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10-29-2007, 10:20 AM | #1 | ||
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Member
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Basically, he's saying, So let's get on with it! We need to study other things. I have gisted some of the medicalese in brackets to make it more comfortable to read.
Jaye //begin quote// Neurology. 2007 Oct 23;69(17):1701-11. Links Beating a dead horse: dopamine and Parkinson disease. Ahlskog JE. Department of Neurology, Mayo Clinic Our collective thinking about Parkinson disease (PD) has been heavily influenced by the dramatic response to dopamine replacement therapy. For progress to continue, however, we need to take a broad view of this disorder, which includes recognition of the following. First, substantial evidence now indicates that dopamine oxidation is unlikely to substantially contribute to the pathogenesis of PD [means roughly that the body's processing dopamine probably doesn't hurt you much]. Second, levodopa therapy is not associated with neurotoxicity [it doesn't damage the brain or nerve cells]. Third, the first neurons affected in PD are nondopaminergic [PD starts first in other places than the substantia nigra layer of the brain, where the dopamine-making cells are]; the substantia nigra and other dopaminergic nuclei are affected only later in the course. Thus, PD is much more than degeneration of the dopaminergic nigrostriatal system. Fourth, in the current era, most of the disability of advancing PD is from involvement of nondopaminergic [non-dopamine-making] systems, including levodopa-refractory motor symptoms, dementia, and dysautonomia [dyskinesia, dystonia, dementia, malfunction of the autonomic nervous system]. Motor complications associated with levodopa therapy can be problematic, but they can be controlled in most, using available medications and deep brain stimulation surgery. We have reached the point of diminishing therapeutic returns with drugs acting on dopamine systems; more dopaminergic medications will provide only modest incremental benefit over current therapies. Finally, the benefits from transplantation surgeries aimed at restoring dopaminergic neurotransmission will be limited because later-stage PD disability comes from nondopaminergic substrates. Scale. PMID: 17954785 [PubMed - in process] //end quote// |
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10-29-2007, 10:53 AM | #2 | |||
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Senior Member
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Jaye - this has to be one of the most significant / provocative journal articles ever about PD (IMHO!)!
The author's conclusion is why I think that stem cells are not the answer (or at least, not the complete answer) for PD. I love that the science is finally catching up to patient experience. If only they had started listening to us earlier!
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Carey “Cautious, careful people, always casting about to preserve their reputation and social standing, never can bring about a reform. Those who are really in earnest must be willing to be anything or nothing in the world’s estimation, and publicly and privately, in season and out, avow their sympathy with despised and persecuted ideas and their advocates, and bear the consequences.” — Susan B. Anthony |
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10-29-2007, 01:01 PM | #3 | ||
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I was so excited when I saw it come in on the AMEDEO feed this morning! We and the generations before us have waited a long time for this.
Trying to remember what dancing shoes were, Jaye |
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10-29-2007, 03:07 PM | #4 | |||
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In Remembrance
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...this should be old news to every researcher and doctor in the world as the paper below shows. Thirty dam*** years ago. My point is that people have to get noisy about this at every opportunity.
