Parkinsons News: 273 headlines
Watch this Muhammad Ali Parkinson's video!
Celebrity Fight Night Video
Presented by MD Health Channel

Celebrity Fight Night:
122 Photo-Slideshow
CLICK HERE
Watch Muhammad Ali fight clips on this Parkinson's video!

Sources used by our Parkinsons News Channel Research Team:
The New York Times, CNN, FOX, CBS, BBC, Mayo Clinic, Johns Hopkins Medicine, UCLA Medical Center, National Institute of Health, Stanford Hospital, Memorial Sloan- Kettering, Yale Cancer Center, Massachusetts General Hospital, Brigham and Women's Hospital, University of Michigan, M. D. Anderson Cancer Center, National Institute of Health, American Cancer Association, NBC, Reuters News, American College of Cardiology, Journal of the American Medical Association & 100's more

Links
Barrow Neurological Institute

Archives

This page is powered by Blogger. Isn't yours?

Saturday

 

Cinnamon could fight Parkinson's as spice found to be source of chemical that helps protect brain

Wednesday

 

Post on parkinsons: UCLA Researchers Identify New Gene Involved in Parkinson’s Disease, a Finding that may Result in New Treatments for the Debilitating Disorder

Monday

 

Prevalence, Determinants, and Effect on Quality of Life of Freezing of Gait in Parkinson Disease

Friday

 
ALZHEIMER'S STUDY FINDS 11 GENES WHICH CONFIRM IT'S OVERLAP WITH MS PARKINSONS














New genes linked to late-onset Alzheimer's have been discovered, giving scientists clues on how to create better drugs to fight off the disease. Researchers in the multinational International Genomics of Alzheimer's Project (IGAP) have found 11 genes which broaden our understanding of the disease and confirm its overlap with other neurodegenerative diseases like Parkinson's and multiple sclerosis.
Read more »

 

Impaired new learning found in persons with Parkinson's disease

Wednesday

 

Santhera Receives US Patent for Fipamezole in the Treatment of Parkinson's

Friday

 

Dr. Sanjay Gupta: 'I'm Doubling Down On The Legalization Of Medical Marijuana'


Dr. Sanjay Gupta — CNN’s chief medical correspondent — revealed on aReddit “Ask Me Anything” this week that he’s “doubling down on the legalization of medical marijuana.”

In the AMA, Gupta tried to dispel some medical myths about pot and pointed out that it’s safer than many narcotic pain pills that doctors prescribe.

Gupta has waged a campaign to change perceptions about pot and argue for its medical legalization since he changed his opinion on the issue in August.

Here are a few highlights:

What are your thoughts towards using high percentage CBD strains to help people with Anxiety? Do you think that using CBD in combination with therapy could be effective and less dangerous than other drugs such as Prozac or Xanax?

I think so. We have a better understanding of how CBD works in the brain, and the receptors where it binds. There are many prescription drugs that have a much higher risk than cannabis, but are prescribed often. Narcotics, in particular. We consume 80% of the world’s pain meds in the United States.

What is the best method of marijuana ingestion?

It is probably vaporizing. I think smoking creates a lot of byproducts that we don’t know enough about. I think eating it leads to very uneven absorption. Vaporizing seems to activate the medicine without burning it. I also think oils absorbed in the mouth are effective, especially for kids.
Read more »

Thursday

 

Relationship between poor decision-making process and fatigue perception in Parkinson’s disease patients

Fatigue is a common non-motor symptom in Parkinson’s disease patients. The reasons for its perception are not completely understood. One suggested possibility might be that perceived fatigue is related with abnormal interpretation of somatic symptoms. It has been described that somatic markers misinterpretation leads to poor decision-making. We hypothesized that fatigued Parkinson’s disease patients would show poorer performance than non-fatigued in a decision-making task. To test our hypothesis, 89 Parkinson’s disease patients were assessed for the presence of fatigue using the Parkinson Fatigue Scale. All patients were also administered scales evaluating psychopathology and neuropsychological tests, including the Iowa Gambling Task. 33 (37.1%) patients fulfilled established criteria for fatigue. In the univariate analysis, fatigued patients showed higher levels of anxiety (state: p =0.001, trait: p< 0.001), impulsivity (p= 0.051), and depression (p <0.001) than non-fatigued patients. No statistically significant differences in other neuropsychological test results (Stroop, Trail Making Test, Tower of London) were found between fatigued and non-fatigued patients except for the Iowa Gambling Task, in which fatigued patients showed poorer performance (p =0.001) after controlling for confounding factors. These results suggest that fatigued Parkinson’s disease patients may present abnormal decision-making process, which may reflect abnormal processing of somatic markers when faced with an activity that requires effort.
Click to read more

Friday

 

New warning suggested for Ambien...the same sleeping pill that landed a Kennedy before a jury: says patients shouldn't drive for 8 hours after they take meds like Ambien

Wednesday

 

Clinical studies still overlook gender difference, which leaves women at a disadvantage and could endanger their health, according to a new report

 

OMG OF THE WEEK: Medical treatments harmed nearly a third of nursing home residents, according to a government watchdog report

Tuesday

 

As Full Disclosure Nears, Doctors’ Pay for Drug Talks Plummets

Sunday

 

