Peripheral Synuclein Tissue Markers: A Step Closer to Parkinson's Disease Diagnosis

Eduardo Tolosa; Dolores Vilas

Disclosures

Brain. 2015;138(8):2120-2122. 

Intraneuronal Lewy bodies and Lewy neurites consisting of aggregated α-synuclein (SNCA) are the hallmark of brain pathology in Parkinson's disease. It is now well established that Lewy-type α-synuclein histopathology also occurs in the peripheral autonomic nervous system (Beach et al., 2010; Gelpi, 2014), and recent efforts have been directed towards detection of this pathology in peripheral tissues in the hope that it could serve as diagnostic biomarker of Parkinson's disease. Such a tissue marker would differentiate Parkinson's disease from mimics and related conditions such as multiple system atrophy (MSA), essential tremor and vascular parkinsonism, which are not associated with Lewy-type α-synucleinopathy. In this issue of Brain, Zange et al. present the results of one such study on peripheral SNCA, and report the presence of phosphorylated α-synuclein (pSNCA) deposits in the dermal nerves of patients with Parkinson's disease, but not MSA or essential tremor, consistent with what one might expect from the known pathology of these disorders (Zange et al., 2015). The results thus suggest that a simple forearm skin biopsy could permit the separation of these conditions. Zange et al. also describe changes compatible with a neuropathy in their subjects with Parkinson's disease. As they observed a correlation between the pSNCA deposits and denervation of autonomic skin elements that was independent of age or disease duration, they suggest, as others have previously (Donadio et al., 2014), that pSNCA is causative for the nerve fibre degeneration. However, no conclusive evidence for this exists. The situation is similar to that in the CNS in Parkinson's disease, where it is unclear if Lewy bodies and neurites are causative factors, or bystanders of the neurodegenerative process.

Differentiating Parkinson's disease from MSA, particularly the so-called parkinsonian variant (MSA-p), can be difficult in clinical practice, especially in the early disease stages. Patients with MSA-p may respond well to levodopa and the usual red flags alerting for MSA may be missing. Ancillary tests can help in the diagnosis (Fanciulli and Wenning, 2015) but not uncommonly fail to solve the problem conclusively. Cardiac scintigraphy, for example, a test that has been found to correctly distinguish idiopathic Parkinson's disease with high sensitivity and specificity from MSA, was normal in a similar percentage of patients with Parkinson's disease and those with MSA (Zange et al., 2015).

The search for peripheral SNCA deposits in living patients started with biopsies of the olfactory epithelium. Braak's elegant demonstration in post-mortem tissue of SNCA immunoreactive inclusions in the gastric wall of patients with Parkinson's disease (Braak et al., 2006) prompted studies looking for abnormal SNCA deposition in the gastrointestinal tract, and several studies have identified pSNCA in gastric and colonic specimens as well as in the salivary glands (Fig. 1; see Cersosimo and Benarroch, 2012 for a review).

(Enlarge Image)

Figure 1.

Peripheral tissues in which pSNCA deposits have been reported to occur in Parkinson's disease. Modified from image by Yoko Design, Shutterstock.

The dermal nerves have also been the focus of studies in search of a peripheral SNCA marker. In post-mortem tissues, pSNCA has been detected in skin samples from the upper extremities, abdomen and scalp (Ikemura et al., 2008; Beach et al., 2010). In vivo studies assessing skin pSNCA deposits have reported on the presence of SNCA aggregates in patients with Parkinson's disease, with variable frequencies ranging from 0% to 100% (Wang et al., 2013; Donadio et al., 2014; Navarro-Otano et al., 2014), probably in part because different sites were selected for the skin biopsy. Zange et al. chose skin tissue obtained from punch biopsies from the forearm for their study and found SNCA aggregates in all 10 of their patients with Parkinson's disease, but in none of the patients with MSA or essential tremor.

