss represents a crucial turning point in PD progression and that pharmacotherapies aimed at restoring NE have important therapeutic potential.

The reference for this review is:
K. S. Rommelfanger, D. Weinshenker, Biochemical Pharmacology 74 (2007) pp. 177-190.

Among other things, they point out that the same cell loss and Lewy body brain pathology seen post mortem in the substantia nigra is almost always also seen in the locus ceroeleus, involving NE neurons. They also present research in which other researchers demonstrated that NE secretion in this region is important in the normal function and maintainence of DA neurons.