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.

Notes from the Movement Disorders Society Annual Meeting

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The Movement Disorders Society held its annual convention in Sydney, Australia recently.  Many interesting topics dealing with Parkinson’s disease were discussed.  Some of those topics will be addressed here.

A report on mild cognitive impairment in Parkinson’s by Alison Yarnell, from Newcastle University in the United Kingdom, showed that if cognitive impairment was present at the time of Parkinson’s diagnosis, the patient had a higher risk for developing dementia later in the disease progression.  A clinical trial compared neurological and cognitive assessments of 219 newly diagnosed subjects with Parkinson’ s to 99 age-matched controls.  Cognitive assessments covered global cognition, attention, memory, executive function, visuospatial function and language.  Subjects were classified dependent on their scores.  Memory impairment was the most common, with 15 percent of the subjects affected followed by visuospatial deficit s in 13 percent, attention in 12 percent and executive function at 11 percent.  Other studies have shown cognitive impairment in as many as 25 percent of the Parkinson’s population with many going on to develop dementia within three years of diagnosis  The author of this study stressed that cognitive testing should be done at the time of diagnosis to both get a baseline and also to determine which patients might be in need of closer monitoring.  By determining cognitive status early on in the course of the disease, therapeutic interventions may provide better results.

Clinical trial design was another interesting topic at the MDS meeting.  Dr. Tiago Mestre from Toronto Western General Hospital in Ontario, Canada, raised the question of how participants’ attitudes and reactions to placebos in double blind trials influenced the evaluations of the effectiveness of the therapeutic agent being evaluated.   To try to understand if this is indeed a real effect, a systematic review of double-blind, randomized, controlled trials of dopamine agonists in Parkinson’s that used a placebo or an active control.  The analysis of their preliminary results did show a clinically significant impact of decreased effectiveness of the medication being tested.  Therapeutic effectiveness might be even higher for the drug being tested than trial results indicate.  This negative effect of a placebo in a trial is called the “Lessebo” effect.

One commenter also raised the question of the “nocebo” effect…where if a patient is given a placebo, or non-therapeutic substance, by an authority figure who assures them of the benefit, a benefit will be experienced.  Another patient who is more skeptical and less trusting  might experience a harmful effect, when, indeed, the “active” ingredient is not known to cause harm.

Dr. Rajesh Pahwah , from the University of Kansas Medical center presented research on a new formulation of an older medication has shown promise in controlling levodopa induced dyskinesias in Parkinson’s. There are currently no approved medications to treat levodopa induced dyskinesias.  It is still in the investigational stages, but a timed-release form of amantidine has been successful in a small clinical trial.  Amantidine has been around for a long time, and has been used to reduce dyskinesias but  doses hight enough to be effective have often not been well tolerated.  .The new formulation is designed to gradually increase the availability of the drug in the day time, when the dyskinesias are the most disturbing, and to limit the overnight concentration thereby helping to relieve insomnia and sleep disturbances.  Because higher doses can be administered gradually in timed-release, effectiveness and tolerability are both improved.  The new formulation, called a “chronotherapeutic” pharmacokinetic  profile, is not yet FDA approved and not out of the clinical trial testing stages.  Some mild adverse events have been reported, but the company is seeking the advice of the FDA on continuing development of this medication.

Diffusion Tensor Imaging to Diagnose Movement Disorders

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A team of researchers at the University of Florida used a special imaging technique to identify markers in brain regions to help identify specific movement disorders whose clinical symptoms often appear similar but have different origins in the brain.  Parkinson’s disease, multiple system atrophy, essential tremor or supranuclear palsy have symptoms that are very similar in the early stages of the disease which makes a definite diagnosis very difficult.

David Vaillancourt is the team’s principal investigator.  He is an associate professor in the department of applied physiology and kinesiology.  Over a three year period, he and his team have examined 72 patients with movement disorders using the imaging technique Diffusion Tensor Imaging.  They also anticipate testing between 150 and 180 new subjects in the next few years.

DTI, as it is called, is a non-invasive imaging process that together with magnetic resonance imaging (MRI) is able to examine structures deep within the brain and characterize the properties of those structures on a microscopic scale much more detailed than imagery alone can provide.  By sensitizing the MRI signal, it can analyze the random molecular motion of water molecules which provides insights ot the organization of the micro structures.

Dr. Vaillancourt stated that the primary goal of this study was to be able to use DTI to accurately predict the correct disease.  When a new patient presents with symptoms, this technique will make diagnosing the symptoms possible early in the disease progression.  Diagnosis and treatment can be tailored from the beginning, eliminating possible changes to diagnosis as various symptoms progress or response to medication is inadequate.

Of the 72 subjects they have so far examined, they have been able to diagnose and separate the patients into specific movement disorder groups very accurately.  The results of this study will be published in the journal Movement Disorders.


Prodoehl, J., Li, H., Planetta, P. J., Goetz, C. G., Shannon, K. M., Tangonan, R., Comella, C. L., Simuni, T., Zhou, X. J., Leurgans, S., Corcos, D. M. and Vaillancourt, D. E. (2013), Diffusion tensor imaging of Parkinson’s disease, atypical parkinsonism, and essential tremor. Mov. Disord.. doi: 10.1002/mds.25491


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