Newl therapy helps Parkinson's patients regain voices


Many people lose the ability to be heard with the onset of any number of neurological conditions consisting of stroke, cerebral palsy, multiple sclerosis and Parkinson’s disease.
Through speech therapy, there’s help for diseases that weaken voices. Solutions also can come with a therapy called Lee Silverman Voice Treatment.
The protocol was developed by two speech language pathologists and is named after one of the first patients to undergo the program.
The greatest silencer of voice comes with Parkinson’s disease. Researchers estimate that 89 percent of people with Parkinson’s exhibit difficulties with speech and voice. Their voice volume decreases, and they have an increase in vocal tremors.
Even Grammy Award-winning singer Linda Ronstadt said she no longer can perform because of Parkinson’s.
The disease also alters the personal capacity to recognize soft speech. Scores of patients are unaware they’re whispering. Family members are affected because, many times, they’re cut off from parts of conversation.
More than 4 million people worldwide have been diagnosed with Parkinson’s. That translates to 1 in every 500. The risks increase with age and the average onset is at 65.
It can be devastating to be diagnosed with a neurological or nervous system disorder that robs control of our bodies. We digress with alarming new rules that govern our posture, muscles and gait. In the course of a few years, we begin to stoop, trip and fall. And all muscles are affected, including the ones that control voices.
“Every aspect of your interaction with others is affected when you lose your voice,” say Lisa M. Purdy, a certified speach language pathologist. She says Parkinson’s has no cure, but there are positive ways to be heard.
Therapy brings additional awareness and teaches a new normal to those patients who have lost their natural speaking voice.
“We bring attention to a louder volume of voice, and through repeated effort, patients adapt to speaking in decibels that can be heard,” Purdy says. “We also work with family members and give them cues to help their loved ones communicate.”
Patients can gain better perception of posture and breathing to enhance communication. Purdy says the new-found techniques instill recognition of correct volume. The knowledge allows patients to self-correct a whisper into an audible sound.
LSVT treatment can help 90 percent of Parkinson’s sufferers, according to extensive clinical trials. The results show a positive impact with improving voice volume disorders. Patients with conditions of stroke, cerebral palsy and multiple sclerosis also benefit from voice therapy.
“Working to restore patients’ interaction with others is very rewarding,” Purdy says.
She says the rewards come by seeing their patients improve with confidence and a better sense of self.
Laureen Lowe-Albrecht is licensed in physical therapy, specializing in senior health and wellness. Contact her at lalbrecht@ 
MelbourneTerraceRehabCenter or call 321-725-3990.

Read more 

 

Study: Pesticide Exposure Tied to PD Risk

Exposure to pesticides and solvents appears to be a risk factor for Parkinson's disease, a meta-analysis found.
Based on an analysis of 89 prospective and case-control studies, exposure to bug or weed killers and solvents increased the risk of developing Parkinson's disease by 33% to 80%, reported Gianni Pezzoli, MD, of the Parkinson Institute, Istituti Clinici di Perfezionamento in Milan, and Emanuele Cereda, MD, PhD, IRCCS University Hospital San Matteo Foundation in Pavia, Italy.


Thursday

 

Video: What works, What Doesn’t

What works and what doesn't work in Parkinson's? We asked four experts in the field for their take:Mahlon R. DeLong, MD, professor of neurology at the Emory University School of Medicine in Atlanta; C. Warren Olanow, MD, chairman emeritus and professor in the department of neurology at the Icahn School of Medicine at Mount Sinai in New York City; Mark Stacy, MD, professor of neurology at Duke University; and David Standaert, MD, PhD, professor and chair of the department of neurology at the University of Alabama at Birmingham. In this video, they discussed surgical interventions, levodopa as the "gold standard," managing disease, the role of exercise, and biomarkers for disease progression. Challenges include looking past levodopa and moving from laboratory targets to drugs.

Click to watch video

Tuesday

 

A Tissue Test for Parkinson Disease?

