Stem Cell Transplantation Shows Promise for PARKINSON’S DISEASE

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Many studies going back many years have investigated the possibility of creating neural stem cells in the lab and transplanting them to regions of the brain damaged by PARKINSON’S DISEASE.  Usually, these studies have been done using mouse models of PD and have involved heavy uses of immunosuppression.  Some studies have used cells obtained from the transplanted mouse itself, but results have rarely shown any benefit and are very difficult to duplicate.

Now, a researcher at Kyoto University’s Center for IPS Cell Research and Application in Japan has experimentally shown that cells derived from the subject’s own body produced almost no immune response when transplanted into the brains of monkeys and actually resulted in viable neural cells.  Doctors Jun Takahashi and Asuka Morizane are interested in promoting new neural pathways to restore dopaminergic cell function in the hope that this approach will help people with PARKINSON’S DISEASE.

When cells are obtained from the subject’s own body, they are called autologus.  Cells derived from other sources are called allergenic and evoke a very strong rejection response from the subject that receives them.  Autologus transplants are generally better tolerated especially in those with Parkinson’s disease.  This study used cells derived from the blood of the donor/subject and grew them into induced pluripotent stem cells (iPSC), which were then differentiated into dopaminergic neural cells.  These same cells were then transplanted back to the monkeys’ brain.  The monkeys were observed for three months and not given any immunosuppressant drugs.   No rejection response was seen and the cells became viable, functioning dopaminergic cells in their new location.

This is a radical approach that shows promise, however much more research will be necessary before it can be translated to human applications.

Credits:

“A direct Comparison of Autologus and Allergenic Transplantation of iPSC-Derived Neural Cells in the Brain of a Nonhuman Primate” Stem Cell Reports, 2013. dx.doi.org/10.1016/j.stemcr.2013.08.007

Blood Bio-Marker Found for Cognitive Impairment in Parkinson’s Disease

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Blood Bio-Marker Found for Cognitive Impairment in Parkinson’s Disease  “There currently is no cure for PARKINSON’S, but the earlier we catch it–the better chance we have to fight it,” says Michelle Mielke, Ph.D.

 

Dr. Mielke is a researcher at the Mayo Clinic in Rochester, Minnesota.  She is studying blood based bio-markers for PARKINSON’S DISEASE, as a simpler, less expensive , less invasive technique for diagnosing this disease than brain scans or spinal taps which are sometimes used.  (A “blood bio-marker” test uses a protein in the blood or urine as a marker for what is going on inside the body. The best known biomarker test is a home pregnancy test which works on the same principle.*)

Her laboratory has found a specific but very rare genetic mutation that can lead to early onset PARKINSON’S DISEASE cognitive impairments.  This occurs in only 4 to 7 per cent of PARKINSON’S DISEASE patients. The mutation is called GBA and it is a marker of lipids in the blood.  This mutation causes lipids, ceramides and glucosylceramides to be incorrectly metabolized.  They found that people with PARKINSON’S DISEASE who have higher levels of lipids in their blood are more at risk for developing dementias or cognitive impairments.

Cognitive impairments in PARKIINSON’S DISEASE together with the other symptoms of PARKINSON’S DISEASE are very challenging for both the patients and their caregivers.  If a blood bio-marker such as this can help diagnose patients who are at greater risk earlier, it might lead to a treatment to slow the progression or reverse some of the damage.

About Dr. Mielke

The principal research interests of Michelle M. Mielke, Ph.D., are to further the understanding of the epidemiology of neurodegenerative diseases and psychiatric disorders.

A primary focus of Dr. Mielke’s research is the identification of biomarkers for the diagnosis, prediction and/or progression of Alzheimer’s disease, as well as other neurodegenerative and neuropsychiatric conditions.

Much of her work has emphasized both lipid markers — particularly sphingolipids (ceramides and sphingomyelins) — and neuroimaging markers.

 

Credits:

* http://abcnews.go.com/Health/Technology/story?id=118256&page=1

http://www.mayo.edu/research/faculty/mielke-michelle-m-ph-d/BIO-00055128

Photo credit: http://www.siemens.com/innovation/en/publikationen/publications_pof/pof_fall_2008/frueherkennung/biomarker.htm

Medications for the Management of Parkinson’s Disease Part 2 – Agonists

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Medications for the Management of Parkinson’s disease Part 2 – Agonists

 

The second “miracle drug” for PARKINSON’S DISEASE  are the dopamine agonists.  Agonists work by making the receptor neurons think they are getting enough dopamine and by keeping available dopamine in the synapse between neurons a little longer.  In the early stages of PARKINSON’S DISEASE , use of agonists alone may be beneficial, but as the disease progresses, they are not as useful alone as they are together with carbi/levodopa.  Agonists can be helpful in managing fluctuations in symptoms from carbi/levodopa treatments.  There are side effects, and they can exacerbate the side effects of the other medications. Some of the more serious side effects have been with impulse control.  Problems such as gambling, impulsive shopping and hyper sexuality have been blamed on these medications.  Excessive sleepiness has also been reported.  It takes an experienced, PARKINSON’S DISEASE  trained neurologist to “fine tune” dosage and timing of all the PARKINSON’S DISEASE  medications.  Dosage of agonists should be started low and built up; if symptoms warrant a withdrawal from agonists, they must be decreased slowly.  The most common agonists are pramipexole (Mirapex) and ropinerole (Requip).  Long acting versions of both are also available as Mirapex ER and Requip XL.

