I have nothing to sell you but hope, and that I give you for free.

The purpose of this web site is to provide you with information for when you meet with a physician to discuss what can be done for someone suffering from brain failure.  You will have a list of questions to ask, and sources to read so that you can ask them intelligently.  I want to share some of the information I've accumulated in my search to help my mother.

Synthetic pharmaceuticals and physician supervised treatment is certainly the preferred course of action to help the brain failure sufferer.  But while you wait for the physicians (who may have treatments) to get off of their duffs and actually try something, here are two substances you can try.  The research papers indicate that this may be the closest you will get to a cure in that these two substances interrupt key steps in the disease process.  Pharmaceutical versions, if and when they ever develop them, should be stronger and more effective:

Nutritional Alternative Treatment Protocol for Tauopathies:
[...such as Alzheimer's disease, Progressive Supranuclear Palsy (PSP), Frontotemporal Dementia (FTD), Corticobasal Degeneration (CBD, corticobasal ganglionic degeneration, CBGD, corticobasal syndrome, CBS), etc]  Tauopathy Discussion Forum

[NOTE:  2009 10 29 This list is very much out of date.  We've added MCT oils, niacinamide, and some other supplements...]
[Update: 2011 09 19 Alzheimer's disease and therefore CBS-AD may be caused by spirochete bacterial infection.  See The Role of Infection and Inflammation in Neurodegenerative Diseases for more information on this topic, and more importantly, what you can do about it.]

Patricia's Protocol:

Cinnamon:          1000mg three times per day, for the first 6 weeks, then twice
                   per day thereafter for maintainance.  Cinnamon in capsules form
                   prevents the degradation of the cinnamon by saliva.
                   If the person can't swallow capsules, it may be possible
                   to substitute 1/2 tsp of ground cinnamon in food for the 1000mg
                   capsules.  However, degradation of the cinnamon by saliva may
                   make this method less effective. 1/2 cup of "cinnamon tea" two
                   or three times per day should also be considered.
                   Target:  Inhibition of tau protein aggregations, disassemble
                   aggregations that have already formed.

Curcumin:          300-500mg 2 to 3 times per day, at least 8 hours apart, if
                   possible.
                   Targetting amyloid beta and "oxidative stress" from iron and
                   copper  (~12mg/lb of body weight)

Lithium???         60mg lithium orotate per day (1/2 of a 120mg tablet)  [????]

Methylene Blue???  1 drop (using an eye dropper) of 2.303% methylene blue solution
                   to every two cups of the cinnamon tea

1)  Cinnamon  University of California, Santa Barbara researcher Donald Graves reports
    finding an "extract of cinnamon" that "inhibits the aggregation of tau and
    disassembles fibers that have already formed".  Subtle improvements should be
    noticed in 4 to 6 weeks.  If after 8 weeks no improvements are noticed, then it
    probably isn't going to work.  There may be enzymes in saliva that degrade
    the active components of cinnamon.
    See the last paragraph of: "Cinnamon, Cloves Improve Insulin Function, Lower Risk
    Factors For Diabetes, Cardiovascular Disease"
    http://www.medicalnewstoday.com/articles/41026.php
    Note:  Cinnamon, especially whole cinnamon, may have components that cause unwanted
           side effects, and may interact with prescription medications.  Do not consume
           excessive ammounts.
    (See below for more information.)

2)  Curcumin (extract of the curry spice turmeric)
    In studies done with transgenic mice, curcumin "disaggregated" the amyloid-β
    plaques that have been proven to cause the symptoms of Alzheimer's disease.
    Curcumin is also an iron and copper chelator.
    Note:  Curcumin may adversely augment the effects of prescription blood thinners,
           and may interfere with certain chemotherapy agents.
    (See below for more information.)

These things are not likely to cure a tauopathy.  They only interrupt key steps in the disease process.  The memories contained in brain tissue lost due to the disease can not be restored.  However, as the disease progresses, neurons first become dormant before finally expiring.  If the tau protein problem is interrupted, those neurons that are dormant, but still viable may be restored, resulting in some degree of recovery.  Also, whatever the biochemical process is that caused the tau proteins to become corrupted in the first place is still present.  It is possible that this process may at some point in time overwhelm any substance that keeps the tau problem in check.  So far, this "protocol" has been effective since April 29, 2008.