Editor's Note:
Medscape recently spoke with Charles H. Adler, MD, PhD, Professor, Department of Neurology, Mayo Clinic College of Medicine, Scottsdale, Arizona, about his past and future research into the potential of submandibular gland biopsy as a useful diagnostic tool in Parkinson disease (PD).
Medscape: Please tell us about your study looking at the potential use of submandibular gland biopsy in PD diagnosis.
Dr. Adler: We have something called the Arizona Study of Aging and Neurodegenerative Disorders that has been ongoing for the past 17 years. As part of the study, all participants agreed to an autopsy at the end of life. Initially, only brain biopsies were performed, but since 2005 the patients have undergone whole-body autopsies.
I run the clinical part of the study, whereas my neuropathologist colleague Dr. Tom Beach handles the autopsy and pathology part. Dr. Beach has done a survey of multiple different organs looking for phosphorylated synuclein staining in areas other than the brain. [Editor's note: Aggregates of the alpha-synuclein protein are a pathologic hallmark of PD.] He found dense synuclein staining in the submandibular gland; all 28 patients with PD who were autopsied had evidence of phosphorylated synuclein staining in their submandibular gland.
Dr. Beach did a proof-of-concept study where by doing a needle biopsy in frozen tissue, he was able to identify 17 of the 19 cases with synuclein staining. It meant that 2 of them did not show synuclein in the needle biopsy, so somehow the tissue that had the synuclein staining was missed.
We then translated that finding to the clinic and did a study looking at 15 patients with advanced PD, meaning patients who had had disease for more than 5 years. The reason we chose that population is that in the autopsy series that Dr. Beach did, the disease duration was pretty advanced because those patients had already come to autopsy -- so the majority of patients had had PD for more than 5 years.
In a biopsy study that's now in press, we did a biopsy in 15 patients, 12 of whom had submandibular tissue we could look at, and 9 of those patients were synuclein-positive. We took that as proof of concept that you actually can find phosphorylated alpha-synuclein staining in living human submandibular glands.
We have moved forward now with the current study, which is to look at 25 patients with earlier or shorter disease duration -- meaning disease duration less than 5 years -- and 10 controls as a comparison group to make sure that the staining is only picking up synuclein in persons who do have PD.
Medscape: Could you talk about the methods of this new study.
Dr. Adler: I first examine all participants -- both those with PD and the controls. For the patients with PD, we then do a dopamine transporter scan called the DaTscan, looking to see whether they have abnormalities in dopamine uptake that would be suggestive of PD. We do a smell test of all the individuals in this study, because individuals with PD usually have loss of the sense of smell. Those are 2 other markers that we're looking at.
Then we have 1 of 2 ear, nose, and throat doctors in the practice do the biopsies. The biopsies are done by putting some numbing medication in the skin overlying the submandibular gland, which sits right under the jawline, and then we do 4 or 5 needle passes per patient. Dr. Beach then stains the samples for synuclein.
Medscape: Have you begun collecting data yet?
Dr. Adler: We've enrolled 18 or so patients out of the 35 who need to be enrolled, so we're a little over halfway through enrollment. We haven't looked at any data yet.
Medscape: Do you have a sense of where in the disease course synuclein might be detected compared with other markers of PD, such as olfactory dysfunction?
Dr. Adler: I think that's part of what we're trying to determine. The question is how early can we actually detect synuclein in the gland, and that's something we don't know yet. My expectation is that of the 25 individuals with PD, we should get a good idea of what percentage of those cases are positive to be able to say that this does or does not happen early in the disease course.
Is it a premotor marker? Is it possible that if you were to biopsy samples from people who have loss of the sense of smell, they would have synuclein in the submandibular gland even before they had tremor or slowness of movement? Those are all questions that would still need to be answered.

Wednesday

 
Trigger Medications and Patient-Related Risk Factors for Parkinson Disease Psychosis Requiring Anti-psychotic Drugs

Read more »

 
A new gene therapy approach was safe and well tolerated for Parkinson's
Read more »

 
STUDY: Inosine Safe, Raises Urate Levels in Early Parkinson's
The findings of the Safety of Urate Elevation in PD (SURE-PD) study suggest that inosine should be further developed as a potential disease-modifying therapy for patients with PD, the investigators, led by Michael A. Schwarzschild, MD, PhD, professor, neurology, Harvard Medical School, and Massachusetts General Hospital, Boston, conclude.
READ MORE

 
Robot-Assisted Walking Training for Individuals With Parkinson's Disease
Robot training is a feasible and safe form of rehabilitative exercise for cognitively intact people with mild PD. This original approach can contribute to increase a short time lower limb motor recovery in idiopathic PD patients. The focus on the gait recovery is a further characteristic that makes this research relevant to clinical practice. On the whole, the simplicity of treatment, the lack of side effects, and the positive results from patients support the recommendation to extend the use of this treatment. Further investigation regarding the long-time effectiveness of robot training is warranted.
READ MORE

 
 Swiss drugmaker Roche has found an efficient way for complex antibody drugs to penetrate the brain
"We have basically designed this module, called shuttle, that binds to this transport mechanism and shuttles a cargo inside the brain," Luca Santarelli.  Results of a study published January 8 in the journal Neuron found the technology helped to increase the concentration of antibodies in the brains of mice, reducing the amount of amyloid plaque -- a hallmark of Alzheimer's.
READ MORE

 
 Studies show that walking frequency is associated with depression among older adults
although significant associations between walking frequency and subsequent depressive symptoms were not found, it seems premature to conclude that promoting walking is not a relevant strategy to protect against depressive symptoms. There are also ample data to recommend walking for physical health reasons. Future research could investigate prospective associations between meeting recommendations for physical activity levels and depressive symptoms in older people.
READ MORE

Monday

 

For Doctors, Nurses and Primary Care Providers


The 2013 Aspen Course on Parkinson’s Disease and Other Movement Disorders

The 2013 Comprehensive Review of Movement Disorders for the Clinical Practitioner (Aspen Course) marked the 23rd anniversary of this long-standing program on Parkinson’s disease (PD) and other movement disorders. Drs Stanley Fahn, Mark Hallett, and Joseph Jankovic are the course founders and directors. Medscape is pleased to have the highlights of this year’s program discussed in the activity below. The faculty will provide updates on Parkinson’s disease, psychogenic movement disorders, and Huntington’s disease (HD).