Several other pharmaceutical products have become available for treatment of PARKINSON’S DISEASE .  While they are not the mainstream medications, they can be very, very useful in certain situations.  A fast dissolving form of carbi/levodopa is available for situations when it would take too long for a regular pill to be effective.  This is Parcopa, and it is now available as a generic.  Another “rescue drug” is apomorphine (Apokyn)  This is an injectable drug, and a patient or a caregiver has to be trained to give the injection.  This is a short acting drug, in the agonist class, but if someone suffers from sudden “off” periods, this can get them going again very quickly.  It does cause nausea, so anti-nausea agents must be taken at the same time.

The rotigotine transdermal patch (Neupro) was hailed as another “miracle” when it first came out.  It delivered a steady dose of medication which was easily and readily absorbed through the skin.  Patients were thrilled to wear a patch instead of taking a regimen of drugs.  And it was effective for many of them, but it had problems, particularlly with the adhesive and the FDA forced it to be recalled from the market for several years.  It is now back.  It is in the agonist class, and while it is very useful, it  too, has side effects, some of which can be quite serious.  Sensitivity to sulfites is one drawback, but among people with PARKINSON’S DISEASE  this is not a common issue.  Drowsiness, nausea and the other side effects noted for drugs in the agonist class apply to this one, too.  Skin irritations can develop from either the ingredients or the adhesive in the patch and care must be taken not to expose the patch to either heat or water.  It comes in various doses.

If PARKINSON’S DISEASE  were the only disease a person needed treatment for, it would still be a very complex matter.  But because PARKINSON’S DISEASE  usually starts later in life, there probably are some other medical issues to consider, complicating the situation even further.  Seeking the advice of a neurologist who is both trained and experienced in movement disorders and especially in PARKINSON’S DISEASE  is essential.  The attention of a caring and dedicated primary care physician is also a high priority, especially if multiple medications for multiple medical issues are involved.  A good primary care physician can treat infections which  cause a person with PARKINSON’S DISEASE  extra distress and disrupt the benefit of the PARKINSON’S DISEASE  meds as well as oversee all the combinations of medications a person is taking to avoid serious drug interactions.

Although there is no cure for Parkinson’s disease, the symptomatic treatments that are available today are able to improve the quality of life and reduce the symptoms better than at any time in the past.  Of course, research is ongoing, new drugs will come along and perhaps that elusive cure will be found.  Living one’s life to the fullest and living well with PARKINSON’S DISEASE  can be possible with the help of a good neurologist and modern medications.

Side Effects

Mirapex

For a full list please see the information at:

http://www.drugs.com/sfx/mirapex-side-effects.html

Applies to pramipexole: oral tablet, oral tablet extended release

Along with its needed effects, pramipexole (the active ingredient contained in Mirapex) may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

Check with your doctor immediately if any of the following side effects occur while taking pramipexole:

More common

  • Dizziness, lightheadedness, or fainting, especially when standing up
  • drowsiness
  • hallucinations (seeing, hearing, or feeling things that are not there)
  • nausea
  • trouble with sleeping
  • twitching, twisting, or other unusual body movements
  • unusual tiredness or weakness

Some side effects of pramipexole may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:

More common

  • Constipation
  • dryness of the mouth
  • headache
  • heartburn, indigestion, or acid stomach

Less common

  • Abnormal dreams
  • decreased sexual drive or ability
  • general feeling of discomfort or illness
  • increased cough
  • increased sweating
  • itching
  • joint pain
  • loss of appetite
  • runny nose
  • skin problems, such as rash or itching weight loss

Requip

For complete information please see: http://www.drugs.com/requip.html

Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have any of these serious side effects:

  • feeling like you might pass out;
  • fever, stiff muscles, confusion, sweating, fast or uneven heartbeats (especially if you stop taking Requip or use a lower dose);
  • hallucinations;
  • tremors (uncontrolled shaking); or
  • tight feeling in your chest, trouble breathing.

Call your doctor promptly if you fall asleep during a daily activity, if you faint, or if you have hallucinations (hearing or seeing something that is not there). Your doctor may want you to stop taking Requip, or take a lower dose.

Less serious Requip side effects may occur, such as:

  • mild nausea, vomiting, stomach pain, or loss of appetite;
  • worsened RLS symptoms early in the morning;
  • diarrhea or constipation;
  • dry mouth, sweating;
  • headache;
  • dizziness, drowsiness;
  • sleep problems (insomnia); or
  • agitation or anxiety.

