Another resarch on the importance of Glutathione ...
I take NAC which is supposed to be a Glutathione precurser ... any body else is taking it???
http://www.associatedcontent.com/art...arkinsons.html

Lack of Glutathione Linked to Parkinson's Disease
By Rafael_B
Published Dec 20, 2007

According to a new study, published in the most recent issue of the prestigious Journal of Neuroscience, researchers have shown (in animal models) that the lack of glutathione is linked to the development of the Parkison's disease. The study was led by Julie Andersen, PhD., from the Buck Institute for Age Research, Novato, California

The Parkison's disease is a neurodegenerative disorder. Common symptoms are: tremor, slowness of movement and rigidity. No cure is available today for the Parkison's disease. Glutathione is recognized as a potent detoxifying antioxidant that helps the body repair damage from stress, pollution, infection and damage.

Scientists have shown in this study that mice exhausting their levels of glutathione in dopamine-producing neurons developed nerve damage and symptoms that mimic the Parkinson's disease (PD) in humans. Dopamine is a neurotransmitter involved in a myriad in nerve functions.

In this study a special kind of mice was bred. These genetically engineered mice cold are induced (chemically) to develop a depletion of glutathione in neurons as adults and in different stages of their adulthood. When the glutathione depletion was induced in young adults no Parkinsonian-like nerve damage and symptoms occurred. On the contrary if the induction was done in late middle age mice developed loss of neurons specifically related to Parkison's disease.

Another interesting effect was seen in this study. Loss of glutathione in neurons may also have a strong effect of energy production. Energy, at the cellular lever is produced in a sub cellular structure known as mitochondria. Mitochondria are true "power plants" within the cell. Lack of glutathione may have an effect on an enzymatic complex of the mitochondria known as mitochondrial complex I.

Glutathione is available to be taken as a dietary supplement. However, the antioxidant glutathione cannot pass the blood-brain barrier to reach the glutathione starving neurons. So no effect can be seen in Parkinson patients taking glutathione orally.

1: Biofactors. 1997;6(3):321-38.

Lipoic acid increases de novo synthesis of cellular glutathione by improving
cystine utilization.

Han D, Handelman G, Marcocci L, Sen CK, Roy S, Kobuchi H, Tritschler HJ, Flohé L,
Packer L.

Department of Molecular and Cell Biology, University of California, Berkeley
94720-3200, USA.

Lipoic acid (thiotic acid) is being used as a dietary supplement, and as a
therapeutic agent, and is reported to have beneficial effects in disorders
associated with oxidative stress, but its mechanism of action remains unclear. We
present evidence that lipoic acid induces a substantial increase in cellular
reduced glutathione in cultured human Jurkat T cells human erythrocytes, C6 glial
cells, NB41A3 neuroblastoma cells, and peripheral blood lymphocytes. The effect
depends on metabolic reduction of lipoic acid to dihydrolipoic acid.
Dihydrolipoic acid is released into the culture medium where it reduces cystine.
Cysteine thus formed is readily taken up by the neutral amino acid transport
system and utilized for glutathione synthesis. By this mechanism lipoic acid
enables cystine to bypass the xc- transport system, which is weakly expressed in
lymphocytes and inhibited by glutamate. Thereby lipoic acid enables the key
enzyme of glutathione synthesis, gamma-glutamylcysteine synthetase, which is
regulated by uptake-limited cysteine supply, to work at optimum conditions. Flow
cytometric analysis of freshly prepared human peripheral blood lymphocytes, using
monobromobimane labeling of cellular thiols, reveals that lipoic acid acts mainly
to normalize a subpopulation of cells severely compromised in thiol status rather
than to increase thiol content beyond physiological levels. Hence lipoic acid may
have clinical relevance in restoration of severely glutathione deficient cells.

PMID: 9288403 [PubMed - indexed for MEDLINE]

I was taking 200 mg per day of N-acetyl cysteine until a few months ago. The vitamin/supplement mix I take now (Vitalizer Gold by Shaklee) contains 50 mg of N-acetyl cysteine. I was also taking acetyl carnitine and alpha lipoic acid but am not currently doing so.