I mentioned before that my mother is suffering from some sort of dementia.  At first we were told she had had a stroke, then they said Alzheimer's disease, then they tested her for normal pressure hydrocephalus, and then finally, in December of last year, a neurologist, a "movement disorder" specialist, diagnosed her (from symptoms!) as having corticobasal ganglionic degeneration (CBD or CBGD).  This is a bad one.  It apparently is a tauopathy, similar in some respects to progressive supranuclear palsy (PSP).  It robs people of the ability to control their bodies, and to speak, but apparently leaves their memory and "higher functions" intact.  So, I started searching the Internet for research on tau protein.  I found these two very interesting developments.  First is that the old drug used to treat bipolar disorder, lithium, has been proven to increase brain mass, slow or even halt the progression of amyotrophic lateral sclerosis, and prevent the hyperphosphorylation of the tau protein.  However, lithium may have some negative side effects in older people, so this option would best be explored with the help of a physician knowledgeable in using it.  The second was that a "cinnamon extract" can actually untangle tau fibers that have already formed!

************
Cinnamon

A key step in the disease process of several neurodegenerative diseases is the corruption of the tau protein.  These molecules normally form part of a intracellular transport system that neurons use to transfer necessary molecules in, and waste products out.  I think of it as a "smart conveyor belt".  Some biochemical process goes haywire, and the tau gets corrupted.  It then twists together to form useless and destructive "fibers" and/or clumps.

A professor of molecular biology at the University of California, Dr. Donald J. Graves, has lead a team that has identified a component of common cinnamon (most likely cassia cinnamon) that will prevent this tau from aggregating, and will in addition disassemble aggregations that have already formed!  It is non-toxic, easily produced in large quantities, and most likely brain permeable (most substances can't get past the chemical barrier of the brains blood supply network). This makes it a good candidate for treating diseases with a corrupted tau protein component.

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

"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

Donald Graves is an adjunct professor of Molecular, Cellular and Developmental Biology at the University of California, Santa Barbara.  He retired from Iowa State University in October 2000.  He divides his time between UCSB and the Sansum Institute.
http://www.ia.ucsb.edu/pa/display.aspx?PKey=1123

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 (which apparently isn't present 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."

Following the trail of using cinnamon to control diabetes, I found this:

Here's the "Cinmamon Tea" recipe:

..... RECIPE .....
Glucose-Lowering Cinnamon Tea Excerpted from
Diabetes: Prevention and Cure,
by C. Leigh Broadhurst, PhD,
Kensington Books, New York, 1999, pp. 192-193

"In the laboratory where I work at the US Department of Agriculture, we have investigated over 60 plant extracts in a special cell culture test that determines how much a particular compound stimulates the uptake and utilization of glucose. While these tests are no substitute for human or animal studies, they are important because they identify safe compounds that act directly on cell metabolism. Plenty of plants
and individual phytochemicals can lower blood sugar, but many accomplish this by imposing toxic effects on the body. Cinnamon was by far the most active compound in our assay, so we focused on it.

"From an extract of commercial cinnamon, we identified new phytochemicals called chalcone polymers that increase glucose metabolism in the cells twentyfold or more. In addition, cinnamon contains anthocyanins of the type thought to improve capillary function, and an extract similar to ours has been shown to inhibit the formation of ulcers and increase blood flow to the stomach in rats. As chalcone polymers strongly inhibit the formation of reactive oxygen species in activated blood platelets, we also know them as antioxidants. A number of antioxidant phytochemicals have already been identified in cinnamon, so that cinnamon may have all three of the beneficial actions mentioned previously.

"Since the first published results that identify cinnamon as a potential therapy for diabetes, we have heard from hundreds of people who found that it works. Since cinnamon is very safe, there is little harm in trying it yourself.

"To use cinnamon to help lower blood sugar and broadly improve Types I and II diabetes, put 3 rounded tablespoons of ground cinnamon and 1/2 to 1 teaspoon of baking soda (use a lesser amount if sodium is a problem for you) in a 32-ounce (quart) canning jar. Fill the jar with boiling water and let steep at room temperature until cool. Strain or decant the liquid and discard the grounds, and then put a lid on the jar and refrigerate. Drink 1 cup (8 ounces) of the tea 4 times per day. After 1-3 weeks, drop to 1-2 cups per day or use as needed. For those with Type I diabetes, start with only 1-2 cups per day and increase by 1 cup per week, monitoring blood sugar closely. Buying cinnamon in bulk is cost-effective and highly recommended...."
http://www.geocities.com/diabetips/cinna.html

This page also describes some challenges in finding a good quality cinnamon to start with. Keep in mind that this information is tailored to those battling diabetes.