This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

See also: Requip side effects (in more detail) 

Medications for the Management of Parkinson’s disease Part 1

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Carbidopa/Levodopa, that miracle drug for the treatment of Parkinson’s disease has only been in use a little over 60 years. In that time frame, research has accelerated, more knowledge of the brain has been revealed and more drugs have been added to the arsenal for fighting the symptoms of Parkinson’s disease. This article will look at the classes of drugs commonly used. It is not intended to replace the advice of your neurologist or physician. Parkinson’s disease is a very complex disease, and no two people with Parkinson’s manifest the symptoms in the same way. Treatments must be tailored to the individual, and only a Parkinson’s disease specialist can effectively determine what is best.

Before carbidopa/levodopa came on the scene, treatment often consisted of anticholinergic drugs. Anticholinergic drugs block the activity of the neurotransmitter acetylcholine which is involved in memory and control of movement; it has no affect on the dopamine systems in the brain. This class of drug is rarely used today because there are more effective ways to treat PARKINSON’S DISEASE now available. In some cases, particularly in people with severe dystonias that develop from periods when their usual medications fail to work, anticholinergic medications may help. One of the main side-effects of this class of drug is mental “fogginess”, problems with memory as well as dry mouth, constipation and blurred vision. The pharmacological name for this medication is trihexiphenidyl (Artane).

MAO-B or monoamine oxidase inhibitor B, is also used early in the treatment of PARKINSON’S DISEASE . It has only a rather limited effect on PARKINSON’S DISEASE symptoms, however, if used very early in the diagnosis, it can delay the need for carbidopa/levodopa medications. Sometimes it can be added later in the course of the disease to enhance the effect of levodopa. Basically, this drug works by breaking down the levodopa in the brain and making it more available to weakened neurons. It too has side effects; it may cause dizziness and low blood pressure, indigestion, nausea and headaches. Some of the drugs in this class may provide some neuroprotection, and studies are on-going, however there has not been any really conclusive evidence . Rasagiline (Azilect) and seligiline or deprenyl (Eldepryl or Zelapar) are the pharmaceutical and trade names for this medication.

Carbidopa/levodopa is the “gold standard” of treatment for symptoms of PARKINSON’S DISEASE . It has been around only since the 1960s, but has made a world of difference in patients’ lives. It is the most effective treatment available but it has also has generated a lot of discussion, both pro and con. There were concerns about extended levodopa replacement becoming toxic, however research has not found that to be true. Other issues revolved about the best time to introduce it into the treatment program. There have been arguments that beginning treatment with carbi/levodopa too early in the course of the disease will limit the length of time its benefits are effective without causing serious side effects. The other side thinks that delaying the introduction of carbi/levodopa lowers the quality of life of the patient and leaves them vulnerable to other aspects of the disease. Most neurologists favor an earlier start, but there are some modifying factors.

Carbidopa/levodopa is available in many different combinations. Dosing strategies have to be carefully worked out in collaboration with the neurologist in order to avoid serious side effects and to obtain maximum benefit. This is not a medication where one size fits all! It is possible that more than one form of this medication may be used at different times of the day, so people who are taking this need to be very aware of which pill is taken at what time; and timing is equally as important as the pill. The formulations come in different shapes and colors, but careful vigilance is still necessary. Perhaps the oversight of a caregiver can be enlisted.

The first “miracle” was carbidopa/levodopa, introduced as “Sinemet”. The small amount of carbidopa listed first in the fraction, was added to reduce the nausea that levodopa can cause. The medical terminology “sin = without” and “emesis = nausea” became the clever name for this drug. A bit later, scientists figured out a way to make a controlled release form of this medication, one that would dissolve slowly over time and eliminate taking so many shorter acting pills. This was called Sinemet-CR. Carbidopa/levodopa does have side effects such as low blood pressure, dizziness, dry mouth and sometimes nausea.

What are the Common Side Effects?
Sinenet (Carbidopa/Levidopa)

  • Nausea
  • Vomiting
  • Loss of appetite
  • Lightheadedness
  • Lowered blood pressure
  • Confusion
  • Dyskinesia (if used as a long-term therapy; between 3-5 years)
  • People who use levodopa longterm may experience dyskinesia at some point, usually three to five years after starting the medication.
  • The term dyskinesia describes involuntary, erratic, writhing movements of the face, arms, legs, and/or trunk, which usually occur one to two hours after a dose of levodopa has been absorbed into the bloodstream and is having its peak clinical effect.

Eating Proteins with Levodopa/Sinemet*

  • It is best to take Sinemet 30 to 60 minutes before eating a meal. This allows the Sinemet to be quickly absorbed before the food can interfere.
  • Take the Sinemet along with foods that don’t contain proteins.
  • Ginger tea is a good choice for many people, because it often “settles the stomach”.
  • A graham cracker or soda cracker along with the ginger tea may help too. These foods are very low in protein and should not interfere with the absorption of Sinemet.

