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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.

Deep Brain Stimulation for Parkinson’s – Sooner Rather Than Later?

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A point of view article by four Canadian and UK neurologists who are very experienced with DEEP BRAIN STIMULATION was published in a recent issue of Annals of Neurology Journal.  They analyzed and reviewed results from current and long term studies of Deep Brain Stimulation in people with Parkinson’s and compared the results of Deep Brain Stimulation to standard medical treatment for Parkinson’s.  Present medical treatment for Parkinson’s consists of medical, surgical and supportive treatment.

Standard medical treatment for PARKINSON’S DISEASE has evolved considerably since the introduction of L-Dopa forty years ago and then the appearance of dopamine agonists.  New brain imaging techniques and greater understanding of the natural history of the disease have come a long way to help new therapies develop.  Advances in surgical technique plus the hardware for Deep Brain Stimulation have also become part of standard medical management.

Medical management has been divided into three areas:  Early Parkinson’s Disease, when it first affects motor function; Late stage PARKINSON’S DISEASE, where motor complications become apparent and surgical intervention.  There are standards for uncomplicated versus complicated and combinations of therapies to treat the motor problems and then complications.  But PARKINSON’S DISEASE also has non-motor symptoms, such as pain or depression, which these therapies are unable to satisfactorily address.  Surgical intervention has generally been reserved for those people for whom medical therapies are not sufficient or whose responses have been irregular and who have dyskinesias that cannot be resolved any other way.  These are often people in the later stages of PARKINSON’S DISEASE.

Deep Brain Stimulation now has a history of 12 to 14 years, since the Food and Drug Administration granted approval.  There are now some people who had Deep Brain Stimulation 10 years ago and are still showing clinically confirmed benefits.  Deep Brain Stimulation has both motor and non-motor benefits.  Deep Brain Stimulation reduces drug induced dyskinesias by as much as 60 to 80 per cent, while decreasing the amount of medication needed.  People who have had DEEP BRAIN STIMULATION demonstrate improvement on the Unified Parkinson’s Disease Rating Scale and also report improved quality of life.  While there are many qualities to recommend DEEP BRAIN STIMULATION, studies have shown that there are some side effects to be considered.  For instance, DEEP BRAIN STIMULATION of the subthalamic nucleus (STN) increased the long term response to L-Dopa medication, but it also worsened the short term response with the effect of mimicking early stage PARKINSON’S DISEASE.  DEEP BRAIN STIMULATION of the globus pallidus internus (GPi) was not as effective on motor symptoms as STN, but verbal fluency increased.  Both types of DEEP BRAIN STIMULATION report improvement in non-motor domains of pain, akathisia, cognitive function, emotion and improvement in the activities of daily living.  Many of the side effects are short term and resolve without problems.

Of course, there are other side effects of DEEP BRAIN STIMULATION, adverse events are always possible.  Surgery is always serious, and DEEP BRAIN STIMULATION surgery, done while the patient is awake, carries its share of potential problems.  The hardware must not only be properly placed, it must be monitored and adjusted from time to time and batteries need to be replaced. The safety profile of DEEP BRAIN STIMULATION has been so good that it is now recognized as an established therapy for PARKINSON’S DISEASE.  Given the improvement of both motor and non-motor symptoms, and the improved quality of life experience with the combination of surgical and medical treatment for PARKINSON’S DISEASE, the guidelines for consideration of DEEP BRAIN STIMULATION as a therapy may need reassessment.  Instead of waiting until later in the course of PARKINSON’S DISEASE to recommend DEEP BRAIN STIMULATION as a “rescue”, perhaps we should consider DEEP BRAIN STIMULATION earlier in order to “preserve” function.

Guidelines for DEEP BRAIN STIMULATION have generally been that the patient be responsive to L-Dopa therapy, be cognitively unimpaired and emotionally stable to undergo the surgery.  However, cognitive impairments, emotional debility and psychotic symptoms are part of PARKINSON’S DISEASE and often occur later in the disease, possibly ruling out DEEP BRAIN STIMULATION.  If DEEP BRAIN STIMULATION could be done before drug induced motor symptoms become problematic, before disease progression affects cognition and emotion, the patient could benefit from improved symptoms and improved quality of life…making it easier to remain working or socially engaged for a longer period of time.