The results of Zange et al. look promising but cannot be considered definitive, and previous studies with peripheral nervous system SNCA in Parkinson's disease suggest caution. Initial studies of colonic SNCA, for example, suggested that pSNCA deposits were highly specific for Parkinson's disease, but a recent study provides evidence for the presence of aggregated pSNCA in individuals with, as well as without Parkinson's disease (Visanji et al., 2015), suggesting that colonic deposition of pSNCA is not a useful diagnostic test.

Before we can consider ordering a skin SNCA study for diagnostic purposes, some important methodological issues need to be solved. The optimal site for study, for example, needs to be determined. We and others (Miki et al., 2010; Navarro-Otano et al., 2014) have failed to find pSNCA deposits in skin from the supramalleolar region and current evidence suggests that the highest yield may occur in skin tissue obtained in the cervical region (Donadio et al., 2014). Zange et al. promote the ventral forearm as the optimal site based on the assumption that there is a higher sweat gland density in this specific area. The issue is not quite settled and it remains possible that in Parkinson's disease the positivity for pSNCA in a given skin tissue also varies depending on disease stage, with distal regions more likely to have SNCA aggregates in very early stages, but perhaps less so later in the disease course. A centripetal propagation of axonal SNCA aggregates has been found to occur in the peripheral autonomic nervous system (Orimo et al., 2008).

The number of biopsies needed to obtain an optimal result is also unclear. While most studies have performed only one biopsy per site, Donadio et al. obtained the highest sensitivity (100%) by analysing two cervical skin samples, whereas the analysis of only one sample yielded a lower positivity rate. They attributed this finding to the likely patchy deposition of peripheral pSNCA. The size of the biopsies has also varied in the reported studies—between 3 and 6 mm—and could influence the rate of positivity, since larger biopsies are likely to enhance the probability of detecting autonomic structures and pSNCA deposits. Finally, methods of tissue fixation, choice of antibodies for immunohistochemistry and criteria for considering a biopsy positive or negative for pSNCA have differed considerably from one study to the next and made it difficult to compare results. For instance, in studies with a sensitivity higher than 80%, such as those of Zange et al. and Donadio et al., the assessment of the SNCA deposits is quite different. In Zange and co-workers' study, the presence of SNCA deposits was assessed qualitatively and semiquantitatively, and the detection rate was defined as the percentage of antibody-positive skin elements (sweat glands, arrector pili muscles and arterial blood vessels) relative to all detected skin elements. In the study by Donadio et al., the pSNCA staining was assessed with a fluorescence microscope and was rated in each skin site as the percentage of autonomic structures or nerve bundles showing a positive staining.

Researchers need to arrive at a consensus on procedure standardization and on how to move forward with studies to determine the sensitivity and specificity of skin Lewy-type α-synucleinopathy as a diagnostic biomarker for Parkinson's disease. This would hopefully reduce the variability of the results obtained and make them comparable. Eventually, studies focusing on expression patterns of pSNCA in the peripheral autonomic nervous system in premotor Parkinson's disease would seem warranted. SNCA accumulation has already been identified in the gastrointestinal tract in premotor Parkinson's disease (Hilton et al., 2014). Prodromic skin studies could be undertaken in subjects with a higher than average risk of developing Parkinson's disease such as those with idiopathic REM sleep behaviour disorder or asymptomatic carriers of leucine-rich repeat kinase 2 (LRRK2) mutations. These would ideally be prospective cohort studies, in which multiple additional markers (clinical, biological and imaging) would be assessed and subjects followed long term to capture the evolution to clinically defined Parkinson's disease. A reliable premotor biomarker could allow treatment to begin earlier and facilitate the development of treatments to slow or even halt disease progression.