COMT Inhibitors

In the mean time, science found that adding another medication to the regimen kept the dopamine active in the brain, prolonging its effect and preventing “wearing off”. This was the addition of a COMT inhibitor. COMT is Catechol-O-Methyl Transferase and it was pharmaceutically known as entacapone (Comtan) or tolcapone (Tasmar). Both prescriptions were given together. This medication, too, must be carefully monitored. Anyone taking Tolcapone (Tasmar) must have regular blood tests to check liver function. COMT can also increase the side effects of carbi/levodopa and hallucinations can occur as well as increased movements, called dyskinesias.

Then a brilliant idea from a pharmaceutical company:…Why not combine the two in one pill? And Stalevo was born; a combination of carbidopa, levodopa and entacapone in one tablet. This medication also comes in multiple strengths. It has the advantage that only one pill is necessary instead of two, simplifying the regimen, but for some people, side effects can limit its usefulness. There is also some consideration that the combination may contribute to prostate problems for men, but this is still under scientific investigation.

What are the Common Side Effects?
Carbidopa/Levodopa/Entacapone(Stalevo®)

  • Dyskinesia
  • nausea
  • diarrhea
  • hyperkinesia (an abnormal amount of uncontrolled muscular action; spasm.)
  • abdominal pain
  • dizziness
  • harmless discoloration of urine
  • saliva and/ or sweat
  • hallucinations

Early Diagnosis of Parkinson’s by Handwriting Analysis

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“Micrographia” or small handwriting has been a signal symptom of Parkinson’s disease (PD) for many years.  Why the handwriting gets smaller and smaller is not well understood.  But now a group of occupational therapists working at University of Haifa and the Rambam Hospital have studied this phenomenon and found what is perhaps and early way to predict and diagnose Parkinson’s disease based on handwriting.

Professor Sara Rosenblum noted that many people who have Parkinson’s disease have often felt there were cognitive changes happening in their brains well before any motor symptoms were seen and they were aware of changes in their handwriting, sometimes years before there were motor symptoms.  Most studies have focused on the motor skills of hand writing and not on the cognitive changes.  Professor Rosenblum decided to look at the cognitive changes by asking the participants to sign their name and write several addresses, as if addressing an envelope, tasks that require cognitive skills.  She chose 40 subjects: 20 healthy and 20 with early stage PD that had no motor symptoms.

Using a plain piece of paper placed on an electronic tablet and a special, pressure sensitive pen, they were able to analyze the writing from several perspectives.  They could see how the subjects formed the letters, the length, height and width as well as how much pressure was applied and the time it took to write them.  They found some interesting differences.

The people with Parkinson’s disease wrote smaller letters, used less pressure and took longer to write them than the healthy group.  Of special note was the longer time the people with PD held the pen in the air before writing, which shows the amount of time their brain was contemplating the next writing action.  This suggests that there is a reduced or slower cognitive ability.

Further development of this research could lead to earlier detection of Parkinson’s disease .  It has the advantage that it could be done my a technologist other than the physician and if the changes are noted, the patient can then be referred to a physician for further evaluation and treatment.

Professor Rosenblum is presently collaborating with Dr. Ilana Schlessinger, the head of the Movement Disorders and Parkinson’s Disease at Rambam Hospital in Haifa, Israel..  They are using handwriting analysis to measure the degree of Parkinson’s patients improved functioning after undergoing deep brain stimulation.

If you enjoyed this article, please help us continue to help others by Donating to Parkinson Research Foundation

Sara Rosenblum, Margalit Samuel, Sharon Zlotnik, Ilana Erikh, Ilana Schlesinger. Handwriting as an objective tool for Parkinson’s disease diagnosisJournal of Neurology, 2013; DOI: 10.1007/s00415-013-6996-x.

Anxiety, Diet and Parkinson’s Disease

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The Reality of Anxiety in Parkinson’s Disease

Anxiety is a common complaint in Parkinson’s disease (PD).  Sometimes it is even present several years before motor symptoms appear or a diagnosis of PD can be made.  It is also a common complaint of older people, and it has been suggested that anxiety may even be a risk factor for development of PD. Anxiety symptoms in people with PD tend to be more severe than in age matched people without PD.   In comparing results of several studies, it appears that about half of the people with PD will have anxiety sufficiently troublesome to cause clinical concern.