A primary goal of the treatment of PD is curing the disease by stopping its progression and restoring the patient to a healthy, normal state. Restoration seems unattainable at present, but slowing disease progression based on the above advances in the basic science of PD seems approachable in the not so distant future. Many attempts at disease modification have been carried out in a number of controlled clinical trials. Most drug trials ended in failure, including trials of coenzyme Q10, creatine, pramipexole, tocopherol, riluzole, and two antiapoptotic agents: TCH346 and CEP-1347. Two controlled surgical trials also failed to slow or reverse PD: intraputaminal infusions of the glial-derived trophic factor (GDNF) and the gene therapy trial of implants of viral vectors containing the gene for neurturin (a member of the GDNF family). So far, only trials of the monoamine oxidase type B inhibitors selegiline[27,28] and rasagiline[29] have provided hints of slowing clinical progression, although a symptomatic effect could possibly account for their benefit. Levodopa was also studied, but interpretation of the results showed incongruity between the clinical and imaging components of the trial.[30] A recent open-label trial suggests that exanatide might have neuroprotective potential.[31] It would be most cost-effective if a suitable animal could be used to test potential neuroprotective agents. As mentioned above, new animal models based on genetics or spread of rogue α-synuclein may prove to be feasible models to study potential neuroprotective agents.

A major development in the clinical understanding of PD is the recognition that the disorder is not simply one marked by motor difficulty (the 6 cardinal features of parkinsonism are tremor-at-rest, bradykinesia, rigidity, loss of postural reflexes, flexed posture, and freezing of gait) but also by the presence of nonmotor features (Table 1).[1] Patients with PD usually have 10 to 12 nonmotor symptoms,[2] some of which often occur several years before the first motor symptom. This is especially true of reduced sense of smell, constipation, and acting out one’s dreams (also known as rapid eye movement [REM] sleep behavior disorder [RBD]). In a 16-year follow-up of men with RBD, 81% developed a parkinsonian disorder with a mean interval of 13 years.[3] Depression and anxiety are also often early features. Cognitive decline with frank dementia is also common, but this condition usually occurs later in the disease course and is more related to the patient’s current age (late 70s through 90s); dementia is eventually seen in up to 80% of patients with PD.[4]

With the typical presentation of insidious onset of unilateral rest tremor and bradykinesia (such as small handwriting, decreased arm swing, and decreased leg swing on walking), the diagnosis is relatively easy. Difficulties arise in distinguishing between tremor of PD and tremor seen in essential tremor; when parkinsonism is present without tremor, raising the possibility of so-called atypical parkinsonism or Parkinson-plus states; and when a gait disorder of a slow shuffling gait with loss of balance is observed. The tremor of essential tremor differs from that of PD in that the former is a tremor of action. This can be seen with writing, including the drawing of Archimedes’ spiral, or with the finger-to-nose maneuver. Occasionally a patient may have both conditions, so the diagnosis can be initially puzzling. The neuroimaging procedure known as DaTscan can help distinguish between the two conditions. DaTscan is a single photon emission computer tomography (SPECT) scan in which the radioligand binds to the dopamine transporter that is located on the dopamine nerve terminals in the striatum. In PD, there is asymmetrical loss of the nerve terminals, and hence, an asymmetrical reduction is detected in the DaTscan. In essential tremor there is no loss of radioligand binding. Although this SPECT scan can be helpful in differentiating between the two conditions, the scan is sometimes difficult to interpret and expertise is required.[5]

The DaTscan is not helpful in distinguishing between PD and Parkinson-plus syndromes (progressive supranuclear palsy, multiple system atrophy, and cortical basal syndromes) because all of these have striatal dopamine deficiency. The presence of additional neurologic signs -- such as ocular involvement, orthostasis and other forms of dysautonomia, early freezing of gait, early falling, and lack of dramatic response to levodopa therapy – is a clue that the patient may have a Parkinson-plus disorder. A slow, short-stride gait with falling or fear of falling is a common gait disorder. This can sometimes be the onset of PD, but often it is due to cerebrovascular insufficiency (vascular parkinsonism), normal pressure hydrocephalus, or a poorly understood syndrome of senile gait disorder. These conditions do not respond well to levodopa, but this medication could be tried to make sure the patient does not have an unusual presentation of PD. READ MORE




Thursday

 

Celebrity Fight Night raises millions for charity


Reporter-Phoenix Business Journal

The annual Celebrity Fight Night event raised more than $7 million last weekend to support charities such as the Muhammad Ali Parkinson Center atBarrow Neurological Institute in Phoenix.
Hollywood stars, singers and professional athletes converged on the J.W. Marriott Desert Ridge Resort and Spa on March 23 for Muhammad Ali’s Celebrity Fight Night XIX. This year’s event raked in $7.2 million for Parkinson’s research.
Celebrities such as Billy Crystal, Jennifer Lopez and Billy Ray Cyrus attended the black-tie event, which featured a live auction featuring one-of-a-kind luxury items as well as a separate silent auction.
The live auction featured a dinner withReba McEntire at her Beverly Hills, Calif. home, with special guests Tom Hanks, Rita Wilson and David Foster, which went for $800,000 – two bidders paying $400,000 each.
Other auctioned prizes included two tickets to Tom Hanks’ upcoming Broadway show “Lucky Guy,” plus a backstage meet and greet, a weeklong trip to Tuscany and a special VIP performance by Andrea Bocelli followed by a private dinner with the musician himself, which sold for $550,000.
Each year dozens of celebrity guests attend the event, which has raised $87 million dollars in 19 years. The Celebrity Fight Night Foundation was founded in 1994.


   
Comparison of Once-Daily Versus Twice-Daily Combination of Ropinirole Prolonged Release in Parkinson's Disease

Background: Ropinirole prolonged release (RPR) is a once-daily formulation. However, there may be individual pharmacokinetic differences so that multiple dosing may be preferred in some individuals. This study compares once-daily and twice-daily RPR in patients with Parkinson's disease.
Conclusions: RPR is a once-daily formulation, but multiple dosing was preferred in many patients. Multiple dosing of RPR might be a therapeutic option if once-daily dosing is unsatisfactory.