Thanks. I take 600mg N-acetyl cysteine and 300mg alpha lipoic acid daily. There is a lot of stuff on the internet on their benifits to PD. But ofcourse the PD doctors never recognise this and we are left to our own judgement. That is why this forum is really valuable.

Any comment on the following?
http://www.medicalnewstoday.com/articles/88119.php

Society For Neuroscience Selects Boston University Medical Center Researcher's Abstract
Main Category: Neurology / Neuroscience News
Article Date: 08 Nov 2007 - 2:00 PST
David Farb, PhD, recently had an abstract selected that was highlighted by the Society for Neuroscience (SFN). The abstract details how antioxidants influence dopamine release from striatal synaptosomes. It was presented at SFN's 37th annual meeting November 7th in San Diego, California.

Farb is the professor and chairman of the Department of Pharmacology & Experimental Therapeutics at Boston University School of Medicine. He is also the director of the Biomolecular Pharmacology Training Program, the interdepartmental program in biomedical neuroscience, and heads the Laboratory of Molecular Neurobiology.

Farb's abstract details the relationship between antioxidants and dopamine. Antioxidants can protect the central nervous system from oxidative damage. The level of oxidation and reduction of molecules reflects conditions within the nervous tissue. Increased levels of oxidative damage are believed to be involved in neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and stroke.

In the brain, neurons communicate with each other via synaptic connections in which signals are transmitted by the release of chemical neurotransmitters from presynaptic axon terminals. Farb and fellow BUSM researchers examined the release of a specific neurotransmitter, dopamine, from isolated pre-synaptic axon terminals.

Researchers sought to determine whether the presence of antioxidant compounds could influence spontaneous dopamine release from synaptosomes. They concluded that the release of dopamine could be influenced by numerous factors, including input from other neurotransmitters as well as the reducing/oxidizing state of the cell. Inclusion of the water soluble, sulfhydryl containing antioxidant glutathione, or the glutathione precursor NAC lowered spontaneous dopamine release by 85 percent. The antioxidant vitamin E had no effect on dopamine release.

"Not all antioxidants are equivalent," said Farb. "Our results suggest that the ability of NAC or glutathione at therapeutic doses to rapidly and reversibly stabilize the release of dopamine raises the possibility that such antioxidants may have significant potential for the treatment of oxidative damage in neurodegenerative diseases."

Farb chairs the Executive Committee for the Medical Sciences Training Program and is a member of the Bioinformatics Program. He also served as neurosciences consultant for WGBH-Boston PBS affiliate on the NOVA episode, Mirror Neurons and, as a member of the Drug Development Work Group of Mass Insight. He also co-authored the Massachusetts Technology Road Map for Drug Discovery.

Farb has served as a consultant to large and small pharmaceutical companies, intellectual property law and portfolio investment firms. He was a member of the founding Scientific Advisory Boards of CoCensys and DOV Pharmaceuticals and the Scientific Founder of Scion Pharmaceuticals (acquired by Wyeth), which commercialized his patents on high throughput electrophysiology and small molecule modulators of amino acid receptors. Farb currently serves on the SAB of DOV Pharmaceuticals and Helicon Therapeutics (pending). He holds nine issued U.S. patents and one patent issued in Australia.

Farb's current research is directed toward understanding the mechanisms of action of abused substances and steroid hormones and their interactions with excitatory and inhibitory amino acid receptors in the central nervous system. The research focuses on the mechanism of action and discovery of neuromodulators as therapeutic agents and on the structure, function, and cellular dynamics of ion channels and receptors in the brain and spinal cord. Recently, Farb's laboratory demonstrated that pregnanolone hemisuccinate inhibits reinstatement of cocaine seeking behavior and this compound has been acquired by NIDA for preclinical development in its Medications Development Program.

...is that Farb sure is cozy with Big Pharma. I just wonder if he would tell us if NAC (which is non-patentable) was just as good as anything that he might hope to find that could patentable.

The second thought that somebody owes Dr. Perlmutter an apology for the years they laughed at his work with glutathione.

And third is a mental note to pick up some NAC.