DEEP BRAIN STIMULATION is certainly not a simple consideration.  There are many aspects to consider: social, familial, personal as well as medical.  Serious conversations with the medical providers, neurologists and neurosurgeon need to be undertaken.  Understanding the current situation and symptoms in relation to the course of the disease while weighing them against the benefits, side effects and adverse events of DEEP BRAIN STIMULATION should be considered.  While DEEP BRAIN STIMULATION now has a longer history and more people have benefited from it, at what point in the course of the disease it is appropriate to be offered needs to be re-evaluated.


deSouza, R.-M., Moro, E., Lang, A. E. and Schapira, A. H. V. (2013), Timing of deep brain stimulation in Parkinson disease: A need for reappraisal?. Ann Neurol., 73: 565–575. doi: 10.1002/ana.23890

Is There a Genetic Link Between Alzheimer’s and Parkinson’s?

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A newly released research paper by Valentina Moskvina, Ph.D., and associates from the Cardiff University School of Medicine in Wales, U.K. looked at both Alzheimer’s and Parkinson’s and did not find a common genetic link between them.  This was a statistical meta analysis of a prodigious number of studies that examined the genetics and pathology of patients with Parkinson’s or Alzheimer’s.  Data was analyzed three different ways and all three ways showed no genetic commonality.

Both diseases can appear to have some similarities,  both being progressive neurodegenerative diseases with onset later in life and the development of dementia in later stages of the disease.  The causes of these diseases are distinct, with Parkinson’s resulting from a lack of dopamine production in the substantia nigra causing a movement disorder.  In Alzheimer’s, it is the hippocampus and the entorhinal cortex that are affected with the depletion of acetylcholine resulting in learning and memory difficulties.  As the diseases progress, neurodegeneration progresses leading to dementia.  However many people with Parkinson’s never experience dementia or memory problems whereas Alzheimer’s is the cause of most dementia and memory problems.

Some genetic studies have suggested there might be genetic connections between the two diseases and there have been reports of Alzheimer’s pathology in Parkinson’s patients and Parkinson’s in Alzheimer’s patients.  Having one disease does not exclude the possibility of having the other, but does not mean that the two are connected.  One of  genome wide studies is finding new genes that are linked to either disease, and Dr. Moskvina has herself found new genes related to Alzheimer’s. This study has helped by showing that there is not a single gene that can give rise to either disease but there are some genetic regions that increase the risk for developing both diseases.

One important note about this study is that they did not include people with Lewy-Body Dementia, which shares some similarities with Alzheimer’s.  The researchers also noted there is always a possibility that more refined methods for research on genetics might become available in the future that could still find a common basis for these diseases.


Valentina Moskvina et al. Analysis of Genome-Wide Association Studies of Alzheimer Disease and of Parkinson Disease to Determine If These 2 Diseases Share a Common Genetic RiskJAMA Neurol., 2013 DOI:10.1001/jamaneurol.2013.448


Testosterone and it’s Possible Link to Parkinson’s in Men

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Sudden Decline in Testosterone May Cause Parkinson’s Disease Symptoms in Men

July 26, 2013 — The results of a new study by neurological researchers at Rush University Medical Center show that a sudden decrease of testosterone, the male sex hormone, may cause Parkinson like symptoms in male mice. The findings were recently published in the Journal of Biological Chemistry.

