[lou_lou]

Curry Spice Curcumin And Parkinson's Disease? Protects Against A53T Alpha-synuclein-induced Toxicity
18 Nov 2008

Johns Hopkins Researchers at Neuroscience 2008 - Curcumin, derived from the curry spice turmeric, has strong antioxidant and anti-inflammatory properties. Both oxidative damage - damage caused by oxygen - and inflammation have been implicated in nerve cell death associated with Parkinson's disease. Now, researchers at the Johns Hopkins University School of Medicine have shown in a laboratory model of Parkinson's disease that curcumin does protect cells from dying.

To test the protective effects of curcumin, the research team used a Parkinson's disease cell model system. They tested curcumin on nerve-like cells that make a mutant form of the protein alpha-synuclein, called A53T, that clumps together inside of cells to cause harmful biochemical and cellular changes that eventually kill the cells. A53T alpha-synuclein causes 50 percent of untreated cells to die, whereas only 19 percent of A53T cells treated with curcumin died. Further research showed that curcumin itself reduces oxidative damage.

"These results suggest that curcumin is a potential candidate for inhibiting the oxidative damage that leads to Parkinson's disease," says Wanli Smith, Ph.D., an assistant professor of psychiatry and behavioral sciences at Hopkins. "This common curry spice could be a weapon to protect the brain."

Johns Hopkins Medicine
www.hopkinsmedicine.org
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Article URL: http://www.medicalnewstoday.com/articles/129787.php

Main News Category: Parkinson's Disease

Also Appears In: Neurology / Neuroscience, Nutrition / Diet,


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more information here
http://www.answers.com/Curcumin?afid...ookup&nafid=27
from the Linus Pauling Institute
Biological Activities

Antioxidant Activity

Curcumin is an effective scavenger of reactive oxygen species and reactive nitrogen species in the test tube (in vitro) (9, 10). However, it is not clear whether curcumin acts directly as an antioxidant in vivo. Due to its limited oral bioavailability in humans (see Metabolism and Bioavailability above), plasma and tissue curcumin concentrations are likely to be much lower than that of other fat-soluble antioxidants, such as alpha-tocopherol (vitamin E). However, the finding that 7 days of oral curcumin supplementation (3.6 g/day) decreased the number of oxidative DNA adducts in malignant colorectal tissue suggests that curcumin taken orally may reach sufficient concentrations in the gastrointestinal tract to inhibit oxidative DNA damage (7). In addition to direct antioxidant activity, curcumin may function indirectly as an antioxidant by inhibiting the activity of inflammatory enzymes or by enhancing the synthesis of glutathione, an important intracellular antioxidant (see below).

http://lpi.oregonstate.edu/infocente...cals/curcumin/

[olsen]

curcumin is a Nrf2 inducer, as are sulphorphanes (of which brocco sprouts are the most potent). Alpha lipoic acid positively affects Nrf2 upregulation. and Deprenyl has been shown in cell models to upregulate Nrf2
(http://cat.inist.fr/?aModele=afficheN&cpsidt=17503734)

[aquario]

However, the finding that 7 days of oral curcumin supplementation (3.6 g/day) decreased the number of oxidative DNA adducts in malignant colorectal tissue suggests that curcumin taken orally may reach sufficient concentrations in the gastrointestinal tract to inhibit oxidative DNA damage (7).


Much as I love the food, that's a lot of curry! And what's the scuttlebutt about needing some form of pepper to properly metabolize the curcumin?

Jon

[reverett123]

A compound from black pepper called piperine or bioperine increases the amount you absorb greatly. It also increases absorption of other things as well. Such as PD drugs as I have discovered over the last two weeks. I find that to be a boon. Just be ready to adjust your doses or spacing as needed.

[lou_lou]

dear all,

I take the "Now Brand" - I do not sell it - or am I suggesting that anyone take what I take ...

however according to the label it reads:

Curcumin is the major component of Turmeric (Curcuma longa L.) and extensive scientific research on Curcumin has demonstrated its potent antioxidant properties. Through its antioxidant mechanisms, Curcumin supports colon health, exerts neuroprotective activity and helps maintain a healthy cardiovascular system.
more info @
http://www.nowfoods.com/index.php?ac...l&item_id=2792

[olsen]

Piperine physiologically acts like an MAO-B inhibitor. Be careful when taking a curcumin preparation which includes this vehicle if you take an MAO inhibitor.

[mrsD]

Drugs R D. 2008;9(4):243-50.Links
Effect of NCB-02, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study.
Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N.

Department of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences, Hyderabad, Andhra Pradesh, India.