 

A New Era in Parkinson Disease Diagnosis

CLICK HERE TO VIEW VIDEO

Biomarkers for Parkinson Disease


Bret S. Stetka, MD: Hello. I am Dr. Bret Stetka, Editorial Director of Medscape Neurology, and I am here today with Dr. Ken Marek. Dr. Marek is President and Senior Scientist at the Institute for Neurodegenerative Disorders, and he also leads the Parkinson's Progression Markers Initiative (PPMI) in collaboration with the Michael J. Fox Foundation for Parkinson's Research. Dr. Marek, welcome.

Kenneth Marek, MD: Thank you very much.

Dr. Stetka: I would like to talk to you today about the diagnosis of Parkinson disease. Although unfortunately, we have no cure yet, a lot of encouraging research is going on with respect to Parkinson diagnosis and monitoring disease progression, particularly with biomarkers and imaging. Can you review for us which biomarkers have been linked with the disease so far?

Dr. Marek: A wide array of biomarkers for Parkinson disease have been developed over the past decade. I can put them into 3 different categories.
The first category is clinical markers. These are clinical features that occur outside of the normal cardinal features of Parkinson disease -- so these are not motor abnormalities, but nonmotor abnormalities, such as loss of smell, autonomic dysfunction, depression, or change in cognition. Second, there are imaging biomarkers like MRI, but more productively, PET and SPECT imaging have provided us with tools that can identify the dopamine loss in Parkinson disease and track that loss.

Finally, there are biologic markers. These are markers in the blood and spinal fluid that may be particularly valuable in identifying early Parkinson disease and tracking the disease as well.

Dr. Stetka: Which of these biomarkers, if any, are being used in the clinic, or are most of them investigational at this point?

Dr. Marek: Many of the biomarkers for Parkinson disease are still investigational or even exploratory, but there are now markers that have made their way into the clinic. The most widely used is an imaging biomarker that is now available in the United States and Europe commercially called the DaTscan™ (GE Healthcare; Arlington Heights, Illinois). It targets the dopamine transporter protein, which is a protein on the dopamine nerve cell, and it has proven to be very useful in identifying early disease, and in a research setting in tracking disease.

It's important to emphasize that although these markers are available, they are not necessary for every patient, because most patients still can be identified clinically. But for those difficult cases, these biomarkers have now proven to be very useful as diagnostic tools.

Dr. Stetka: What about simpler biomarkers, such as olfactory dysfunction or sleep disorders? Are people screening for these in primary care yet, or are they still investigational?

Dr. Marek: An exciting aspect of Parkinson disease has been that the disease has broadened from a disorder of motor dysfunction and perhaps even beyond a disorder of central nervous system dysfunction to a more widespread disease of the nervous system. Such problems as olfactory dysfunction and autonomic dysfunction of cardiac or gastrointestinal neurons have begun to be useful predominantly as research tools, but hopefully soon will become more useful as clinical adjuncts to a diagnosis, and we will be able to identify individuals at risk for Parkinson disease at an earlier stage.

Newer Targets in Neuroimaging

Dr. Stetka: Let's move on to neuroimaging. I know that several groups, including your own, are researching various neuroimaging approaches in Parkinson disease. For example, some groups are trying to develop an alpha-synuclein tracer to localize Lewy body pathology. Can you review for us some of the more promising imaging studies that are under way?

Dr. Marek: Neuroimaging in Parkinson disease has had a fairly long history. In part, we have been very fortunate because the dopamine deficit in Parkinson disease has offered us a number of neuroimaging targets, and those targets are very useful, but as you suggest, newer targets are perhaps going to be even more useful. Such targets as alpha-synuclein and inflammatory changes that occur in Parkinson disease might be approaching the actual underlying pathology of the disease, so they are exciting tools that are just being developed. They are not here with us yet, but we would expect that they will be coming along over the next couple of years and will significantly change our ability to detect and monitor Parkinson disease.

Data for Everyone: The PPMI

Dr. Stetka: You are the principal investigator on the PPMI, in collaboration with the Fox Foundation, and you released some of your first biomarker data this week in JAMA Neurology.[1] Can you tell us what the PPMI is, and more about the new data?

Dr. Marek: PPMI is a large initiative that is designed to identify better progression biomarkers for Parkinson disease. The underlying goal is to provide neurologists and those in the pharmaceutical and biotechnical industries with the tools that they need to objectively measure changes in Parkinson disease. This is crucial for the development of drugs to slow down or even prevent the onset of Parkinson disease. This is an international observational study, which involves at this point 32 sites in the United States, Europe, and Australia. We are identifying and following rather comprehensively individuals with Parkinson disease, healthy persons, and individuals in their prodromal states (before they develop the motor symptoms of Parkinson disease) with a wide array of clinical imaging and biologic biomarkers.

Dr. Stetka: Is the idea that these data will be of open use to other researchers?

Dr. Marek: A very crucial aspect of this study is that we are fully committed to making these data available as they are acquired, so these data are available on the PPMI Website. I would urge anyone to go on the PPMI Website, where it is possible to have access to these data. We would love to have people in the neurologic community take a look at these data and contribute their thoughts to the study.

