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Very interesting. Does this relate somehow to inosine, which affects urate levels? And might this have something to do with how dogs pick up the smell of PD? I swear, for the last year or so, I've been aware of an ammonia smelll that seems to emanate from me. I wonder if this smell masks other odors, resulting in the anosmia experienced by many of us PD sufferers. Could PD be a urea cycle disorder? Kathleen ----------------------------------------------------------------------------------------------------------------------------------------------------- From the University of Rochester, here is something on ammonia testing. Link: https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=ammonia Ammonia Does this test have other names? Blood ammonia test, NH3 What is this test? This test checks the level of ammonia in your blood. The test helps find out why you may have changes in consciousness and also helps diagnose a liver disease called hepatic encephalopathy. This disease affects how your brain works, because of excess toxins, or poisons, in your body. Your liver may not work properly if you have high levels of ammonia in your blood. Ammonia is a chemical made by bacteria in your intestines and your body's cells while you process protein. Your body treats ammonia as a waste product. It turns it into an amino acid called glutamine and a chemical compound called urea. Your bloodstream moves the urea to your kidneys, where it is eliminated in your urine. But ammonia will build up in your body if you can't get rid of urea. This can sometimes happen if you have kidney or liver failure. It can also happen if you have a urea cycle disorder, a genetic disorder that means your body is missing one of the enzymes that remove ammonia from the blood. The ammonia blood test is the gold standard for diagnosing urea cycle disorders. On 9 November 2015 at 20:04, Rayilyn Brown <[log in to unmask]> wrote: > another abstract from Joanie McGuire > > Program#/Poster#: > 12.02 > > > > > Presentation Title: > Stopping progression of Parkinson's disease with the drug > phenylbutyrate > > > > > Location: > N230 > > > > > Presentation time: > Saturday, Oct 17, 2015, 1:15 PM - 1:30 PM > > > > > Topic: > ++C.03.a. Human studies > > > > > Authors: > *C. R. FREED1, M. WANG1, J. CUMMISKEY1, K. B. BJUGSTAD1, B. A. > SYMMES1, C. A. JOHNSON2, R. C. MURPHY2, M. A. LEEHEY3, W. ZHOU1; > 1Div. of Clin. Pharmacol., 2Dept. of Pharmacol., 3Dept. of > Neurol., Univ. Colorado Sch. of Med., Aurora, CO > > > > > Abstract: > Parkinson's disease has excellent symptomatic treatment with > drugs such as L-DOPA, but the underlying disease process causes a > relentless downhill course. > > > > Several drugs have been tested in an effort to alter disease > progression, but all have failed. We have developed a new concept for > stopping the progression of Parkinson’s disease by turning on a > neuroprotective gene with an FDA-approved drug. In Parkinson’s disease, the > protein alpha-synuclein forms abnormal deposits called Lewy bodies as well > as toxic fibrils which contribute to the death of dopamine neurons. We have > discovered that the drug phenylbutyrate can prevent aggregation of > alpha-synuclein in transgenic mice which are genetically programmed to > develop a form of Parkinson’s disease as they age. > > > > The drug works by upregulating the neuroprotective gene DJ-1. > Gene activation leads to an increase in lysosome and exosome activity, > promoting transfer of alpha-synuclein from neurons into the bloodstream > where the protein is eliminated. In mice, phenylbutyrate increased plasma > alpha-synuclein by about 100 per cent compared to non-treated control > animals. > > > > To see if phenylbutyrate has the same effect in people, we > have given the drug for three weeks to 20 people with newly diagnosed > Parkinson’s disease and to 20 age-matched subjects without the disease. We > found that the drug increased the level of alpha-synclein in plasma of all > 40 subjects from 50 to 150 per cent of baseline values, just as it had done > in transgenic mice, strongly suggesting that the drug can mobilize > alpha-synuclein from neurons into blood plasma. While baseline plasma > alpha-synuclein varied between subjects, the average alpha-synuclein plasma > concentrations at baseline and during phenylbutyrate administration did not > differ between patients with Parkinson's disease and normal subjects. > Results are compatible with a neuroprotective effect of phenylbutyrate by > accelerating clearance of alpha-synuclein from brain into plasma. > > > > A double-blind, placebo-controlled trial in newly diagnosed > Parkinson patients will be needed to prove whether phenylbutyrate can stop > the progression of Parkinson’s disease in humans. > > > > > Disclosures: > C.R. Freed: C. Other Research Support (receipt of drugs, > supplies, equipment or other in-kind support); Hyperion Pharmaceuticals. M. > Wang: None. J. Cummiskey: None. K.B. Bjugstad: None. B.A. Symmes:None. C.A. > Johnson: None. R.C. Murphy: None. M.A. Leehey: None. W. Zhou: None. > > > > > Keyword (s): > PARKINSON'S DISEASE > > > > > > NEUROPROTECTION > > > > > > DOPAMINE > > > > > Support: > Walter S. and Lucienne Driskill Foundation > > > > > > Michael J. Fox Foundation > > > > > > Mr. Charles Ackerman > > > > > > Mr. Ray Sidhom > > > > > > Mr. John Anderson > > > > > > > > > Ray > Rayilyn Brown > Past Director AZNPF > Arizona Chapter National Parkinson Foundation > > ---------------------------------------------------------------------- > To sign-off Parkinsn send a message to: mailto: > [log in to unmask] > In the body of the message put: signoff parkinsn > ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn