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- Cinnamon -

General Information:

Names:
Wikipedia entry:
Dr. Ray Shahelien entry: 

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Observations:

Cinnamon:

See also Tau Busters
         Inflammation

I ran across this rather tantalizing statement in a Web page: "cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed"

The title is "CINNAMON EXTRACT USEFUL FOR INHIBITING THE AGGREGATION
OF TAU AND TREATING ALZHEIMER'S DISEASE" by a researcher at the
University of California, Santa Barbara by the name of Donald Graves
Published on 2/22/2008???
http://www.ibridgenetwork.org/UCSB/cinnamon-extract-useful-for-inhibiting-the-aggregation-of-tau

Here is the first piece of information I found about this:

Cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed

"Researchers at the University of California, Santa Barbara have discovered an extract of common cinnamon that contains a class of small organic molecules that inhibit several key processes in Alzheimer's disease. The cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed, suggesting that neurofibrillary tangles can possibly be reversed by these compounds. The extract exhibits potent inhibitory activity, is orally available, water-soluble, non-toxic, and the bioactive molecules are likely brain permeable. The extract is readily produced in large quantities and can be encapsulated in powder form for oral administration. These properties make the cinnamon extract a highly favorable substance for development into an effective therapeutic to slow or prevent Alzheimer's disease."
http://www.ibridgenetwork.org/innovations/download_tech_brief/3417

I'm amazed that in the whole wide universe of the Internet, there is little mention of this.

What I have found out is that there are several types of "cinnamon", depending on what plant they come from. Look it up on Wikipedia:  http://en.wikipedia.org/wiki/Cinnamon

There is no indication of which species of cinnamon plant was used in the research. Since Chinese cinnamon (cassia, or Cinnamomum aromaticum) is the most common species found in the United States, and the research was done at the University of California in Santa Barbara; it is reasonable to assume that they used cassia cinnamon.

There is some debate about a toxic components of cassia cinnamon, especially coumarin (which apparently isn't present in significant proportions in Ceylon cinnamon). The toxins seem to be present in the lipid (fat) soluble components, but not the water soluble parts. Now, in his previous research publications, Graves was looking at "water soluble" components of cinnamon for controlling sugar metabolism. Perhaps a connections between some recent speculation that Alzheimer's disease is, in some cases, a product of sugar metabolism, in essence a "type III" diabetes; and the possible use of a cinnamon extract to treat AD, may have lead them to examine the effects on tau. This would then be one of those surprise discoveries. So, they were looking at water soluble cinnamon extracts. I take it from reading other web pages on using cinnamon to control diabetes (http://www.mendosa.com/newsletter_april.htm) that the water soluble extracts are relatively easy to separate by "boiling cinnamon in water and pouring off the soluble portion and discarding the solid cinnamon."

(See Patricia's Protcol for more on making a "cinnamon tea"-- extracting the water soluble components of cinnamon.)

Just how much coumarin is in cassia cinnamon?  According to the German government, from "between approximately 2100 and approximately 4400 mg/kg cinnamon powder".  I've found several references on various web sites stating that cassia has a 5% courmarin content.  I think these folks must be mathematically challenged.  There are 1000 grams in a kilogram.  There are 1000 milligrams in a gram.  So, if there are 4400 mg per kg, that is 4400mg per 1000x1000mg or 4400/1,000,000 or 0.44%.  Maximum. So, if you take 1 gram of cassia cinnamon, you get 4.4mg of coumarin. The recommended Tolerable Daily Intake (TDI) established by the European Food Safety Authority is 0.1 milligram per kilogram (kg) of body weight.  There are 2.2 pounds per kilogram.  So, a 120 lb woman would weight about 55 kg.  She would have to eat 1250mg of cassia cinnamon. If this is a problem, use the "aqueous extract". 

The following is from a German government publication, "High daily intakes of cinnamon: Health risk cannot be ruled out" BfR Health Assessment No. 044/2006, 18 August 2006:

When it comes to individual ingredients the coumarin concentration in cassia cinnamon is particularly problematic. The values measured in cinnamon capsules (CVUA Stuttgart) confirm the high coumarin levels in cassia cinnamon (between approximately 2100 and approximately 4400 mg/kg cinnamon powder) as had also been previously measured by CVUA (Münster, BfR 2006). By contrast, coumarin can only be found in traces or below the measurement limit in Ceylon cinnamon.

Depending on the dose recommendation the taking of capsules with cinnamon powder can lead to an exceeding
of the tolerable daily intake of 0.1 milligram coumarin per kilogram body weight that can be ingested daily over a lifetime without posing a risk to health (Tolerable Daily Intake, TDI) established by the European Food Safety Authority (EFSA).
 
The consumption of capsules containing cassia cinnamon powder is also likely to lead to an exceeding of the above-mentioned TDI for coumarin. Solely regarding this coumarin exposure, there are theoretically two steps which could be taken to reduce it:

¤ the replacement of cassia cinnamon by Ceylon cinnamon (so far we do not know whether it has a similar effect on the blood sugar level of diabetics to that of cassia cinnamon; the recommendation of replacement is subject to the assumption that the effects of cassia cinnamon are confirmed by reliable studies),

¤ the use of aqueous extracts of cassia cinnamon which, according to the CVUA analyses in Stuttgart, leads to far lower coumarin exposure (exhaustion of the TDI only in the single-digit percentage range). These extracts probably also have a far lower proportion of essential oils (in particular cinnamaldehyde).

http://www.bfr.bund.de/cm/245/high_daily_intakes_of_cinnamon_health_risk_cannot_be_ruled_out.pdf

[I am highly suspicious of EU regulation and certification, and of that from any individual EU country.  There is a high degree of industrial protectionism in them.  They create artificial barriers to competitors entering a market.  The governments protect their businesses, not only from foreign competitors, but from domestic entrepreneurs.  The "old boys network". People are expected to not disrupt the order of things, and definitely not aspire to attain wealth beyond their class.]

I haven't been able to find much more about this, but as you can imagine, I'm extremely interested. I don't know what the "extract" is, exactly, and if regular old cinnamon has enough of this stuff to do the job.  You would think that, if real, this would be a MAJOR news story.  Yet I found it difficult to even find mention of it.

I want to make it clear that I'm not saying that this WILL work. There haven't been any formal studies done yet.  At least, I haven't been able to find any.  All I've found are reports from people giving it to someone afflicted with AD.  I believe that it MIGHT work; that it is cheap, easy enough and safe enough to try.  You don't have to get government funding, insurance coverage, or a physician to administer it.  If it doesn't work, you are out a small amount of money, time, and someone ate a lot of cinnamon for two months.  But if it does work... Instead of watching your loved one slip away from you a little each day, here you have the chance to DO something more than just watch in frustration.

In the bigger picture are the millions of other people suffering with these tauopathies, and their families who have no idea that there is a spice in their own cupboards that might help.  If this works-- if this water-soluble cinnamon extract actually is able to interrupt the tau protein step of the disease process-- millions of people might find relief from these horrible afflictions.  But they will need to know about it, and they will need to believe in it enough to try it.

On the down side, the price of cinnamon is likely to skyrocket. I wonder if it is possible to buy "cinnamon futures"?  ;)

Another point.  These tauopathies eventually lead to the loss of brain tissue.  Interrupting the disease process will not restore this.  Other compounds or therapies will be needed to do that job, if it is possible.  The information and memories lost with when neurons expire obviously can not be recovered.  The conditions and processes that produced the corrupted tau in the first place will not be affected and will continue to exist.  The best you can hope for is some slight recovery while neurons that are still viable but just inactive come back on line, followed by a period of stabilization.  I would be happy with this.

Update Feb. 25, 2009
I have found more information!  A patent appliation on the World Intellectual Property Organization web site, proves that this idea is real. It was published on October 9, 2008. I still wonder if there is enough of this stuff in raw, ground cinnamon, of whatever species, to help. For now, I can still hope.

For those who doubted...

Title: PROANTHOCYANIDINS FROM CINNAMON AND ITS WATER SOLUBLE EXTRACT INHIBIT TAU AGGREGATION

Abstract: Compositions comprising proanthocyanidin compositions (e.g. those extracted from cinnamomum species) that are observed to bind tau and inhibit its aggregation as well as methods for making and
using such compositions are disclosed. In certain embodiments of the invention, the proanthocyanidins can be used as a probe to identify and/or characterize tau isoforms in a variety of contexts. In other embodiments of the invention, these compositions are used in methods designed to treat neurological disorders associated with tau aggregation (e.g. Alzheimer's disease).

Pub. No.: WO/2008/121412 International Application No.: PCT/US2008/004236
Publication Date: 09.10.2008 International Filing Date: 31.03.2008

IPC: A61K 36/54 (2006.01)
Applicants: THE REGENTS OF THE UNIVERSITY OF CALIFORNIA [US/US]; 1111
Franklin Street, 12th Floor, Oakland, CA 94607 (US) (All Except US).
LEW, John [CA/US]; (US) (US Only).
GRAVES, Donald, J. [US/US]; (US) (US Only).
Inventors: LEW, John; (US).
GRAVES, Donald, J.; (US).
http://www.wipo.int/pctdb/en/wo.jsp?WO=2008121412
http://www.wipo.int/pctdb/en/wo.jsp?WO=2008121412&IA=US2008004236&DISPLAY=DESC

Update November 5, 2009

Cinnamon Extract Inhibits Tau Aggregation Associated with Alzheimer's Disease In Vitro
Journal Journal of Alzheimer's Disease
Publisher IOS Press
ISSN 1387-2877 (Print) 1875-8908 (Online)
Issue Volume 17, Number 3 / 2009
DOI 10.3233/JAD-2009-1083
Pages 585-597
Subject Group Neurosciences
Authors
Dylan W. Peterson¹, Roshni C. George¹, Francesca Scaramozzino¹, Nichole E. LaPointe¹, Richard A. Anderson², Donald J. Graves¹, John Lew^1
1Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA, USA
²Beltsville Human Nutrition Center, Beltsville, MD, USA

Abstract
An aqueous extract of Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer's disease (AD). The extract can also promote complete disassembly of recombinant tau filaments and cause substantial alteration of the morphology of paired-helical filaments isolated from AD brain. Cinnamon extract (CE) was not deleterious to the normal cellular function of tau, namely the assembly of free tubulin into microtubules. An A-linked proanthocyanidin trimer molecule was purified from the extract and shown to contain a significant proportion of the inhibitory activity. Treatment with polyvinylpyrolidone effectively depleted all proanthocyanidins from the extract solution and removed the majority, but not all, of the inhibitory activity. The remainder inhibitory activity could be attributed to cinnamaldehyde. This work shows that compounds endogenous to cinnamon may be beneficial to AD themselves or may guide the discovery of other potential therapeutics if their mechanisms of action can be discerned.
http://iospress.metapress.com/content/06h5g61751404678/
http://www.ncbi.nlm.nih.gov/pubmed/19433898?dopt=Abstract
http://www.diabetesaction.org/site/DocServer/Tau_J_Alzheimers_09.pdf?docID=781

Here is some information on Dr. Richard Anderson:

http://www.sparc.ars.usda.gov/pandp/people/people.htm?personid=144

There is also a commercial water-soluble product available called Cinnulin for those who want to avoid the inconvenience of making the cinnamon tea.  It appears to be made using the process detailed in the above patent application.  This is just for your information and should not be construed as an endorsement of the product.

Study Confirms Cinnulin PF Effectively Increases Insulin Sensitivity in Pre-Diabetes Sufferers
2005-08-10 - Integrity Nutraceuticals International (INI)
...Cinnulin PF, a 20:1 water extract of cinnamon, retains the active components without the potentially harmful compounds, making it completely safe for every day use.  Cinnulin PF is the only cinnamon extract standardized for the recognized active component in cinnamon, double-linked Type-A Polymers...
http://www.npicenter.com/anm/templates/newsATemp.aspx?articleid=13268&zoneid=23

http://www.npicenter.com/images/profile/integ/INI_BloodSugarGotYouDown_8.5x11_4pgs.pdf

INSULIN ENHANCING PRODUCTS FROM CINNAMON
PROJECT DIRECTOR: ANDERSON R A
PERFORMING ORGANIZATION
BELTSVILLE AGR RES CENTER
BELTSVILLE,MD 20705
http://www.reeis.usda.gov/web/crisprojectpages/410118.html

http://www.integritynut.com/products-and-services/cinnulin_pf_

http://www.cinnulin.com/more_info.html

http://www.planetarynutrition.com/Cinnulin_PF_s/233.htm

Cinnamon may also inhibit the effects of TNF-alpha (See Immune System effects and Enbrel for more info.)
Research Project: CHROMIUM AND POLYPHENOLS FROM CINNAMON IN THE PREVENTION AND ALLEVIATION OF GLUCOSE INTOLERANCE

Research Project:  CHROMIUM AND POLYPHENOLS FROM CINNAMON IN THE PREVENTION AND ALLEVIATION OF GLUCOSE INTOLERANCE

Location: Diet, Genomics and Immunology Lab

Title: Tumor Necrosis Factor-alpha Stimulates the Overproduction of Intestinal Apolipoprotein B48-containing Very Low Density Lipoproproteins

Authors
item    Qin, Bolin - ARS RESEARCH ASSOCIATE
item    Khosrowl, Adeli - UNIV OF TORONTO, ONTARIO
item    Anderson, Richard

Research conducted cooperatively with:
item    Integrity Nutraceuticals International

Submitted to: Diabetes
Publication Type: Abstract
Publication Acceptance Date: March 12, 2008
Publication Date: June 10, 2008
Citation: Qin, B., Khosrowl, A., Anderson, R.A. 2008. Tumor Necrosis Factor-alpha Stimulates the Overproduction of Intestinal Apolipoprotein B48-containing Very Low Density Lipoproproteins. Diabetes. 888:102.

Technical Abstract: Tumor necrosis factor-alpha(a)(TNFa), a proinflammatory cytokine, is involved in obesity-associated pathologies including type 2 diabetes and atherosclerosis. TNFa enhanced postprandial apoB48-VLDL1 overproduction by about 89% compared with the control after 90 min olive oil loading; TNFa did not significantly affect apoB-48 VLDL2 expression. In addition, acute oral treatment of Cinnulin PF (a water soluble cinnamon extract, 50 mg per kg BW), which has insulin-like metabolic actions, inhibits TNFa-induced postprandial overproduction of apoB48-containing lipoproteins. Fresh isolated primary enterocytes of hamsters were stimulated with TNFa (10 ng per mL for 4hs), to investigate the expression of insulin signaling pathway genes, insulin receptor (IR), IRS1, IRS2, Akt1, and phosphatidylinositol3-kinase (PI3K), and the key regulators of lipid metabolism, microsomal triglyceride transfer protein(MTP), sterol regulatory element-binding protein (SREBP)1c, and phosphatase and tensin homology (PTEN), as well as the inflammatory factor genes, ILa, ILBeta, IL6, and TNFa. Quantitative real-time PCR assays showed that TNFa decreased IR, IRS1, IRS2, PI3K and Akt1 mRNA levels of enterocytes by 45, 59, 60, 59, and 38%, respectively, of controls. In summary, TNFa stimulates the postprandial apoB-48 VLDL1 overproduction via regulation of mRNA levels of proteins in the intestinal insulin signaling pathway, and perturbs the expression of MTP, PTEN, and SREBP1c, as well as enhances the expression of inflammation factors. Taken together with previous studies, the improvement of insulin sensitivity will inhibit the overproduction of apoB48-containing lipoproteins induced by factors and diets that increase TNFa levels.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=222820

And also...

Location: Diet, Genomics and Immunology Lab (United States Department of Agriculture Agricultural Research Service)

Project Number: 1235-51520-037-00
Project Type: Appropriated

Start Date: Nov 18, 2004
End Date: Jan 22, 2009

Objective:
Overall objective of the proposed research is to help control the incidence of impaired glucose metabolism and decrease the conversion of glucose intolerance to diabetes. Specific objectives include the following. 1)Elucidate the role of Cr in the onset of impaired glucose metabolism using a stress-induced rat model for Cr deficiency. 2)Determine methods to assess Cr status and elucidate its functions in human nutrition. 3)Define the role and mechanistic effects of insulin potentiating polyphenols from cinnamon on intracellular signals that regulate insulin-induced glucose uptake and oxidative stress.

Approach:
Compounds that enhance insulin activity lead to a more sensitive response to insulin and improve glucose tolerance. Increased levels of stress lead to loss of nutrients including chromium (Cr), a nutrient that is involved in glucose and insulin metabolism. We propose to elucidate the role of Cr in a stress-induced diabetes rat model. Steroid-induced diabetes in people taking steroids such as prednisone has been shown to be reversed by increased intake of chromium. This project is designed to elucidate the role of the chronic stress of low level administration of the steroid, dexamethasone, in the augmentation of deficiency of chromium. These studies will facilitate our collaborative human study to elucidate the roles of Cr in human nutrition and also methods to assess Cr status. There are currently no reliable methods to assess Cr status. This study will combine reliable analytical measures of chromium status with studies to elucidate the function of chromium in human nutrition. We also propose to define the role and mechanistic effects of insulin potentiating polyphenols from cinnamon on intracellular signals that regulate insulin-induced glucose uptake, oxidative stress and NF-'B activation. These studies should lead to a greater understanding of the roles of chromium and polyphenols from cinnamon in the prevention and alleviation of glucose intolerance and type 2 diabetes.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408448

Update July 30, 2010
There has been some reports on the Alz.org message board that whole cinnamon has been more effective than the water-soluble extract.  Most people have been opting to use Ceylon cinnamon rather than the cheaper and more readily available cassia (Chinese) cinnamon because Ceylon cinnamon contains less of the blood-thinning chemical coumarin.  This allows people to take more of it-- say 1 tsp three times per day-- without being concerned with the buildup of coumarin.

See Inflammation/Infection

Comparison of bacteriostatic and bactericidal activity of 13 essential oils against strains with varying sensitivity to antibiotics

22 AUG 2008

Letters in Applied Microbiology
Volume 47, Issue 3, pages 167–173, September 2008

Abstract

Aims: To compare the bacteriostatic and bactericidal activity of 13 chemotyped essential oils (EO) on 65 bacteria with varying sensitivity to antibiotics.

Methods and Results:

Fifty-five bacterial strains were tested with two methods used for evaluation of antimicrobial activity (CLSI recommendations): the agar dilution method and the time-killing curve method.

EO containing aldehydes (Cinnamomum verum bark and Cymbopogon citratus), phenols (Origanum compactum, Trachyspermum ammi, Thymus satureioides, Eugenia caryophyllus and Cinnamomum verum leaf) showed the highest antimicrobial activity with minimum inhibitory concentration (MIC) <2% (v/v) against all strains except Pseudomonas aeruginosa.

Alcohol-based EO (Melaleuca alternifolia, Cymbopogon martinii and Lavandula angustifolia) exhibited varying degrees of activity depending on Gram status.

EO containing 1·8-cineole and hydrocarbons (Eucalyptus globulus, Melaleuca cajeputii and Citrus sinensis) had MIC90% ≥ 10% (v/v). Against P. aeruginosa, only C. verum bark and O. compactum presented MIC ≤2% (v/v).

Cinnamomum verum bark, O. compactum, T. satureioides, C. verum leaf and M. alternifolia were bactericidal against Staphylococcus aureus and Escherichia coli at concentrations ranging from to 0·31% to 10% (v/v) after 1 h of contact. Cinnamomum verum bark and O. compactum were bactericidal against P. aeruginosa within 5 min at concentrations <2% (v/v).

Conclusions: Cinnamomum verum [Ceylon cinnamon] bark had the highest antimicrobial activity, particularly against resistant strains.
http://onlinelibrary.wiley.com/doi/10.1111/j.1472-765X.2008.02406.x/full

Alzheimer's Prevention in Your Pantry
ScienceDaily (June 27, 2011)
>...An extract found in cinnamon bark, called CEppt, contains properties that can inhibit the development of [Alzheimer's] disease, according to Prof. Michael Ovadia of the Department of Zoology at Tel Aviv University. His research, conducted in collaboration with Prof. Ehud Gazit, Prof. Daniel Segal and Dr. Dan Frenkel, was recently published in the journal PLoS ONE...
http://www.sciencedaily.com/releases/2011/06/110627123144.htm

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Known sources:
    Ceylon Cinnamon:  Penzey's Spices in Brookfield, WI

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Natural sources:

