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04-01-2007, 08:18 AM | #111 | ||
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In the U.K look for one that says for dry coughs.There are quite a few that follow the above criteria but theyare kept behind the counter so you have to ask for them.My pharmacist friend suggest one asks their doctor for a presciption as it is for off licence use here and chemist would have to refuse to sell it to you if they thought you were purchasing too much.The amount required would hardly alarm any chemist I would have thought.I have had no trouble obtaining it. Besides there are more than one chemist in most towns.
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04-02-2007, 10:36 AM | #112 | ||
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This is one of the latest research papers from the NIH on a more potent form of dextromethorphan, 3-HM, shown to be 90% neuroprotective in rodents. In the paper, there is a graph comparing five forms of DM. While 3-HM was 90% effective, the next most effective form seems to be DM at about 70% to 80%. Don't know if 3-HM is sold as a drug.
Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Science/National Institutes of Health, Research Triangle Park, North Carolina, USA. We investigated the neuroprotective property of analogs of dextromethorphan (DM) in lipopolysaccharide (LPS) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models to identify neuroprotective drugs for Parkinson's disease (PD). In vivo studies showed that daily injections with DM analogs protected dopamine (DA) neurons in substantia nigra pars compacta and restored DA levels in striatum using two different models for PD. Of the five analogs studied, 3-hydroxymorphinan (3-HM), a metabolite of DM, was the most potent, and restored DA neuronal loss and DA depletion up to 90% of the controls. Behavioral studies showed an excellent correlation between potency for preventing toxin-induced decrease in motor activities and neuroprotective effects among the DM analogs studied, of which 3-HM was the most potent in attenuating behavioral damage. In vitro studies revealed two glia-dependent mechanisms for the neuroprotection by 3-HM. First, astroglia mediated the 3-HM-induced neurotrophic effect by increasing the gene expression of neurotrophic factors, which was associated with the increased acetylation of histone H3. Second, microglia participated in 3-HM-mediated neuroprotection by reducing MPTP-elicited reactive microgliosis as evidenced by the decreased production of reactive oxygen species. In summary, we show the potent neuroprotection by 3-HM in LPS and MPTP PD models investigated. With its high efficacy and low toxicity, 3-HM may be a novel therapy for PD. http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract Also, Dr. John Hong, Head of Neuropharamacology at the NIH, will be a speaker at the 3rd annual LDN Conference this October in Tenn. He will speak on opioid receptor antagonists like DM and naltrexone being neuroprotective for PD and Alzheimers. Hopefully, he will be able to suggest the most optimal DM dosage for people even though they don't test with humans, I don't think. http://www.lowdosenaltrexone.org/events.htm Ashley |
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04-03-2007, 12:13 PM | #113 | |||
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3-HM, a major metabolite of DM, is rapidly produced from DM by one or more of a family of drug-metabolizing P450 enzymes in the liver. These enzymes add hydroxy groups to a variety of drugs and other molecules which allows them to be more rapidly excreted, usually in the urine.
The upside of this is that one does not have to separately obtain the apparently more effective neuroprotective 3-HM if one is taking DM. At least one limitation to this situation could exist if the 3-HM made in the liver and released into the circulation were less able to cross the blood-brain barrier than the parent DM. |
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04-03-2007, 05:56 PM | #114 | |||
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In Remembrance
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Be alert to possible reactions between DM and other drugs which also use the CYP450 metabolic paths. That may have been my problem since Requip is such. Sinemet is not and I think at least one of the other agonists is not. If you have doubts Google "CYP450" and your drug at a minimum. Then just be extra observant the first few days.
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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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04-05-2007, 09:42 PM | #115 | |||
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Today..Its almost 11 pm, and I havent taken any meds since 2 pm this afternoon without any consequences whatsoever..I will be taking my last dose of Sinamet in a half hour..then DM and hour later
Neuro appoimtment on the 11th..Should be interesting
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There are those who see things as they are and ask..Why?..I dream of things that never were and ask..Why not?..RFK |
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04-12-2007, 11:54 PM | #116 | |||
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I saw my neuro yesterday..My motor skill exam was a bit above average, and my BP was 128/80..Down from 140/92 last time..I didnt tell him about the DM
He said to stay the course
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There are those who see things as they are and ask..Why?..I dream of things that never were and ask..Why not?..RFK |
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04-20-2007, 07:19 AM | #117 | ||
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My husband(PWP) who has been diagnosed just over two years, has been taking the appropriate cough medicine for about a month.I am sure I am not imagining it but he seems to be tremoring less often and is walking better although his gait was never that bad.He thinks this is true also .But to him the main advantage has been much better sleep:no more waking at 3am and then being drowsy in the day. The only prescibed medicine he is on is Requip (4mg,4mg 4mg,1mg)Unfortunately, there are too many variable to say it is definately only the DM as he also takes cucumin,cod liver oil. an antioxidant pill and ALC/ALA.The last having been added since starting the cough medicine.
Combination could interact.He takes his blood pressure very reqularly.The reason I have written this follow up is that as he is not on Sinemet it cannot be an interaction with that.Incidently,last time we saw the neurologist he said he thought it would not benifit him or improve his tremor if he upped his Requip so if it works in the same way.....? |
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04-20-2007, 07:33 AM | #118 | ||
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ALA/ALC improves my memory.I am positive about that.
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04-20-2007, 07:47 AM | #119 | |||
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Senior Member
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Quote:
Fatigue?:..Still shows a bit of improvement as well as reduced stuttering
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There are those who see things as they are and ask..Why?..I dream of things that never were and ask..Why not?..RFK |
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05-07-2007, 12:56 PM | #120 | ||
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This study shows how activated microglial (killer cells), which are believed to destroy dopamine neurons, can be be greatly attenuated by dextromethorphan and another even more effective drug. Though the research was done for drug abuse, it implies that DXM could be used for PD. I don't know what an equivalent human DXM dose would be but this study seems to back Dr. Hongs research done at the NIH.
Ashley http://www.nida.nih.gov/NIDA_notes/N...N6/Evokes.html Drs. Kuhn and Thomas injected mice with either MK-801 or DXM and then methamphetamine (5 mg/kg of body weight) 15 minutes later, repeating this sequence four times at 2-hour intervals. A control group of mice received the same regimen, but with saline substituted for methamphetamine. Forty-eight hours after the last injection, the researchers assayed the brains of the mice for Cox-2 and TNF-α, the indicators of microglia activation, and for striatal dopamine levels, a widely used index of damage to dopamine neurons. Dr. Kuhn says, "We found that both DXM and MK-801 significantly reduced the markers of striatal microglial activation associated with methamphetamine exposure and protected against dopamine nerve terminal damage in the striatum. The close association between the ability of MK-801 and DXM to significantly lower both microglial activation and neuronal damage suggests a causal link between the two. It looks as though the damage associated with methamphetamine abuse is the result of microglial action." |
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"Thanks for this!" says: | Drevy (07-01-2014) |
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