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04-27-2010, 11:48 PM | #1 | ||
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Junior Member
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Would someone with more scientific knowledge than me please would read the statement below.
It's written in arcane language but seems to be saying that curcumin makes PD symptoms WORSE, or maybe I'm not reading it right. Here's the quote: "The LRRK2 gene has emerged as the gene most commonly associated with both familial and sporadic PD. Here, we report that exposure of rat mesencephalic cells to curcumin induces the expression of LRRK2 mRNA and protein in a time-dependent manner." |
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04-28-2010, 01:09 AM | #2 | |||
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In Remembrance
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Hi Togo,
Even as a scientist, that sentence means nothing to me. It seems that the important few words are "curcumin induces the expression of LRRK2 mRNA and protein". But what do they mean by expression. Also, protein is "expressed" also, yet you can't say all protein is bad. There is such a wealth of positive information about curcumin's beneficial effects that I should not spend time trying to decipher this reference. Do a search both on the web and on this site, and you will only find beneficial properties for curcumin. Ron
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Diagnosed Nov 1991. Born 1936 |
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04-28-2010, 03:01 PM | #3 | ||
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Junior Member
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Ron, thanks so much for your help. I feel much better.
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04-28-2010, 03:45 PM | #4 | |||
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In Remembrance
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Another indicator- India consumes tons of curcumin yet has much less PD than the US which consumes little.
Also, we have no way to translate the lab's exposure to that of the dinner table. That's important because many of these complex plants are bi-phasic and lose or even reverse their effects at high dosages. Those cells in the flask may have been blasted with a mega dose. We have no way of knowing. The best evidence comes from the lab verifying tradition and confirmed by the patient. Turmeric has that. Have some curry?
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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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04-29-2010, 05:01 AM | #5 | ||
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Junior Member
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Quote:
I'm particularly interested in what you say about curcumin and bioperine, and would be very grateful if you could tell me your source for this, as there are so many to choose from on the internet. I hope you're allowed to do this on this forum, but, if not, would it be possible for you to e-mail me direct - again, I don't know if this is possible, but would appreciate your advice. Many thanks in anticipation. |
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04-29-2010, 07:18 AM | #6 | ||
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Member
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Hi togo,
LRRK2 is a protein which is needed for the normal function of a cell. Mutations in LRRK2 gene results in a faulty protein and that is what is correlated with PD. If curcumin induces the expression of LRRK2, which simply means that exposure to curcumin results in making of LRRK2 protein is not a bad thing. As long as curcumin induces normal LRRK and not the mutated one, we are safe!! Here is an abstract on LRRK2 Trends Neurosci. 2006 May;29(5):286-93. Epub 2006 Apr 17. LRRK2 in Parkinson's disease: protein domains and functional insights. Mata IF, Wedemeyer WJ, Farrer MJ, Taylor JP, Gallo KA. Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA. Abstract Parkinson's disease (PD) is the most common motor neurodegenerative disease. Mutations in the gene encoding leucine-rich repeat kinase 2 (LRRK2) have been linked recently with autosomal-dominant parkinsonism that is clinically indistinguishable from typical, idiopathic, late-onset PD. Thus, the protein LRRK2 has emerged as a promising therapeutic target for treatment of PD. LRRK2 is extraordinarily large and complex, with multiple enzymatic and protein-interaction domains, each of which is targeted by pathogenic mutations in familial PD. This review places the PD-associated mutations of LRRK2 in a structural and functional framework, with the ultimate aim of deciphering the molecular basis of LRRK2-associated pathogenesis. This, in turn, should advance our understanding and treatment of familial and idiopathic PD. Hope it helps girija Quote:
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"Thanks for this!" says: | lindylanka (04-30-2010), Ronhutton (04-29-2010) |
04-29-2010, 01:40 PM | #7 | |||
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In Remembrance
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Hi Budgies,
See you private messages for my reply, as I would not want anyone to think I was pushing a particular supplier. Rick is quite right about India having a low incidence rate for PD. The actual figures are USA/ UK have around 280 cases of PD per 100,000 people, whilst India has 14 per 100,000. There has to be a reason for such a huge discrepancy, and it is thought that it m,ust be due to the copious quantities of curcumin consumed in India,. Best wishes Ron. PS Girija, Thanks for clarifying the abstract.
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Diagnosed Nov 1991. Born 1936 |
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04-30-2010, 06:53 AM | #8 | ||
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Senior Member
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Hi Ron,
Just wanted to say that perhaps the differential in rates between India and US/UK figures is as likely to be do do with the incidence of undiagnosed PD as the use of turmeric. That is not to say that I discount curcumin, it has powerful antibiotic properties and is used in ayurvedic preparations. I just think that looking at figures from countries with less developed health care and high poverty levels does not give a true picture of the incidence, for this you would have to correlate it with the figures for people who actually have access to medical treatment. Even then I doubt if you would come up with anything like the true incidence. Even in the UK there are people, mainly older, who do not get treated for PD, either because they do not seek help for what they see as the problem of getting older, or because there is still a stigma attached to PD and they do not want the baggage that come along with it, or worse, to be seen as a disease and not a person. I know of at least two people who fall into this bracket........ There's a lot still to be done for PD awareness.... Lindy |
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04-30-2010, 02:13 PM | #9 | ||
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Member
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every body: following article confirms your input. Inspired by Ron's postings, I have been taking 900 mg curcumine + bioperin for few years and because it is cheap I am tempted to double the dose .. how ever I did not .. following an arabic saying " Too much of a good thing will turn it into a bad thing "
but seriously: dose is a real issue Imad Curcumin reduces alpha-synuclein induced cytotoxicity in Parkinson's Disease cell model Overexpression and abnormal accumulation of aggregated alpha-synuclein (alphaS) have been linked to Parkinson's disease (PD) and other synucleinopathies. AlphaS can misfold and adopt a variety of morphologies but recent studies implicate oligomeric forms as the most cytotoxic species. Both genetic mutations and chronic exposure to neurotoxins increase alphaS aggregation and intracellular reactive oxygen species (ROS), leading to mitochondrial dysfunction and oxidative damage in PD cell models. Results: Here we show that curcumin can alleviate alphaS-induced toxicity, reduce ROS levels and protect cells against apoptosis. We also show that both intracellular overexpression of alphaS and extracellular addition of oligomeric alphaS similarly increase ROS which induces apoptosis, suggesting that aggregated alphaS may induce similar toxic effects whether it is generated intra- or extracellulary. Conclusions: Since curcumin is a natural food pigment that can cross the blood brain barrier and has widespread medicinal uses, it has potential therapeutic value for treating PD and other neurodegenerative disorders. Author: Min WangShanta BoddapatiSharareh EmadiMichael Sierks Credits/Source: BMC Neuroscience 2010, 11:57 Last edited by imark3000; 04-30-2010 at 03:14 PM. |
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04-30-2010, 02:56 PM | #10 | |||
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In Remembrance
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Lindy-
In general, I agree. But this is a special case. The culture has recognized and treated PD for five thousand years or so. -Rick
__________________
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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