One of the major roadblocks for discovering drugs against Parkinson’s disease* is the unavailability of a reliable animal model for this disease

“While scientists use different toxins and a number of complex genetic approaches to model Parkinson’s disease in mice, we have found that the sudden drop in the levels of testosterone following castration is sufficient to cause persistent Parkinson’s like pathology and symptoms in male mice,” said Dr. Kalipada Pahan, lead author of the study and the Floyd A. Davis endowed professor of neurology at Rush. “We found that the supplementation of testosterone in the form of 5-alpha dihydrotestosterone (DHT) pellets reverses Parkinson’s pathology in male mice.”  “In men, testosterone levels are intimately coupled to many disease processes,” said Pahan. Typically, in healthy males, testosterone level is the maximum in the mid-30s, which then drop about one percent each year. However, testosterone levels may dip drastically due to stress or sudden turn of other life events, which may make somebody more vulnerable to Parkinson’s disease. “Therefore, preservation of testosterone in males may be an important step to become resistant to Parkinson’s disease,” said Pahan.

Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson’s disease. Nitric oxide is an important molecule for our brain and the body.  “However, when nitric oxide is produced within the brain in excess by a protein called inducible nitric oxide synthase, neurons start dying,” said Pahan.  “This study has become more fascinating than we thought,” said Pahan. “After castration, levels of inducible nitric oxide synthase (iNOS) and nitric oxide go up in the brain dramatically. Interestingly, castration does not cause Parkinson’s like symptoms in male mice deficient in iNOS gene, indicating that loss of testosterone causes symptoms via increased nitric oxide production.”

“Further research must be conducted to see how we could potentially target testosterone levels in human males in order to find a viable treatment,” said Pahan.

Other researchers at Rush involved in this study were Saurabh Khasnavis, PhD, student, Anamitra Ghosh, PhD, student, and Avik Roy, PhD, research assistant professor. This research was supported by a grant from the National Institutes of Health that received the highest score for its scientific merit in the particular cycle it was reviewed.

Parkinson’s is a slowly progressive disease that affects a small area of cells within the mid-brain known as the substantia nigra. Gradual degeneration of these cells causes a reduction in a vital chemical neurotransmitter, dopamine. The decrease in dopamine results in one or more of the classic signs of Parkinson’s disease that includes resting tremor on one side of the body; generalized slowness of movement; stiffness of limbs and gait or balance problems. The cause of the disease is unknown. Both environmental and genetic causes of the disease have been postulated.

*Parkinson’s disease affects about 1.2 million patients in the United States and Canada. Although 15 percent of patients are diagnosed before age 50, it is generally considered a disease that targets older adults, affecting one of every 100 persons over the age of 60. This disease appears to be slightly more common in men than women.


Story Source:

Rush University Medical Center. “Sudden decline in testosterone may cause Parkinson’s disease symptoms in men.” ScienceDaily, 26 Jul. 2013. Web. 8 Aug. 2013.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

  1. S. Khasnavis, A. Ghosh, A. Roy, K. Pahan. Castration Induces Parkinson Disease Pathologies in Young Male Mice via Inducible Nitric-oxide Synthase. Journal of Biological Chemistry, 2013; 288 (29): 20843 DOI: 10.1074/jbc.M112.443556


Scientists Find a Potential Cause of Parkinson’s Disease that points to a new Therapeutic Strategy

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Scientists Find a Potential Cause of Parkinson’s Disease that Points to a New Therapeutic Strategy

Biologists at The Scripps Research Institute (TSRI) have made a significant discovery that could lead to a new therapeutic strategy for Parkinson’s disease.

The findings, recently published online ahead of print in the journal Molecular and Cell Biology, focus on an enzyme known as parkin, whose absence causes an early-onset form of Parkinson’s disease. Precisely how the loss of this enzyme leads to the deaths of neurons has been unclear. But the TSRI researchers showed that parkin’s loss sharply reduces the level of another protein that normally helps protect neurons from stress.

“We now have a good model for how parkin loss can lead to the deaths of neurons under stress,” said TSRI Professor Steven I. Reed, who was senior author of the new study. “This also suggests a therapeutic strategy that might work against Parkinson’s and other neurodegenerative diseases.”

Genetic Clues

Parkinson’s is the world’s second-most common neurodegenerative disease, affecting about one million people in the United States alone. The disease is usually diagnosed after the appearance of the characteristic motor symptoms, which include tremor, muscle rigidity and slowness of movements. These symptoms are caused by the loss of neurons in the substantia nigra, a brain region that normally supplies the neurotransmitter dopamine to other regions that regulate muscle movements.

Most cases of Parkinson’s are considered “sporadic” and are thought to be caused by a variable mix of factors including advanced age, subtle genetic influences, chronic neuroinflammation and exposure to pesticides and other toxins. But between 5 and 15 percent of cases arise specifically from inherited gene mutations. Among these, mutations to the parkin gene are relatively common. Patients who have no functional parkin gene typically develop Parkinson’s-like symptoms before age 40.

Parkin belongs to a family of enzymes called ubiquitin ligases, whose main function is to regulate the levels of other proteins. They do so principally by “tagging” their protein targets with ubiquitin molecules, thus marking them for disposal by roving protein-breakers in cells known as proteasomes. Because parkin is a ubiquitin ligase, researchers have assumed that its absence allows some other protein or proteins to evade proteasomal destruction and thus accumulate abnormally and harm neurons. But since 1998, when parkin mutations were first identified as a cause of early-onset Parkinson’s, consensus about the identity of this protein culprit has been elusive.

“There have been a lot of theories, but no one has come up with a truly satisfactory answer,” Reed said.

Oxidative Stress

In 2005, Reed and his postdoctoral research associate (and wife) Susanna Ekholm-Reed decided to investigate a report that parkin associates with another ubiquitin ligase known as Fbw7. “We soon discovered that parkin regulates Fbw7 levels by tagging it with ubiquitin and thus targeting it for degradation by the proteasome,” said Ekholm-Reed.

Loss of parkin, they found, leads to rises in Fbw7 levels, specifically for a form of the protein known as Fbw7β. The scientists observed these elevated levels of Fbw7β in embryonic mouse neurons from which parkin had been deleted, in transgenic mice that were born without the parkin gene, and even in autopsied brain tissue from Parkinson’s patients who had parkin mutations.

Subsequent experiments showed that when neurons are exposed to harmful molecules known as reactive oxygen species, parkin appears to work harder at tagging Fbw7β for destruction, so that Fbw7β levels fall. Without the parkin-driven decrease in Fbw7β levels, the neurons become more sensitive to this “oxidative stress”—so that more of them undergo a programmed self-destruction called apoptosis. Oxidative stress, to which dopamine-producing substantia nigra neurons may be particularly vulnerable, has long been considered a likely contributor to Parkinson’s.

“We realized that there must be a downstream target of Fbw7β that’s important for neuronal survival during oxidative stress,” said Ekholm-Reed.

A New Neuroprotective Strategy

The research slowed for a period due to a lack of funding. But then, in 2011, came a breakthrough. Other researchers who were investigating Fbw7’s role in cancer reported that it normally tags a cell-survival protein called Mcl-1 for destruction. The loss of Fbw7 leads to rises in Mcl-1, which in turn makes cells more resistant to apoptosis. “We were very excited about that finding,” said Ekholm-Reed. The TSRI lab’s experiments quickly confirmed the chain of events in neurons: parkin keeps levels of Fbw7β under control, and Fbw7β keeps levels of Mcl-1 under control. Full silencing of Mcl-1 leaves neurons extremely sensitive to oxidative stress.

Members of the team suspect that this is the principal explanation for how parkin mutations lead to Parkinson’s disease. But perhaps more importantly, they believe that their discovery points to a broad new “neuroprotective” strategy: reducing the Fbw7β-mediated destruction of Mcl-1 in neurons, which should make neurons more resistant to oxidative and other stresses.

“If we can find a way to inhibit Fbw7β in a way that specifically raises Mcl-1 levels, we might be able to prevent the progressive neuronal loss that’s seen not only in Parkinson’s but also in other major neurological diseases, such as Huntington’s disease and ALS [amyotrophic lateral sclerosis],” said Reed.

Finding such an Mcl-1-boosting compound, he added, is now a major focus of his laboratory’s work.