"As for the baking soda, it should make MHCP more soluble in water. Baking soda is sodium bicarbonate, which is a weak base. MHCP is a phenolic compound and therefore slightly acidic. Acids are most soluble in bases (and vice versa), meaning that MHCP is more soluble in a baking soda solution than in pure water."
http://forum.lowcarber.org/archive/index.php/t-151040.html

++++++++++++++++++++++++++++++++++
Cinnamon Tea Recipe & Procedure
++++++++++++++++++++++++++++++++++

Also, check out:

Mary McKinlay's blog "MY JOURNEY WITH ALZHEIMERS OR FRONTOTEMPORAL DEMENTIA"
http://www.simplesite.com/MotherMary/2926947
(Check out her Thursday, March 27, 2008 posting for her report on her two week experiment (so far) with cinnamon.)

Alzheimer’s Association Online Community forum: "Cinnamon really Helps!!!!"
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/6821006162

++++

NOTE:
There has been a lot of excitement recently over a new Alzheimer's disease drug from the UK derived from methylene blue called Rember.  But it seems that it targets EXACTLY the same step in the disease process as the "water-soluble cinnamon extract" does:

Rember:  "The drug works by dissolving the tangle of tau fibres which releases waste products that kill nerve cells, and by preventing the fibres from becoming tangled."
http://www.dailymail.co.uk/health/article-1039677/Daily-pill-halts-Alzheimers-hailed-biggest-breakthrough-disease-100-years.html
http://www.msnbc.msn.com/id/25918231
http://www.telegraph.co.uk/news/uknews/2471076/Alzheimerandrsquos-sufferers-given-hope-by-new-generation-of-drugs.html
Cost/Availability:  Unobtainable for the next couple of years

Cinnamon:  "The cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed..."
Cost/Availability:  $8 per month in capsule form from Target, Walmart, etc., less if in powder form from a grocery store.
http://www.ibridgenetwork.org/innovations/download_tech_brief/3417

The really sad thing is that so few people know that they may be able to halt the progression of a tauopathy with a common spice found in most grocery stores.

However, the Rember study does demonstrate that interrupting the tau protein corruption step does in fact arrest the progression of a tauopathy, or at least slow it dramatically.

**************
Curcumin

Curcumin Inhibits Formation of Amyloid {beta} Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo
J. Biol. Chem., Vol. 280, Issue 7, 5892-5901, February 18, 2005

"Alzheimer's disease (AD) involves amyloid {beta} (A{beta}) accumulation, oxidative damage, and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation. Since the molecular structure of curcumin suggested potential A{beta} binding, we investigated whether its efficacy in AD models could be explained by effects on A{beta} aggregation... When fed to aged Tg2576 mice with advanced amyloid accumulation, curcumin labeled plaques and reduced amyloid levels and plaque burden. Hence, curcumin directly binds small {beta}-amyloid species to block aggregation and fibril formation in vitro and in vivo. These data suggest that low dose curcumin effectively disaggregates A{beta} as well as prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or treating AD."
http://www.jbc.org/cgi/content/full/280/7/5892


Curcumin stimulates proliferation of embryonic neural progenitor cells and neurogenesis in the adult hippocampus.
Kim SJ, Son TG, Park HR, Park M, Kim MS, Kim HS, Chung HY, Mattson MP, Lee J.
Pharmacy, Pusan National University, Busan 609-735.

"Curcumin is a natural phenolic component of yellow curry spice, which is used in some cultures for the treatment of diseases associated with oxidative stress and inflammation. Curcumin has been reported capable of preventing the death of neurons in animal models of neurodegenerative disorders, but its possible effects on developmental and adult neuroplasticity are unknown. In the present study, we investigated the effects of curcumin on mouse multi-potent neural progenitor cells (NPC) and adult hippocampal neurogenesis. Curcumin exerted biphasic effects on cultured NPC - low concentrations stimulated cell proliferation, whereas high concentrations were cytotoxic. Curcumin activated extracellular signal regulated kinases (ERKs) and p38 kinases, cellular signal transduction pathways known to be involved in the regulation of neuronal plasticity and stress responses. Inhibitors of ERKs and p38 kinases effectively blocked the mitogenic effect of curcumin in NPC. Administration of curcumin to adult mice resulted in a significant increase in the number of newly-generated cells in the dentate gyrus of hippocampus, indicating that curcumin enhances adult hippocampal neurogenesis. Our findings suggest that curcumin can stimulate developmental and adult hippocampal neurogenesis, a biological activity that may enhance neural plasticity and repair."

PMID: 18362141 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/18362141?dopt=Abstract


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If you don't try, there is no way in the world you will succeed.

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Updated: October 29, 2009
Inception: April 30, 2008