Common Ground in Neurodegenerative Disease

Dr. Stetka: There is a good deal of overlap among Alzheimer disease, Parkinson disease, and dementia with Lewy bodies, in terms of pathology. Do you see a day when a patient with a suspected neurodegenerative disease undergoes a battery of these biomarker or imaging tests to evaluate his or her risk for a particular condition, and how far off might that day be?

Dr. Marek: It is very intriguing that many neurodegenerative diseases seem to have some commonality with respect to etiology, as well as many of the symptoms that are manifested, and it is very likely that some of the biomarkers we are identifying for Parkinson disease could be useful in other disorders, such as Alzheimer disease and Lewy body disease. The reverse is also true. Results of ongoing efforts in Alzheimer disease may inform our work in Parkinson disease. An example of that is the research focused on spinal fluid markers in Parkinson disease. In that study, we are using the identical markers that were used in studies of Alzheimer disease and Lewy body disease. Comparing biomarkers among these disorders can be very informative.

Dr. Stetka: The ultimate goal of many of these biomarker studies is to facilitate more effective, earlier treatment. Can you speak about the broader implications of these studies in terms of how they may one day affect the management of Parkinson disease?

Dr. Marek: The entire goal of this study is to help us to accelerate therapies. The general way in which we can do that is by simply having tools that can be used to objectively measure disease, but the more specific way is that many of these biomarkers will hopefully identify subsets of individuals who may be affected in different ways. For example, some individuals with Parkinson disease might have more of a synuclein problem, whereas others have more of a LRRK2 problem. Using these biomarkers to direct therapy will also be extremely valuable in making those therapeutic trials more likely to be effective.
Dr. Stetka: Are there any therapeutic avenues you find particularly promising at this point?
Dr. Marek: A number of therapeutic avenues are promising, and many of them focus on our recent understanding of the genetics of Parkinson disease. We now understand that there are different genetic mutations that contribute to risk in Parkinson disease, and these afford us an opportunity to develop targeted therapies. Therapies focused on alpha-synuclein or LRRK2 are the 2 most prominent genetically derived therapeutic targets, but there are other more general approaches, such as looking at growth factors, that also have merit in Parkinson disease.

Dr. Stetka: It is great to know that this research is ongoing. Do you have any final thoughts?

Dr. Marek: I would encourage readers to take a look at the PPMI Website. We want everyone to contribute and be involved in this program.

Dr. Stetka: Dr. Marek, thanks so much for coming today. I hope that you can come back and update us on all of this exciting Parkinson disease research.

Dr. Marek: I look forward to doing that. Thank you very much.

 


Wednesday

 

Muhammad Ali Parkinson Center at Barrow Neurologial Institute

 

Muhammad Ali Parkinson Center at Barrow Neurologial Institute

 

FIGHT NIGHT



Thursday

 

ICPDMD: Long-Acting Ropinirole Eases Parkinson's Sleep Symptoms

PARIS, June 10 -- A new once-a-day formulation of ropinirole eases nighttime symptoms for Parkinson's disease patients, researchers here say.

Patients in two randomized controlled trials had an approximately 20% improvement in symptoms such as sleep disruption, cramping, nocturia, and confusion, according to lead author K. Ray Chaudhuri, M.D., of Kings College Hospital in London.

"Nocturnal symptoms are one of the most common complications of Parkinson's disease," Dr. Chaudhuri told attendees at the International Congress of Parkinson's Disease and Movement Disorders here. And these symptoms worsen as the disease progresses, he said.

Levodopa, the mainstay treatment for Parkinson's, usually controls these symptoms early in the disease. But effective duration of a single dose decreases as the disease progresses, so that by morning, advanced patients have little benefit from their last dose in the evening.

Dr. Chaudhuri and his colleagues tested the ability of prolonged release ropinirole (PRR) to address this problem in two large, phase III, 24-week clinical trials, one comparing PRR to placebo, and the other comparing it to standard ropinirole, given three times a day....full report in MedPage Today

Tuesday

 

VIDEO WEBCAST - Levodopa-Unresponsive Parkinson's Disease

Kapil D. Sethi, MD, Professor of Neurology; Director, Movement Disorders Program, Medical College of Georgia, Augusta
Medscape Today

Friday

 

Deep Brain Stimulation Bests Medical Therapy for Advanced Parkinson's Disease

January 8, 2009 — Results of a randomized trial show that compared with best medical therapy, deep brain stimulation (DBS) increased "on" time without dyskinesias and improved motor function as well as quality of life at 6 months in patients with moderate to severe Parkinson's disease (PD), but at the cost of increased serious adverse events (SAEs).......full story in Medscape Today

Tuesday

 

10 Techie Ways to Fight the Flu

Technologies like a flu-tracking app and phone wipes could help you get through flu season unscathed.
PC Magazine

Wednesday

 

Lifelong Management of Parkinson's Disease

Lifelong Management of Parkinson’s Disease: Diagnosis, Treatment and Emerging Therapies is an Internet-based educational activity containing two separate modules: Early Treatment Options; and Advanced Stage Parkinson’s Disease. There is no cost to participate.

Please note that each module must be viewed in its entirety before continuing education credits or a certificate of participation can be awarded.

To access the program for the first time you must register by clicking on the Register:Log In button (also located in the menu bar on the top left of the screen). As a registered user, you may view either module by clicking on the Activites button of the menu bar to select the module of your choice. You may return at a later date by logging in at the Register:Log In button. We encourage you to complete both modules.