In people with Parkinson’s disease, symptoms of anxiety may be difficult to discern from symptoms of PD.  Sleep disturbance, restlessness, increased tremor and motor problems may be part of Parkinson’s disease, but with anxiety, they are considerably worsened.  Anxiety in Parkinson’s disease can lead to social phobia, obsessive-compulsive disorders or even panic disorders. Anxiety affects the quality of life of people with PD. It affects their relationships with other people, their over-all sense of well-being and lowers substantially their emotional sense of well being. This, in turn, can affect their activities of daily living, their interactions with loved ones and lead to feelings of isolation and depression. Cognitive function is also affected by excessive worry, and anxiety is often a predictor of future cognitive decline. Depression is another factor that is common between older people and people with PD. In people with PD, there is a much stronger correlation between depression and anxiety and this can make treating the motor symptoms more difficult. People with Parkinson’s disease may be reluctant to discuss these symptoms with their physicians, not wishing to discuss their worries and if they do, hurried physicians may see them as minor problems in their overall treatment.

Given the dopaminergic changes in the brain, the responses of serotonin and norepinephrine to those changes may drive the effects of anxiety and depression in people with Parkinson’s disease.  There may even be a genetic predisposition.  Some of the characteristics of anxiety may cause cognitive impairment which may in turn cause more anxiety as tasks such as problem solving in certain situations are anxiety producing in and of themselves.  Parkinson’s drugs have also been suggested as possible causes of anxiety as the relationship between dopamine and anxiety has not been fully investigated.The relationship of anxiety and PD is an important area needing more research.  Because anxiety and motor symptoms are interconnected, that relationship will affect the outcome of treatment.

The Reality of Diet and Parkinson’s Disease

Remember the diet affects anxiety as well.  Many tend to ignore the need for truly good nutrition.   The chemistry of the body needs to be addressed as it is affected by the chemistry in our food.  A lack of the essential vitamins and minerals needed in our diet can complicate anxiety issues. 

What Foods Help With Anxiety?

It is important that everyone get enough Magnesium in their diet but especially those challenged with neuro-degenerative issues.  Magnesium relaxes muscles and nerves.  Magnesium rich foods like: Raw Cocoa 50%, Pumpkin Seeds  47.7%, Spinach  39.1%, Swiss Chard  37.6%, Soybeans  36.9%, Sesame Seeds  31.5%, Halibut  30.3%, Black Beans  30.1%,  Sunflower Seeds  28.4%, Cashews  25%, Almonds  24.6% can be added to the diet to help keep up magnesium levels to assist in minimizing anxiety.

 Special Note on Raw Cacao and Parkinson’s

What is Cacao? Cacao is the seed of a fruit of an Amazonian tree that was brought to Central America during or before the time of the Olmecs. Cacao beans were so revered by the Mayans and Aztecs that they used them as money! Cacao beans contain no sugar and between 12% and 50% fat depending on variety and growth conditions. Nature’s First Law cacao beans are around 40% fat content (low compared to other nuts). There is no evidence to implicate cacao bean consumption with obesity.The raw cacao bean is one of nature’s most fantastic superfoods due to its wide array of unique properties, many of which are destroyed or corrupted by cooking.

Five Reasons For Eating Raw Cacao

Contains Nearly Half of Your Daily Magnesium

Cacao is remarkably rich in magnesium. Cacao seems to be the #1 source of magnesium of any food. This is likely the primary reason women crave chocolate during the menstrual period. Magnesium balances brain chemistry, builds strong bones, and is associated with more happiness. Magnesium is the most deficient major mineral on the Standard American Diet (SAD); over 80% of Americans are chronically deficient in Magnesium! Raw chocolate has a good amount of magnesium, which has many benefits. You need a certain amount of magnesium every day to keep your body functioning properly. Raw chocolate can have anywhere from 100 to 170 milligrams of magnesium per 100 grams of raw chocolate. Men need around 400 milligrams per day, while women need a little over 300 milligrams. This makes it a good source for magnesium, and an easy way to consume the amount you need daily.

Brain Chemistry and Raw Cacao

There is a chemical in chocolate called tryptophan. This is an essential amino acid that the body uses to help produce serotonin in the brain. Serotonin is important neurotransmitter in your brain that is involved in your behavior and moods. It is an important part of the functioning of your body, which is why you need a certain serotonin in your brain. Tryptophan can raise those levels, because it gives a small boost to serotonin production.

Phenylethylamine (PEA) is found in chocolate. PEA is an adrenal-related chemical that is also created within the brain and released when we are in love. This is one of the reasons why love and chocolate have a deep correlation. PEA also plays a role in increasing focus and alertness.

Anandamide (The Bliss Chemical)
A neurotransmitter called anandamide, has been isolated in cacao. Anandamide is also produced naturally in the brain. Anandamide is known as “The Bliss Chemical” because it is released while we are feeling great. Cacao contains enzyme inhibitors that decrease our bodies’ ability to breakdown anandamide. This means that natural anandamide and/or cacao anandamide may stick around longer, making us feel good longer, when we eat cacao.

