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Possible Parkinson's disease cure

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    Possible Parkinson's disease cure

    Researchers at Iowa State University have found an essential key to possibly cure Parkinson's disease and are looking for others.

    Anumantha Kanthasamy, a distinguished professor of biomedical sciences and W. Eugene and Linda R. Lloyd Endowed Chair in Neurotoxicology at the ISU College of Veterinary Medicine, has been working to understand the complex mechanisms of the disease for more than a decade and thinks he has found hope for the cure.

    Parkinson's disease sufferers lack a sufficient amount of a brain chemical called dopamine.

    Kanthasamy's research shows that there is specific protein that is naturally present in human brains that -- for no known reason -- kills the brain cells that make dopamine.

    The cells that are being killed are the ones that produce the needed dopamine.

    "We have millions of cells in our brains," said Kanthasamy, "In Parkinson's, about 10,000 of these brain cells die; no one knows why."

    Kanthasamy discovered that a novel protein -- known as protein kinase-C (specifically PKCδ) - is killing the dopamine-producing cells.

    Kanthasamy and his research staff discovered a compound that neutralizes the cell-killing kinase-C and allows the dopamine-producing cells to survive and function.

    source and details:
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    I hope so too.

    I really hope Michael J Fox sees progress during his lifetime. The last time I saw an interview with him, he looked terrible.
    Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

    T-11 Flaccid Paraplegic due to TM July 1985 @ age 12


      Thank you for posting this. I will forward this to a former co-worker who was diagnosed with Parkinson's. He needs some good news.
      2012 SCINetUSA Clinical Trial Support Squad Member
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        Before people jump to conclusions, I don't think that this study has shown anything that can be called a "cure" for Parkinson's disease. There are many theories of what causes death of dopaminergic cells and this is just one of several theories and the study, as far as I can tell, is from 2007.

        Anumantha Kanthasamy at Iowa State University has been working on Protein kinase C for some time. In 2007, he and his colleagues published a study, claiming that rottlerin (a protein kinase C inhibitor) protected dopaminergic neurons against MPTP (a toxin that kills dopaminergic cells) in culture and in mice.

        J. Pharmacol. Exp. Ther. 322 (3): 913-922

        Copyright © 2007 by the American Society for Pharmacology and Experimental Therapeutics.

        Neuroprotective Effect of Protein Kinase C Inhibitor Rottlerin in Cell Culture and Animal Models of Parkinson's Disease

        Danhui Zhang, Vellareddy Anantharam, Arthi Kanthasamy, and Anumantha G. Kanthasamy

        Parkinson's Disorder Research Laboratory, Department of Biomedical Sciences, Iowa Center for Advanced Neurotoxicology, Iowa State University, Ames, Iowa

        Abstract: Recent studies from our laboratory demonstrated that the protein kinase C (PKC) isoform is an oxidative stress-sensitive kinase and a key mediator of apoptotic cell death in Parkinson's Disease (PD) models (Eur J Neurosci 18:1387–1401, 2003; Mol Cell Neurosci 25:406–421, 2004). We showed that native PKC is proteolytically activated by caspase-3 and that suppression of PKC by dominant-negative mutant or small interfering RNA against the kinase can effectively block apoptotic cell death in cellular models of PD. In an attempt to translate the mechanistic studies to a neuroprotective strategy targeting PKC, we systematically characterized the neuroprotective effect of a PKC inhibitor, rottlerin, in 1-methyl-4-phenylpyridinium (MPP+)-treated primary mesencephalic neuronal cultures as well as in an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of PD. Rottlerin treatment in primary mesencephalic cultures significantly attenuated MPP+-induced tyrosine hydroxylase (TH)-positive neuronal cell and neurite loss. Administration of rottlerin, either intraperitoneally or orally, to C57 black mice showed significant protection against MPTP-induced locomotor deficits and striatal depletion of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid. Notably, rottlerin post-treatment was effective even when MPTP-induced depletion of dopamine and its metabolites was greater than 60%, demonstrating its neurorescue potential. Furthermore, the dose of rottlerin used in neuroprotective studies effectively attenuated the MPTP-induced PKC kinase activity. Importantly, stereological analysis of nigral neurons revealed rottlerin treatment significantly protected against MPTP-induced TH-positive neuronal loss in the substantia nigra compacta. Collectively, our findings demonstrate the neuroprotective effect of rottlerin in both cell culture and preclinical animal models of PD, and they suggest that pharmacological modulation of PKC may offer a novel therapeutic strategy for treatment of PD.
        I was not able to find any new studies that warrant a press release in 2010. In August 2009, Fan et al. [source][/source] apparently confirmed the results in culture but Rottlerin has not gone to clinical trial yet. Rottlerin [source] anchor=&view=c&_searchStrId=1175394495&_rerunOrigi n=google&_acct=C000050221&_version=1&_urlVersion=0 &_userid=10&md5=9fe8d2c8f2a39710ab46e0e4f7586ed 9[/source] is a complicated drug that has many effects besides inhibiting PKC delta. It also uncouples mitochondria and is used to prevent chlamydia and other infections [source] text=fig&searchid=1&FIRSTINDEX=1720&resourcetype=H WFIG[/source]. I don't know why it hasn't gone to clinical trial but one possibility is that the drug is quite toxic. Incidentally, Protein Kinase C (PKC) is an essential intracellular messenger and I suspect that blockade of PKC is not good for cells and Rottlerin has a variety of serious side effects.

        A much more exciting finding, in my opinion, is a recent study indicating that uric acid protects against Parkinson's disease [source][/source]. For many years, people who suffer from gout apparently do not have progressive Parkinson's disease. Two studies in the past six months have reported that high uric acid levels significantly reduce progression of Parkinson's disease in people. Uric acid of course comes from wine, women, and song... Actually, the last two are not true. Uric acid comes from eating foods with high concentrations of DNA, including meat. A drug called inosine (which by the way has been reported to be useful for spinal cord injury) raises uric acid levels and there is talk about such a clinical trial starting.

        Acid associated with gout 'could help Parkinson's sufferers'
        Monday, January 11, 2010
        By Kate Devlin,

        Parkinsons disease progresses more slowly inpatients with naturally high levels of the acid which triggers gout,suggesting a possible new treatment for the disease.

        Patientswith high levels of uric acid were a third less likely to needtreatment over the course of two years than those with low levels, theresults of a new study show.

        Researchers are now testing whether increasing Parkinsons patients uric acid levels safely can help their condition.

        An antioxidant, the acid is created naturally as we digest food.

        But too much uric acid, or urate, can cause bouts of gout, an extremely painful joint condition, and kidney stones.

        Dietsrich in liver, seafood and dried beans have been linked to high uricacid levels but researchers warn that because of the side effectspatients should not try to increase their urate levels themselves.

        Asmaller study published last year also suggested that high uric acidlevels could slow the progression of Parkinsons Disease.

        DrAlberto Ascherio, from the Harvard School of Public Health, who led thestudy, said: Only now we can be reasonably sure that the slower rateof progression in patients with higher concentrations of urate is realand not a chance occurrence."

        However, the researchers stressthat they do not yet know if it is the acid itself which carries theprotective benefit or some other process of the body which producesuric acid as a by-product.

        The latest research looked at 800 sufferers of the condition.