Authors of the study, “Parkin-Dependent Degradation of the F-box protein Fbw7 β Promotes Neuronal Survival in Response to Oxidative stress by Stabilizing Mcl-1,” include Matthew S. Goldberg of The University of Texas Southwestern Medical Center at Dallas and Michael G. Schlossmacher of the University of Ottawa. For more information about the paper, see

Funding for the study was provided in part by the National Institutes of Health (NS059904 and CA078343).

“We now have a good model for how parkin loss can lead to the deaths of neurons under stress,” says TSRI Professor Steven I. Reed.



The Scripps Research Institute. “Potential cause of Parkinson’s disease points to new therapeutic strategy.” ScienceDaily, 24 Jul. 2013. Web. 5 Aug. 2013.

American Society for Microbiology:  Parkin-Dependent Degradation of the F-box protein Fbw7β Promotes Neuronal Survival in response to oxidative stress by Stabilizing Mcl-1.  Published ahead of print 15 July 2013, doi: 10.1128/MCB.00535-13




Stem Cell Breakthrough

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Why don’t brain cells in Parkinson brains communicate better? A team of researchers in Aukland, New Zealand, have been working on that question for the last five years and have found some clues that may help both Parkinson’s and Alzheimer’s.
As new stem cells, immature cells, emerge in the brain, they need to grow into neurons and find their proper place in the brain and begin communicating with other neurons. In order to reach their destination, through a complex and tight inter cellular matrix, they become coated with a slippery substance, polysialic-acid-neutral cell adhesion molecule. This slippery substance reduces the friction so they can migrate and saves cell energy, but once the cell has found the right location, in order to be secured in position, the substance must be removed. Removal of the polysialic acid substance is also necessary for the dendrites (neural appendages) to connect with other neurons and begin to communicate. This process has been well known for many years, but what controls the process has been a mystery.
What happens to the slippery molecules when the cell no longer needs it? This team spent years trying many growth processes under various conditions before finding a clue. Actually, they found two clues. First, they learned that cells internalize the polysialic molecule dependent on cues received from collagen in the extra cellular matrix and gaseous molecules of nitrc oxide.
Then they found that if there is insulin in the matrix, the cell cannot absorb the slippery molecules. Parkinson’s and Alzheimer’s brains are less sensitive to insulin, so insulin is blocking the removal of the polysialic acid causing the cell to be unable to connect or communicate properly with other cells.
Dr. Maurice Curtis was the director of the study, and the experiments were done at the Centre for Brain Research laboratories in Aukland, New Zealand. Other researchers on the team were Dr. Hector Monzo, Distinqguished Professor Richard Fauli, Dr. Thomas Park, Dr. Birger Dieriks, Diedre Jansson and Professor Mike Dragunow. They have now begun testing new drug compounds to target the removal of polysialic acid from cells in hopes of improving the migration and connectivity of new stem cells in the brain.

Insulin and IGF1 modulate turnover of polysialylated neuronal cell adhesion molecule (PSA-NCAM) in a process involving specific extracellular matrix components
Hector J. Monzo1,2, Thomas I. H. Park1,3,Victor Birger Dieriks1,2, Deidre Jansson1,3,Richard L. M. Faull1,2, Mike Dragunow1,3,Maurice A. Curtis1,2,*
DOI: 10.1111/jnc.12363 Article Accepted for Publication

Video Games for Therapy – Nintendo Wii Benefits PD

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Video game aficionados have pretty much abandoned the Nintendo Wii….moving on to the next generation and looking for more action, excitement and better screen images.  Medical doctors, physical therapists and people with Parkinson’s are embracing the Wii…and its ability to improve balance and reduce falls.

Spending just 20 minutes a day playing three different Wii games along with workouts on treadmill and exercycle improved scores on the Unified Parkinson’s Disease Rating Scale (UPDRS) and the Tinnetti Balance Test. Dr. Antonella Peppe, a research professor at the Fondazione Sana Lucia in Rome did a pilot study with people with Parkinson’s and found the Wii balance board stimulated the central nervous system.  Improvements in rigidly, movement fine motor skills and energy levels were reported by all the participants  Dr. Peppe’s study confirms the results of other studies.