This program was recorded at a live presentation in New York City on June 12, 2007. Each module consists of an educational presentation and Q&A derived from the meeting and employs a combination of audio, video and slides. At the conclusion of each module a quiz will become available. (Please disable pop-up blocking in order to access the quiz.) After achieving a passing score (at least 70%) and completing the program evaluation, you will be asked to select one of three credit certificates appropriate to your professional credentials: AMA PRA category 1 Credits™ (for physicians), ACPE credit (for pharmacists), a certificate of participation and completion (for other learners.) The certificate cannot be saved so be sure that your printer is connected before starting. We will however maintain a record of your participation.

http://www.pdtreatmenttrends.com/go/Home

 

A drink only occasionally may reduce the risk of dementia, perhaps because long exposure to low alcohol levels help brain cells survive other stresses

Judicious Drinking Associated with Reduced Risk of Dementia
MAYWOOD, Ill., Dec. 30 -- Having a drink only occasionally may reduce the risk of dementia, perhaps because long exposure to low alcohol levels help brain cells survive other stresses, researchers here said.
Medscape Today - Full story

 

Keeping Blood Sugar Low May Help Lessen Memory Loss

NEW YORK, Dec. 30 -- Lowering blood glucose levels may help lessen the cognitive decline of normal aging, even in diabetes-free patients, researchers here said.
MedPage Today - Full story

Monday

 

Sleep Disorder May Lead to Parkinson's Disease or Dementia

Risk Is More Than 50% After 12 Years
December 24, 2008 — Patients with rapid-eye-movement (REM)–sleep behavior disorder (RBD) face close to a 20% 5-year risk of developing Parkinson's disease (PD) or dementia, and that risk rises to more than 40% after 10 years and exceeds 50% after 12 years, new research shows.
MEDSCAPE TODAY

Thursday

 

Early Management of Parkinson's Disease: When to Start, What to Start With, and Why

Wednesday

 

Stem cells: What they are and what they do - MayoClinic.com

 

Early Management of Parkinson's Disease

CLICK ON LINK TO WATCH VIDEOEarly Management of Parkinson's Disease

 
Virtual reality device helps multiple sclerosis patients walk

Technion-Israel Institute of Technology scientists have created a virtual reality device that combines auditory and visual feedback to improve walking speed and stride length in patients suffering from Multiple Sclerosis (MS) and Parkinson's disease.

According to lead researcher Professor Yoram Baram of the Faculty of Computer Science, the device combines a wearable, cell phone-sized audio component - which measures body movement, processes it and sends feedback to the user through earphones - with a visual feedback apparatus he developed for Parkinson's patients 10 years ago.

The visual component presents users with a virtual, tiled-floor image displayed on one eye via a tiny piece that clips onto glasses worn by the user. This allows the user to distinguish between the virtual floor and real obstacles, making it possible to navigate even rough terrain or stairs.

Baram and Prof. Ariel Miller of the Faculty of Medicine and the Multiple Sclerosis and Brain Research Center at the Carmel Medical Center in Haifa examined the effects of the patented device on the gait quality of MS patients.

The researchers found that auditory feedback significantly improved the gait of both MS and Parkinson's patients (though the improvement was less pronounced in Parkinson's patients).

With regard to walking speed, patients showed an average improvement of 12.84% while wearing the device. There were also positive residual short-term therapeutic effects (18.75% improvement) after use. Average improvement in stride was 8.30% while wearing the device and 9.93% residually.

"Healthy people have other tools, such as sensory feedback from muscles nerves, which report on muscle control, telling them whether or not they are using their muscles correctly," says Baram. "This feedback is damaged in Parkinson and MS patients and the elderly, but auditory feedback can be used to help them walk at a fixed pace."

Results from a small study (14 randomly selected patients with gait disturbances predominantly due to MS) on the device are published in the February 2007 issue of the Journal of the Neurological Sciences.

The integrated device - the first to respond to the patient's motions rather than just providing fixed visual or auditory cues - is already in use at a number of medical centers in Israel and the United States, including the University of Cincinnati and the State University of New York.

The Technion-Israel Institute of Technology is Israel's leading science and technology university. Home to the country's winners of the Nobel Prize in science, it commands a worldwide reputation for its pioneering work in nanotechnology, computer science, biotechnology, water-resource management, materials engineering, aerospace and medicine.

The majority of the founders and managers of Israel's high-tech companies are alumni. Based in New York City, the American Technion Society is the leading American organization supporting higher education in Israel, with 17 offices around the country.

Tuesday

 

Telephone-Based Psychotherapy Shows Durability in Depression - CME Teaching Brief® - MedPage Today

SEATTLE, March 22 -- For depressed patients on medication but too sad to seek psychotherapy as well, lasting help may be available by phone researchers found in a follow-up study.

For more than 75% of nearly 400 patients, the positive effects of six months of brief telephone psychotherapy at the start of antidepressant medication endured for 18 months after the first session, including six months beyond the end of all phone therapy, said Evette Ludman, Ph.D., of the Group Health Cooperative Center for Health Studies here, and colleagues.

This study, reported by Dr. Ludman and colleagues in the April issue of the Journal of Consulting and Clinical Psychology, was a follow-up to a 2004 report on the same sample of 393 patients, published in the Journal of the American Medical Association.