The study by Zange et al. provides evidence that skin SNCA assessment may reliably separate Parkinson's disease from MSA, with no overlap between the two conditions in positivity for pSNCA in dermal nerves. This biomarker study, centred on a disease-related protein, needs to be replicated in an independent cohort and with a larger number of cases, and preferably with blind rating of the immunohistochemistry sections. The results of the study suggest though that we may be getting closer to finding an inexpensive and non- or minimally invasive diagnostic tissue marker of Parkinson's disease. Such a marker would be useful for separating Parkinson's disease from MSA and other parkinsonisms not associated with Lewy-type histopathology, and may eventually be used for confirming the diagnosis of very early, or even prodromal, disease.

http://www.medscape.com/viewarticle/850685?src=wnl_edit_tpal

A new study maps the path Parkinson's takes as it spreads from affected to healthy tissue in the early stages of the brain-wasting disease.

By comparing scans of people affected by the disease and healthy counterparts, a new study has mapped the early stages of Parkinson's disease progress in the brain.

The results should increase our understanding of how Parkinson's disease spreads, say researchers from McGill University in Montreal, Canada, who report their findings in the journal eLife.

The map is the first to show the extent and distribution of the atrophy that Parkinson's disease causes as it spreads through brain regions.

Previous studies have not been able to consistently show regional atrophy in the early stages of Parkinson's disease because the data sets and sample sizes have been too small and the methods were not sensitive enough, says senior author Dr. Alain Dagher.

For their study, the team used the open source Parkinson's Progression Markers Initiativedatabase.

This gave them access to more MRI scans and clinical data than had ever been used on such a study before. This, together with their more sensitive methods, is what allowed them to pick out the brain regions that atrophy in the early stages of Parkinson's disease.

The scans and data allowed them to compare the brain structure of 232 patients in the early stages of Parkinson's disease (PD) with 117 healthy individuals of similar ages.

They found that the disease progresses from cell to cell through the brain along networks, as Dr. Dagher - a neurologist specializing in movement disorders and functional brain imaging - explains:

"The atrophy pattern on MRI is compatible with a disease process that spreads via brain networks - something that had never been shown in human patients before, and would support the hypothesis that PD is caused by a 'toxic agent' that spreads trans-neuronally."

This adds weight to the idea that Parkinson's is a prion-like disease caused by a toxic, misfolded protein called alpha-synuclein. The protein copies itself and travels along brain networks, clogging up cells on its way.

Similar mechanisms have been proposed for Alzheimer's disease and Bovine Spongiform Encephalopathy (BSE - commonly known as mad cow disease).

Mapping will continue as disease progresses in the participants

Monitoring of the patients in the study will continue, with yearly evaluations expected to yield a wealth of data so researchers can continue to map disease progression through the brain.

Treatments for the symptoms exist, but there is no cure for Parkinson's - a disease that affects an estimated 7-10 million people worldwide. The disease kills brain cells that release dopamine, a chemical messenger that helps to regulate movement, emotional responses and other functions.

As the disease progresses, the brain's supply of dopamine dwindles, giving rise to a range of symptoms such as tremor, stiffness, slowness of movement and impaired balance. The symptoms gradually get worse and everyday aspects of life that most of us take for granted - like walking, talking and taking care of oneself - become increasingly difficult.

The team behind the current study hopes the map will help develop new tests for drugs that target the culprit protein, an avenue that may lead to treatments that prevent, slow or even reverse Parkinson's disease.

The findings follow other research Medical News Today learned about that proposes Parkinson's may be a consequence of brain cell burnout. A study led by the University of Montreal suggests Parkinson's disease may be the result of an energy crisis in brain cells that have unusually high energy needs in order to control movement.

Written by Catharine Paddock PhD

Research-towards-stem-cell-treatments

16 September 2015

This week researchers at the University of Saskatchewan and Harvard Medical School have been talking about their research using skin cells to replace brain cells lost in Parkinson's.

Stem cells carry real hope as a treatment and potential cure for people with Parkinson's.

Dr Beckie Port, Research Communications Officer

The research study that has been highlighted in press and social media today could represent a step towards new a treatment for the condition.

But clinical trials in people are still a long way off.

Stem cells and Parkinson's

People with Parkinson's don't have enough of a chemical called dopamine because some of the brain cells that produce this chemical have died.