1: Natl Inst Drug Abuse Res Monogr Ser. 1975 Nov;(3):13-21. Brain monoamines and parkinsonism. Hornykiewicz O. In Parkinson's disease there is a derangement of the metabolism of at least 3 major brain monoamines, namely, dopamine (DA), norepinephrine (NE) and serotonin (5-HT). Of these alterations the severe deficiency of DA in the striatum is most characteristic, being (a) found in Parkinsonian syndromes of any etiology and (b) significantly correlated with the degree of cell loss in the substantia nigra, and the severity of the main symptoms. On the basis of neurochemical-clinical correlations Parkinson's disease may be subdivided into (a) an asymptomatic stage during which the striatal DA deficiency may reach a marked degree but can be compensated by the remaining DA neurons, and (b) the stage of decompensation (i.e. clinically manifest disease) which ensues when the depetion of striatal DA reaches 70% or more. L-Dopa's main feature as a specific antiparkinson drug may be seen in its potential to revert the decompensated stage of the disease to the stage of functional compensation. This is in many cases possible because (a) the DA turnover in the remaining DA neurons is increased, providing for a high rate of formation (from L-dopa) and release of DA; (b) the "denervated" striatal receptors are supersensitive to DA; and (c) the newly-formed DA can be expected to reach a wide area of the striatum due to the high degree of divergence of the dopaminergic innervation. Compared with the striatal DA deficiency, the degree of NE and 5-HT decrease in the Parkinsonian brain is moderate. The decrease in NE may be due to the (moderate) cell loss in the locus coeruleus; at present no morphological basis for the lowering of brain 5-HT is known. The functional significance of the changes in brain NE may be an aggravation of akinesia. The decrease in brain 5-HT may be related to aspects of Parkinson's disease in turn related to affective behavior and mood. PMID: 787796 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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10-29-2007, 03:25 PM | #5 | |||
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Senior Member
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That's just the point - it's not old news to most researchers. Or else it's known but they have chosen to ignore it. That's why I think it's so provocative - because it bucks the prevailing trend/wisdom of mainstream research. But a few voices are starting to speak up - Bill Langston from the Parkinson's Institute is one - he uses the Braak stages (another maverick) as the basis for the talks he gives lately. Hopefully it's an old theory that will take on a new life.
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Carey “Cautious, careful people, always casting about to preserve their reputation and social standing, never can bring about a reform. Those who are really in earnest must be willing to be anything or nothing in the world’s estimation, and publicly and privately, in season and out, avow their sympathy with despised and persecuted ideas and their advocates, and bear the consequences.” — Susan B. Anthony |
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10-29-2007, 03:59 PM | #6 | |||
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Senior Member
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I just said this:
Quote:
"Translational Medicine" is the new thing at the NIH - very much needed and over due!
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Carey “Cautious, careful people, always casting about to preserve their reputation and social standing, never can bring about a reform. Those who are really in earnest must be willing to be anything or nothing in the world’s estimation, and publicly and privately, in season and out, avow their sympathy with despised and persecuted ideas and their advocates, and bear the consequences.” — Susan B. Anthony |
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10-29-2007, 04:25 PM | #7 | |||
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Member aka Dianna Wood
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This is Vicky from Minnesota who has heard Dr. Ahlkskog speak in person. I still have the handout from the event he spoke some years ago. At that time I had been trying to keep my amount of Sinemet to as low a doseage as I was able to stand. Dr. J. Eric Ahlskog presented his opinion of 10 myths that sabotage treatment of Parkinson's Disease:
Myth #1 - Levodopa stops working after a few years.
Myth #2 - Levodopa may be toxic
Myth #3 - Almost everyone develops dyskinesias of levodopa
Myth #4 - Dyskinesias are worse than parkinsonism Dyskinesias (excessive movement):
Myth #5 - Levodopa should be delayed
Myth #6 - The levodopa dose should be limited
Myth #7 - The dopamine agonist are nearly as effective as levodopa Dopanine agonist=synthetic form of dopamine
Myth #8 - The dopamine agonist drugs may slow the progression of PD Suggested by Brain Imaging studies
Myth #9 - Controlled-release carbidopa/levodopa is preferred (Sinemet CR) Facts about the CT formulation:
Myth #10 - Levodopa disrupts sleep Facts:
I believe not one person on this forum can be in complete agreement with Dr. Ahlskog with all of his myths. PD comes in too many forms. I agree with you Indigogo, it is good to revisit older theories. I also agree with Jaye. But the patients have to bear some responsibility for the attempts to prove theories rather than learn more about the disease. The lobbying and pressure that advocates applied to congress for funding theories to find a quick cure rather than learning the etiologie of PD slowed down the scientific community's research efforts. By trying to appease the patient lobbyists, the pharmaceutical companies let the patients' (their market) determine the direction of research, not hard science. Vicky |
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