The follow-up found that at 18 months, 77% of those given phone-based therapy reported that depression was "much" or "very much" improved, compared with only 63% of those receiving usual care.

In the 18-month analysis, the benefits of telephone psychotherapy in the first six months were sustained during the second six months when only brief booster sessions were provided. Significantly a "robust clinical benefit" endured for six months after all treatment contact was discontinued, the researchers found.

"As with weight control," Dr. Ludman said, "maintaining improvement is the hardest part of treating depression."

Traditional in-person psychotherapy has limited reach among the large number of patients beginning antidepressant treatment in primary care, the researchers wrote. Expanding access to therapy calls for considering new therapy approaches, such as phone-based sessions, that place greater emphasis on accessibility, outreach, and patient convenience, the investigators concluded.

Of the participants, 195 were randomly assigned to antidepressant medication and usual care while 198 got medication and phone therapy. Of these, 348 (89%) completed the six-month blinded assessment, and 334 (85%) completed the 18-month follow-up.

On average, all patients reported a moderate level of depressive symptoms at baseline, two to four weeks after starting antidepressants prescribed by a primary-care provider.

Phone psychotherapy sessions, delivered by masters-level therapists, included eight core sessions (about 30 minutes) during the first six months, with 15- to 20-minute booster sessions every two months up to a year. After that, phone therapy ended.

According to a structured cognitive behavioral-based psychotherapy program, patients were encouraged to identify and counter their negative thoughts (cognitive behavioral therapy), pursue activities they had enjoyed in the past, and develop a plan to care for themselves....[MORE]


Thursday

 
CME Teaching Brief® - MedPage Today - FDA Warns of Sedative-Aided Sleep Driving and Anaphylaxis

ROCKVILLE, Md., March 14 -- The FDA has taken steps to ensure that clinicians and patients are aware of rare bizarre effects associated with sedative hypnotics, including driving or eating while sleeping.

The agency has ordered makers of all sedative-hypnotic drugs to strengthen label warnings about the risk of "complex sleep-related behaviors" and also severe allergic reactions. The FDA defined sleep driving as "driving while not fully awake after ingestion of a sedative-hypnotic product, with no memory of the event."

Last December, the FDA sent letters to manufacturers of products approved for the treatment of sleep disorders requesting that the whole class of drugs revise product labeling to include warnings about the following potential adverse events:

Anaphylaxis and severe facial angioedema, which can occur the first time the product is taken. Complex sleep-related behaviors which may include sleep-driving, making phone calls, and preparing and eating food while asleep.

"There are a number of prescription sleep aids available that are well-tolerated and effective for many people," said Steven Galson, M.D., MPH, director of FDA's Center for Drug Evaluation and Research. "However, after reviewing the available post-marketing adverse event information for these products, the FDA concluded that labeling changes are necessary to inform health care providers and consumers about risks."

Russell Katz, M.D., director of the FDA's division of neurology products at the center, said the new label will warn that a number of complex-sleep related behaviors "including cooking and eating, using the telephone, having sex, and driving" have been reported by persons using the drugs. Typically, the patient has no memory of these actions.

At a press briefing today, Dr. Katz repeatedly emphasized that the allergic reactions, including anaphylaxis and angioedema, and the complex sleep-related behaviors,"are rare by any definition" and he said the FDA has not received any reports of death associated with either side effect....[MORE]


 
Newswise - When Your Brain Talks, Your Muscles Don't Always Listen

Newswise — Have your neurons been shouting at your muscles again? It happens, you know.


As we grow older, neurons--the nerve cells that deliver commands from our brains--have to “speak” more loudly to get the attention of our muscles to move, according to University of Delaware researcher Christopher Knight, an assistant professor in UD's College of Health Sciences.


“As a result of age-related changes in muscle and neurons, elderly people are often frustrated by poor control during precision tasks, and slowed physical responses contribute to more falls as people grow older,” Knight said.


Knight and co-author Gary Kamen, who directs the Exercise Neuroscience Laboratory at the University of Massachusetts, recently published the results of a study on motor-unit firing rates in the Journal of Applied Physiology, and Knight is now beginning a new project focusing on motor-control mechanisms in the elderly. Both studies are sponsored by the National Institutes of Health.


The ultimate goal of the research, Knight said, is to improve movement quality in older adults, as well as patients with disorders such as cerebral palsy or multiple sclerosis, or who are recovering from strokes.


Every move you make is made possible through a miraculous communications network involving the brain at the command center, the spinal cord, billions upon billions of nerve cells, and thousands of muscle fibers.


“Muscles are the driving force behind our movements,” Knight said. “Every time they get a command from the neurons, the muscle fibers contract. In the generation of muscular force, the smallest controllable unit consists of an individual neuron and the muscle fibers it stimulates. We believe that our research is very important to our understanding of motor-control mechanisms in general and impaired control in patient populations.”


Shedding light on the communication between neurons and muscles, and how it changes as we age, may lie right at our fingertips, according to Knight's research.


Using an experimental apparatus he and his students created in UD's Human Performance Lab, Knight has been examining muscular force on a very small scale in the index finger, specifically, the first dorsal interosseous muscle. Located between the index finger and the thumb, this muscle contains 120 “motor units”--in other words, 120 individual neurons, or nerve cells, and the muscle fibers they activate.


“It's a relatively simple muscle, so you get to see more of a one-to-one relationship between the activity of the neurons and the resulting muscular force,” Knight said....[MORE]