Rich in Heart Healthy Antioxidants

The flavanoids in cacao are what give it the antioxidant properties. Antioxidants help fight heart disease and can lower the risk of some types of cancer. They help protect your body’s cells against the threat of free radicals. Free radicals are harmful to your health and may play a role in long-term diseases such as cancer. If you have a high number of free radicals that are not being taken care of by your body, then they will accumulate and cause serious damage over a long period of time.

MAO Inhibitors: Cacao seems to diminish appetite, probably due to its monoamine oxidase enzyme inhibitors (MAO inhibitors) – these are different from digestive enzyme inhibitors found in most nuts and seeds. These rare MAO inhibitors actually produce favorable results when consumed by allowing more serotonin and other neurotransmitters to circulate in the brain. According to Dr. Gabriel Cousens, MAO inhibitors facilitate youthening and rejuvenation.

Can Open Your Blood Vessels

The chemical compound Theobromine is an alkaloid, and it has a few benefits. One is that it has the effect of a mild stimulant. It is used in medicine as a diuretic and a blood vessel opener. It is used to treat high blood pressure because of these characteristics. The diuretic component gives the chemical use as a cleansing aid, because it causes frequent urination. The levels of the chemical in chocolate will give you an extra boost by opening your blood vessels a little bit.

Has Multiple Vitamins

Cacao is full of vitamins. These vitamins include A, B1, B2, and B3 are only a few found in cacao. Vitamin A can strengthen immunity and help with eyesight. Vitamin B1 can help brain function and cardiovascular health. Vitamin B2 protects against carcinogens and may help to prevent migraines. Vitamin B3 can help lower bad cholesterol and protect against heart disease. The combination of these vitamins in cacao can produce multiple helpful benefits for your long-term health.

These five health benefits from eating raw cacao are not to be overlooked. The amount of magnesium is another daily benefit that can help keep you healthy. If you want a reason to eat raw cacao every day, you don’t have to look very far because there are many.

Footnotes and credits

Cacao contains subtle amounts of caffeine and theobromine. However, experiments have shown that these stimulants are far different when consumed raw than cooked.

Consider the following: Experimental provings of chocolate by homeopaths indicate its stimulating effect when cooked. One experiment conducted with a decoction of roasted ground cacao beans in boiling water produced an excitement of the nervous system similar to that caused by black coffee, an excited state of circulation, and an accelerated pulse. interestingly, when the same decoction was made with raw, unroasted beans neither effect was noticeable, leading the provers to conclude that the physiological changes were caused by aromatic substances released during roasting.

EDITOR’S TIP:

If you want to eat cacao for its benefits, the product should be at least 70 percent cacao. But there are products that have a good amount of cacao that do not have as much of a benefit. This is because the process they go through to be produced destroys some of the healthy flavanoids in the process, therefore the reasoning for RAW Cacao.

Allergies?
A recent study showed that only one out of 500 people who thought they were allergic to chocolate actually tested positive. Allergies to chocolate are quite rare. It is typically the case that the person is in fact allergic to milk and dairy products.

Article by Marcia McCall

Vegetarian Answers: Benefits of Raw Cacao

Raw Super Foods:Benefits of Raw Cacao

Chocolate and the brain: Neurobiological impact of cocoa flavanols on cognition and behavior

Alexander N. Sokolova, Corresponding author contact information, E-mail the corresponding author, Marina A. Pavlovab, Sibylle Klosterhalfena, Paul Encka

Compound Identified That Alleviates Parkinson’s Symptoms in Mice

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Researchers from Johns Hopkins and the National Cancer Institute (NCI) highlighted

a novel mechanism underlying Parkinson’s disease while simultaneously putting to

rest a previously held theory regarding progression of the disorder. They also

identified a compound that alleviates the disease’s symptoms in mice.

 

The investigators describe their work in a paper titled “Parthanatos mediates

AIMP2-activated age-dependent dopaminergic neuronal loss,” published online in

Nature Neuroscience.

 

“Not only were we able to identify the mechanism that could cause progressive cell

death in both inherited and noninherited forms of Parkinson’s, we found there were

already compounds in existence that can cross into the brain and block this from

happening,” said Valina Dawson, Ph.D., director of the stem cell biology and neuro-

regeneration programs at the Johns Hopkins University School of Medicine’s Institute

for Cell Engineering (ICE). “While there are still many things that need to happen

before we have a drug for clinical trials, we’ve taken some very promising first steps.”

 

Dr. Dawson and her husband, Ted Dawson, M.D., Ph.D., the director of ICE, have

collaborated for decades on studies of the molecular chain of events that lead to

Parkinson’s. One of their findings was that the function of an enzyme called parkin,

which malfunctions in the disease, is to tag a bevy of other proteins for destruction

by the cell’s recycling machinery. This means that nonfunctional parkin leads to the

buildup of its target proteins, and the Dawsons and others are exploring what roles

these proteins might play in the disease.