BACKGROUND AND OBJECTIVE: Hyperglycaemia leads to increased oxidative stress resulting in endothelial dysfunction. ACE inhibitors, antioxidants and HMG-CoA reductase inhibitors (statins) have been shown to improve endothelial function. The aim of this study was to compare the effects of NCB-02 (a standardized preparation of curcuminoids), atorvastatin and placebo on endothelial function and its biomarkers in patients with type 2 diabetes mellitus. METHODS: A total of 72 patients with type 2 diabetes were randomized to receive NCB-02 (two capsules containing curcumin 150 mg twice daily), atorvastatin 10 mg once daily or placebo for 8 weeks. Endothelial function assessment was performed at baseline and post-treatment using digital volume plethysmography (salbutamol [albuterol] challenge test) to measure change in reflective index, an indicator of arterial vascular tone. Blood samples were similarly collected at baseline and post-treatment for estimations of malondialdehyde, endothelin-1 (ET-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha). Pre-and post-treatment safety assessments were also conducted. ANOVA and paired t-test evaluations were used for comparison. RESULTS: A total of 67 patients completed the study. At baseline, there was no significant difference in the various parameters tested. In all three groups, the change in reflective index at baseline was <6% as assessed by the salbutamol challenge test, indicating the presence of endothelial dysfunction. Compared with baseline, there was a significant improvement in endothelial function after treatment with atorvastatin (mean +/- SD: -3.63 +/- 3.17% vs -8.95 +/- 6.80%, respectively) and NCB-02 (-2.69 +/- 3.02% vs -8.19 +/- 5.73%, respectively). Similarly, patients receiving atorvastatin or NCB-02 showed significant reductions in the levels of malondialdehyde, ET-1, IL-6 and TNFalpha. No significant improvements were obtained in patients administered placebo. CONCLUSION: NCB-02 had a favourable effect, comparable to that of atorvastatin, on endothelial dysfunction in association with reductions in inflammatory cytokines and markers of oxidative stress. Further studies are needed to evaluate the potential long-term effects of NCB-02 and its combination with other herbal antioxidants.

PMID: 18588355 [PubMed - indexed for MEDLINE

Given that Lipitor's actions are now being thought to be more helpful with this factor than the cholesterol lowering
the curcumin effects are very promising.

Here is another: on GI inflammation:
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

I am trying to find the preparation used for the studies
NCB-02...
I found this as far as dose..
http://www.ingentaconnect.com/conten...00004/art00004

But I wonder if an enhancing substance is included in the prep?
Anyone know?

I just found this:
http://www.lef.org/magazine/mag2007/...urcumin_01.htm
(without piperine)

and here it is:
http://www.epic4health.com/cuenbicu.html

I've been using Curcumin for almost a month, for my arthritis. (I stopped my SAMe for comparison)
So far so good. I have not had a relapse which I typically did when I tried to stop SAMe in the past.

I am interested in the endothelial actions of curcumin for myself, to perhaps lower
C-reactive protein, which I will have tested in 3 months. I am going to try this version I just
found! I have used Epic4health before. Their carnitine fumarate was helpful to me in the
past. So I know they are a reliable company. I do not see Bioperine listed as an ingredient!

I just found a double strength 500mg curcumin gel at the above website...and ordered 2 of them!
That is a 4 months supply for me, and came to $49.00. Not bad!

[olsen]

another aspect of pleiotropic effects of statins to consider:

Negative impact of statins on oligodendrocytes and myelin formation


J Neurosci. 2008 Dec 10;28(50):13609-13614.

Negative Impact of Statins on Oligodendrocytes and Myelin Formation In Vitro and In Vivo.
Klopfleisch S, Merkler D, Schmitz M, Klöppner S, Schedensack M, Jeserich G, Althaus HH, Brück W.
Statins are widely prescribed drugs in cardiovascular diseases. Recent studies also demonstrated anti-inflammatory and immunomodulatory properties of statins by modulating the activity of small GTPases. Statins are thus considered as potential therapeutic drug for the inflammatory demyelinating disease multiple sclerosis (MS). However, little is known about the effects of statins on myelin-forming oligodendrocytes. Here, we show that statins hamper process and myelin formation in vitro by interfering with Ras and Rho signaling in mature oligodendrocytes and provide evidence that statins impair ongoing remyelination in vivo. Our findings may have significant implications for the application of statins in MS patients and in other demyelinating diseases of the CNS.

[olsen]

Biochem Biophys Res Commun. 2004 Apr 16;316(4):1065-72. Links
Curcumin blocks NF-kappaB and the motogenic response in Helicobacter pylori-infected epithelial cells.Foryst-Ludwig A, Neumann M, Schneider-Brachert W, Naumann M.
Institute of Experimental Internal Medicine, Otto-von-Guericke-University, Leipziger Str. 44, Magdeburg 39120, Germany.

Infection of epithelial cells by the microbial pathogen Helicobacter pylori leads to activation of the transcription factor nuclear factor kappaB (NF-kappaB), the induction of pro-inflammatory cytokine/chemokine genes, and the motogenic response (cell scattering). Here we report that H. pylori-induced NF-kappaB activation and the subsequent release of interleukin 8 (IL-8) are inhibited by curcumin (diferuloylmethane), a yellow pigment in turmeric (Curcuma longa L.). Our results demonstrate that curcumin inhibits IkappaBalpha degradation, the activity of IkappaB kinases alpha and beta (IKKalpha and beta), and NF-kappaB DNA-binding. The mitogen-activated protein kinases (MAPK), extracellular signal-regulated kinases 1/2 (ERK1/2) and p38, which are also activated by H. pylori infection, were not inhibited by curcumin. Further, the H. pylori-induced motogenic response was blocked by curcumin. We conclude that curcumin, due to inhibition of NF-kappaB activation and cell scattering, should be considered as a potential therapeutic agent effective against pathogenic processes initiated by H. pylori infection.

PMID: 15044093 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/15044093