A different study was done at the Medical College of Georgia.Twenty people with Parkinson’s used the Wii for an hour, three times a week for four weeks.  They played bowling, tennis and boxing, all of which require balance, quick thinking, movement and exercise.  It not only improved all their motor scores, it improved energy levels and alleviated depression, too.  Dr. Ben Herz was the investigator.  He is program director for the school of occupational therapy at the Allied School of Health Sciences.  This study used people who had never had therapy for Parkinson’s,  so they had no preconceived notions of what therapy should be like.  Finding that it involved video games was a big surprise.  But in the end, it was so useful and made them feel so good that more than half of them bought the Wii to use at home.  Dr. Herz says he thinks game systems like the Wii are the future of occupational rehabilitation.

Medical College of Georgia (2008, April 7). Occupational Therapists Use Wii For Parkinson’s Study. ScienceDaily. Retrieved June 25, 2013, from­/releases/2008/04/080407074534.htm

Alexithymia and Impulsive Behavior in Parkinson’s Disease

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A very interesting preliminary report presented at the annual Movement Disorders Society meeting in Sydney looks at impulsive behavior in people with Parkinsons.  Dr. Katharina Goerlich-Dobre from the Department of Neurology at Christian-Albrechts University in Kiel, Germany studied 91 people with Parkinson’s and tested them for alexithymia and found a close correlation between impulsive behaviors and a risk for pathological additive behaviors in people who scored high in alexithymia.

The word alexithymia comes from the Greek “A” for “lack”, ,”lexis”  for “word” and “thymos” meaning emotion.  It was first described by psychiatrists Peter E. Sifneos and John C. Nemiah in 1972 when patients they were working with displayed a marked difficulty in talking about their emotions.  Since then, it has received more attention in psychology and has come to be understood as difficulty identifying feelings or distinguishing between bodily sensations and emotions, a lack of certain types of imagination and difficulty talking about their own feelings or the feelings of others.  People with alexithymia often are rather rigid in the way they relate to life events, tending to be more focused on the mundane or the minute details of daily living.  They are more externally oriented, and tend to prefer to live with strict rules, social conformity and in predictable patterns and may try to maintain them compulsively.  They may be very intellectually accomplished, but are unable to relate to spontaneously imagined or inspired situations or events.   When presented with situations that they find unpredictable, they may make hasty decisions , impulsively, because they are unable to imagine what the outcome of the decision might be.

Anxiety, compulsivity, impulsivity and depression are often discussed in Parkinson’s literature, but little attention has been given to alexithymia.  Dr. Goerlich-Dobre found that many individuals with Parkinson’s are unable to identify their feelings or may suppress feelings they cannot put into words.  She says “The possibly intense emotional arousal accompanying those feelings may prompt alexthymic individuals to engage in impulsive-compulsive behaviors in order to quickly alleviate their distress, as their access to healthier ways of processing those feelings is compromised.”

Neuropsychiatric assessments of Parkinson’s patients’ emotional awareness with an inclusion of alexithymic evaluations my help identify patients who are at risk of impulsive or compulsive behaviors, including pathological addictive behaviors.

Parkinson’s Symptoms Reduced by Smoking Cannabis

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Ruth Djaldetti, M.D., of Tel Aviv University in Israel, presented the findings of her research at a recent International Congress on Parkinson’s Disease and Movement Disorders.  She reported improvement in tremor, pain, rigidity and bradykinesia (slowness of movement).  Twenty subjects, all in their mid-sixties, and were rated using the Unified Parkinson’s Disease Rating Scale (UPDRS) both before and after smoking.  Their overall “before” scores were over 30 and within 30 minutes of smoking, their scores dropped to 24..  Their tremor scores averaged 7.5 on the UPDRS before and dropped to a score of 3.5 after smoking cannabis.  Bradykinesia scores dropped from 13.2 to 8.6 and rigidity went from 7.4 to 6.4.  Dr. Djaldetti also saw a marked relief in the pain her subjects were experiencing and this relief of pain led to better sleep and feeling more rested.