 

In the new study, the Dawsons collaborated with Debbie Swing and Lino Tessarollo of the

NCI to develop mice whose genes for a protein called AIMP2 could be switched into higher

performance. AIMP2 is one of the proteins normally tagged for destruction by parkin, so

the genetically modified mice enabled the research team to put aside the effects of

defective parkin and excesses of other proteins and look just at the consequences of

too much AIMP2.

 

They found that the mice developed symptoms similar to those of Parkinson’s as they aged.

The brain cells that make dopamine were dying. Since AIMP2 is known for its role in the

process of making new proteins, the researchers thought the cell death was caused by

problems with this process. But when graduate student Yunjong Lee looked at the efficiency

of protein-making in the affected mice, everything appeared normal.

 

Searching for an alternative explanation, Lee tested how cells with excess AIMP2 responded

to compounds blocking various paths to cell death and found that the AIMP2 was activating a

self-destruct pathway called parthanatos, discovered and named by the Dawsons years ago.

 

Lee found that AIMP2 triggered parthanatos by directly interacting with a protein called PARP1,

which was long thought to respond only to DNA damage and not to signals from other proteins.

Dr. Valina Dawson notes that AIMP2 is actually the second protein found to activate PARP1, but

the idea that PARP1 is only involved in detecting and responding to DNA damage is still firmly

entrenched in her field.

 

Since the Dawsons had been studying PARP1 for some time, they knew of compounds drug companies

had designed to block this enzyme. Such drugs are already in the process of being tested to

protect healthy cells during cancer treatment.

Parkinson’s Disease, Music and Mystery

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Parkinson’s Disease what effect does music have on its sufferers? What mysterious thing happens to us when we are exposed to or even participate in song?

When you sit back and listen to music, say Samuel Barber’s Adagio for strings, something happens.  What is that something?  Your heart rate synchronizes with the music, your mind quiets and your thoughts melt away into the melodies.  Your whole being transcends time and space and you float on the harmonies and gentle rhythm of the piece.  If you listen to say, Buddy Holly’s That’ll be the day, again, something happens.  Your pulse quickens, you begin tapping your feet to the rhythm, you break into a smile and memories of dancing and happy times flood into your consciousness.  Wherever you were, whatever you were doing, suddenly you are transported somewhere else and you feel the change.  If you have ever sung in a group or been part of a choir, you have experienced first- hand the surge of serotonin and the uplifting feeling that blending your voice with other voices all singing the same song brings.

So perhaps all this has something to do with why music therapy is so good for Parkinson’s.  Music is complex, music is dynamic, and it operates on many levels. It lifts the mood and lifts the spirit.  Parkinson’s is also a complex disease.  It is more than a tremor, stiffness and gait disturbance, more than a lack of dopamine in the substantia nigra, more than the alpha-synuclein, the mitochondria or cell surfaces or the chaperone molecules within the cells.  Music in all its complexity seems to harmonize with the complexity of Parkinson’s disease.  Taking what may be a depressed mood and turning it to happier thoughts and perhaps a lighter mood.

Music is one area that although it can be quantified into individual parts, is; as Aristotle commented “The whole is greater than the sum of its parts”.  It is a process.  Music’s effects on the human psyche and the variability of those effects defy explanation. Parkinson’s disease is also a process that has tended to defy explanation.  Reducing disease to cellular function can explain the cellular function or “mis-function” and the interactions between the cellular relationships.  It can show the how and what of the disease process, but it cannot tell us the why.  Parkinson’s is a dynamic system, with many effects changing from moment to moment.  Sometimes it is the “whole”; sometimes it is just a “part”.

Adding music therapy to treatment for Parkinson’s is bringing two dynamic systems (really many more) together to change the course of yet another.  Exactly how music calms the Parkinson’s beast has yet to be determined.  Yet more important is the fact that it is all a process, not an end point. The complexity of both dynamic systems interacting to bring the human state or the disease state to the edge of that creative process, to the edge of energy and potential and to stimulate new dynamic processes.

In complex systems, such as music and disease, there will always be missing information, unanswered questions.  Part of the process is knowing there are limits, there are things perhaps we cannot quantify or “know”.   Life is still, and hopefully will always be a mystery.  It is releasing and letting go, accepting those limits, and allowing “magic” to happen.  Music is magic…. and mystery; and what a sweet mystery it is!.

Investigational Gene Therapy Trial for Parkinson’s Disease

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A Phase I clinical trial for the treatment of Parkinson’s with Glial Cell Line Derived Neurotrophic Factor (GDNF) has completed the first procedure on the first patient at the University of California, San Francisco.  Krystof Bankiewicz, M.D., Ph.D. of UCSF and John D. Heiss, M.D., from the National Institutes for Neurological Diseases and Stroke are the joint chief investigators.  This trial will treat 24 patients in four cohorts that will receive varying doses of the GDNF. This is the first stage of testing for safety and dose response.