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References:

Cinnamon:

CINNAMON EXTRACT USEFUL FOR INHIBITING THE AGGREGATION OF TAU AND TREATING ALZHEIMER'S DISEASE
by Donald Graves, University of California, Santa Barbara
Published on 2/22/2008???
http://www.ibridgenetwork.org/UCSB/cinnamon-extract-useful-for-inhibiting-the-aggregation-of-tau


"Researchers at the University of California, Santa Barbara have discovered an extract of common cinnamon that contains a class of small organic molecules that inhibit several key processes in Alzheimer's disease. The cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed, suggesting that neurofibrillary tangles can possibly be reversed by these compounds. The extract exhibits potent inhibitory activity, is orally available, water-soluble, non-toxic, and the bioactive molecules are likely brain permeable. The extract is readily produced in large quantities and can be encapsulated in powder form for oral administration. These properties make the cinnamon extract a highly favorable substance for development into an effective therapeutic to slow or prevent Alzheimer's disease."
http://www.ibridgenetwork.org/innovations/download_tech_brief/3417


PROANTHOCYANIDINS FROM CINNAMON AND ITS WATER SOLUBLE EXTRACT INHIBIT TAU AGGREGATION

Abstract: Compositions comprising proanthocyanidin compositions (e.g. those extracted from cinnamomum species) that are observed to bind tau and inhibit its aggregation as well as methods for making and
using such compositions are disclosed. In certain embodiments of the invention, the proanthocyanidins can be used as a probe to identify and/or characterize tau isoforms in a variety of contexts. In other embodiments of the invention, these compositions are used in methods designed to treat neurological disorders associated with tau aggregation (e.g. Alzheimer's disease).

Pub. No.: WO/2008/121412 International Application No.: PCT/US2008/004236
Publication Date: 09.10.2008 International Filing Date: 31.03.2008

IPC: A61K 36/54 (2006.01)
Applicants: THE REGENTS OF THE UNIVERSITY OF CALIFORNIA [US/US]; 1111
Franklin Street, 12th Floor, Oakland, CA 94607 (US) (All Except US).
LEW, John [CA/US]; (US) (US Only).
GRAVES, Donald, J. [US/US]; (US) (US Only).
Inventors: LEW, John; (US).
GRAVES, Donald, J.; (US).
http://www.wipo.int/pctdb/en/wo.jsp?WO=2008121412
http://www.wipo.int/pctdb/en/wo.jsp?WO=2008121412&IA=US2008004236&DISPLAY=DESC

Cinnamon Extract Inhibits Tau Aggregation Associated with Alzheimer's Disease In Vitro
Journal Journal of Alzheimer's Disease
Publisher IOS Press
ISSN 1387-2877 (Print) 1875-8908 (Online)
Issue Volume 17, Number 3 / 2009
DOI 10.3233/JAD-2009-1083
Pages 585-597
Subject Group Neurosciences
Authors
Dylan W. Peterson¹, Roshni C. George¹, Francesca Scaramozzino¹, Nichole E. LaPointe¹, Richard A. Anderson², Donald J. Graves¹, John Lew^1
1Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA, USA
²Beltsville Human Nutrition Center, Beltsville, MD, USA

Abstract
An aqueous extract of Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer's disease (AD). The extract can also promote complete disassembly of recombinant tau filaments and cause substantial alteration of the morphology of paired-helical filaments isolated from AD brain. Cinnamon extract (CE) was not deleterious to the normal cellular function of tau, namely the assembly of free tubulin into microtubules. An A-linked proanthocyanidin trimer molecule was purified from the extract and shown to contain a significant proportion of the inhibitory activity. Treatment with polyvinylpyrolidone effectively depleted all proanthocyanidins from the extract solution and removed the majority, but not all, of the inhibitory activity. The remainder inhibitory activity could be attributed to cinnamaldehyde. This work shows that compounds endogenous to cinnamon may be beneficial to AD themselves or may guide the discovery of other potential therapeutics if their mechanisms of action can be discerned.
http://iospress.metapress.com/content/06h5g61751404678/
http://www.ncbi.nlm.nih.gov/pubmed/19433898?dopt=Abstract

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Updated: July 2, 2012
Inception: July 2, 2012