This bears out the results of other studies.  A study done in Great Britain that was published in 2011 found the principal ingredient in cannabis provided neuroprotection for people with Parkinson’s disease.  Its neuroprotective properties included reduction of inflammation and control of spasms, making it an ideal drug for treating Parkinson’s.  However, its confusing legal status make it very difficult for people to obtain or consider using and for doctors to even recommend to patients.

Another interesting study done in 2010 found that cannabinoid receptors are located in many parts of the brain and that cannabinoids are produced naturally in the brain.  People with Parkinson’s have even higher levels of endocannabinoids (cannabinoids produced within the brain).  The main ingredient in cannabis, Tetrahydrcannibol (THC) actually increases dopamine production temporarily.  Cannabidiol (CBD) another component of cannabis, also provides neuroprotective properties and has been shown to reduce dystonias .  CDB could be a very vital improvement for treating Parkinson’s, and a recent study has shown it useful in treating certain cancers as well.

While there have been many, many people reporting the anecdotal benefits of smoking cannabis, clinical trials are lagging behind.  Laboratory and animal studies have shown many benefits, but perplexing issues around the legality of cannabis are slowing the efforts and impeding progress.


For a review on Cannabis for Treatment of Movement Disorders go to:

More News from the Movement Disorder Society Annual Meeting

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Three more stories from the annual Movement Disorder Society meeting that was held in Sydney, Australia.

Researchers from Lund University in Lund, Sweden and the Van Andel Research Institute in Grand Rapids, Michigan, have developed a potentially useful new mouse model for studying Parkinson’s disease.

The accumulation of α-synuclein is one of the hallmarks of the development of Parkinson’s disease.   If scientists can recreate this process in a mouse model, it will go a long way toward furthering their understanding of the cause of Parkinson’s.  While some mouse models demonstrate certain particular pathologies of PD, they do have limitations.  One such limitation is in demonstrating the progressive development that duplicates the slow accumulation of α-synuclein and loss of motor and non-motor symptoms as it happens in humans.  This team of researchers has developed a new transgenic mouse model that parallels the slow age dependent  accumulation of α-synuclein and demonstrates the behavioral deficits seen in humans.  Understanding how α-synuclein increases in the brains of mice gives research a new tool to study how to treat it in humans and to better understand the causes of PD.

It has been suspected for some time that people with Parkinson’s develop malignant skin cancers more often than the general population.  A study done through the University of Rochester demonstrated that Parkinson’s does bring a four fold greater risk.   A new clinical trial followed 1700 newly diagnosed Parkinson subjects and researchers estimated that in this population there should be about just under four cases of malignant melanoma.  In fact, they found 13 cases of new malignant melanoma.  Why this is so is not yet understood.  These findings prompted Matthew Stern, M.D. the Movement Disorder Society President-elect to say “This study underscores the importance for dermatologic screening in PD patients.  Further, elucidating the relationship between PD and melanoma may shed light on the pathogenesis of both disorder.”

Reducing cognitive impairment in Parkinson’s is the goal of another study out of Newcastle University in Great Britain.  They tested the effects of the drug apomorphine that has been used for over 20 years in Europe to reduce motor fluctuations in advanced PD.  α-Synuclein accumulations are one known cause of dementia in PD, but amyloid -beta  (Aβ) accumulations also contribute to dementia.  This study looked at the brain tissue samples from both cognitively impaired and not impaired deceased Parkinson’s patients.  They found that brain tissues of people treated with apomorphine for motor complications while living and found  lower levels of Aβ.  These findings suggest that apomorphine treatment may have significantly lowered the Aβ burden in the brains of non cognitively impaired individuals and alsomay have reduced the cognitive impairment in the cases of noted dementia.

Researchers stressed that this is an on-going investigation, but that it may be able to lead to a therapeutic treatment for dementia in PD and eventually lead to clinical trials.


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