GDNF provides neuro regeneration and is expected to provide neuro-protective properties to strengthen dopamine producing cells in the brain.  It will be delivered directly to the putamen region of the brain, where dopamine is normally produced but is disrupted by Parkinson’s disease.   According to Dr. Bankiewicz “The success of gene therapy in patients requires accuracy in delivery.”  To achieve this accuracy, a program from the company MRI Interventions called “ClearPoint” is used.  “ClearPoint” is a system of technology to enable precise and exact placement of the gene therapy using MRI.  The infusion of the gene therapy to this very small and precise region of the brain is actually considered “minimally invasive” surgery.  The first patient received treatment on May 20th and there have been no safety issues.

This study is a collaboration between MRI Interventions, the manufacturers of the “ClearPoint” system for precise visualization, uniQure V.B. a Dutch Company that is providing the GDNF and UCSF.   It is sponsored by National Institutes of Health.  MRI Interventions “ClearPoint” system has received FDA approval.  UniQure specializes in human gene therapy treatments with potentially curative results.  They currently have one product that has been successful and are eager to bring new therapies to patients with severe disorders.

Additional note: This treatment of Parkinson’s with Glial Cell Line Derived Neurotrophic Factor (GDNF) was used in the UK in 2003 with remarkable results.  After one year, there were no serious clinical side effects, a 39% improvement in the off-medication motor sub-score of the Unified Parkinson’s Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living sub-score. Medication-induced dyskinesias were reduced by 64% and were not observed off medication during chronic GDNF delivery. Positron emission tomography (PET) scans of [(18)F]dopamine uptake showed a significant 28% increase in putamen dopamine storage after 18 months, suggesting a direct effect of GDNF on dopamine function.

Nat Med. 2003 May;9(5):589-95. Epub 2003 Mar 31.Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease. Gill SS, Patel NK, Hotton GR, O’Sullivan K, McCarter R, Bunnage M, Brooks DJ, Svendsen CN, Heywood P. Source: Frenchay Hospital, Institute of Neurosciences, Bristol, UK. steven.gill@north-bristol.swest.nhs.uk

http://finance.yahoo.com/news/mri-interventions-clearpoint-system-enables-140603875.html

Photo Credit: http://www.raybiotech.com/recombinant-human-gdnf-protein-en.html, http://www.ucsf.edu/about/about-ucsf , Wiki

NEW HOPE FOR PARKINSON SUFFERERS

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Turning Off and Turning On Parkinson Proteins   An amazing discovery was announced today that should lead to help for people with Parkinson’s disease soon.  Science has known how to turn off enzymes that affect various disorders, but turning them on has never been done.  Now a team of researchers from the Howard Hughes Medical Institute in San Francisco, California has done just that!  Through an extremely extensive search for the right molecule, they found it in an unexpected place:  a molecule long used as the basis for anti-wrinkle cream!

The gene PINK1, discovered in a familial strain of Parkinson’s, is known to help the mitochondria (energy suppliers) of neurons involved in Parkinson’s Disease.  PINK1 helps Parkin accumulate in the damaged mitochondria, but prevents further damage and helps the damaged cells to survive and not die.  If PINK1 could be increased, it might help keep those neurons functioning longer and prevent progression   In people who have mutations of PINK1Parkin is not found in the cells, and neuronal cell death follows.

The team wanted to find a way to strengthen PINK1 and started looking at the way that it is turned on by a particular molecule called ATP.  If they could understand how it was turned on, they might be able to find a less direct way to accomplish that task.  They started looking at molecules that were very similar to ATP, hoping to find one they could engineer to fit.  To their surprise, they found KTP, kinetin triphosphate, a very close relative of ATP that worked.  Not only did it turn on PINK1, but it also turned on the mutated forms of PINK1.

To verify that the addition of KTP did the same thing as ATP, they measured the amount of PINK1 activity and also the amount of Parkin that PINK1 brought to the mitochondrial surfaces as well as cell death.  Adding the precursor of KTP, kinetin, to the cells of both PINK1 and mutated PINK1 increased the activity, increased the Parkin and lead to less neuronal cell death.  Not only will this help people with the familial strain of Parkinson’s Disease, but also people who have the sporadic strain.

The group is now working to demonstrate the effectiveness of this discovery in animal models of Parkinson’s Disease.  There are several animal models, but the effects and results in animal models often are not the same as in humans.  However, since kinetin and KTP already have Food and Drug Administration approval and are not known to cause adverse reactions in humans, this should both speed up and simplify the process leading to clinical trials in humans.

Nicholas T. Hertz, Amandine Berthet, Martin L. Sos, Kurt S. Thorn, Al L. Burlingame, Ken Nakamura, Kevan M. Shokat. A Neo-Substrate that Amplifies Catalytic Activity of Parkinson’s-Disease-Related Kinase PINK1Cell, 2013; 154 (4): 737 DOI: 10.1016/j.cell.2013.07.030

Picture Credits: Melbourne Dermatology, Science Direct, Buy Me Beauty, and the above abstract.

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