For people with the Parkinson's, the hope is that we will be able to grow new dopamine-producing brain cells from stem cells.

And that these could one day be used to replace the cells that are lost in Parkinson's.

What the research team are doing

The Canadian research team is testing a new therapy that uses new dopamine-producing cells made from skin cells to repair the brain in an animal model of Parkinson's.

They hope that the experiments they are doing now in the lab will lead to clinical trials in people with Parkinson's within the next couple of years.

A step towards stem cell treatments for Parkinson's

Dr Beckie Port, Research Communications Officer, comments:

"Stem cells carry real hope as a treatment and potential cure for people with Parkinson's.

It is an exciting time for stem cell research in Parkinson's, but therapies for people with Parkinson's based on this research are still some way off.

"However, we need to be sure that the cells that are transplanted will work safely and effectively.

"The researchers are still testing this therapy in animal models of Parkinson's.

"At the same time research using brain cells made from foetal stem cells is happening in the UK.

"It is an exciting time for stem cell research in Parkinson's, but therapies for people with Parkinson's based on this research are still some way off."

- See more at: http://www.parkinsons.org.uk/news/16-september-2015/research-towards-stem-cell-treatments-parkinsons#sthash.KZJGHFwj.dpuf

Ask the MD: Dystonia and Parkinson’s

FoxFeed Blog

Posted by  Rachel Dolhun, MD, September 21, 2015

September is Dystonia Awareness Month. MJFF will be sharing more information on the different types and causes of dystonia, and its relationship to Parkinson’s. Keep an eye on the FoxFeed blog and our social channels (#dystoniaawareness) throughout the month for more on this topic. 

Dystonia — unfamiliar to most not affected by the condition — is a neurological disorder that causes involuntary muscle contractions. These lead to painful twisting, turning or pulling postures or movements that can interfere with normal function. Imagine, for example, that your neck was constantly pulled to the side or your toes randomly cramped under your foot.

Dystonia can involve almost any body part and can be isolated to one area or impact the entire body. It can be a distinct condition on its own — meaning there are no other neurological symptoms — or a component of another syndrome, such as Parkinson’s disease (PD). Within Parkinson’s, dystonia can be the initial sign that leads to the diagnosis, an associated symptom or related to the cycle of medication administration.

Dystonia as an Initial Symptom of PD 

Most people do not demonstrate dystonia at the beginning of their Parkinson’s disease, but in rare cases some will develop dystonia before any other symptoms of PD. In this context, dystonia is most often in the lower leg and it forces the foot to turn inward or the big toe to rise up on its own.

A person with dystonia as the first sign of Parkinson’s may be misdiagnosed with another condition until other PD symptoms (stiffness, slowness or tremor) appear.

Dystonia as an Associated Symptom of Parkinson’s

More commonly dystonia occurs with the other motor symptoms of Parkinson’s and most often affects the eyes, neck and trunk.

Dystonia can cause people to blink excessively or keep their eyelids closed; this is typically associated with a sense of eye irritation and light sensitivity. The treatment of choice is botulinum toxin injections into the muscles surrounding the eyes. For those who get incomplete relief with injections or who don’t want to use them, oral medications may be effective. Eye drops might soothe eye irritation, and special eyelid crutches or glasses with wire loops may help keep the eyelids up.

Dystonia can also cause a forward tilt of the neck that makes it difficult to keep the head upright. This can lead to pain in the neck, interfere with vision and walking, and make speech and swallowing problems worse. Management options include a soft cervical collar for support; physical or occupational therapy for strengthening exercises; oral medications like dopamine therapy and muscle relaxants; and, under the care of specialists, botulinum toxin injections. In select cases, spinal fusion surgery or deep brain stimulation (DBS) is offered.

The torso is another place people with Parkinson’s can experience dystonia, where it can cause a person to lean forward or bend sideways and backward. Dystonia of the trunk can yield pain, shortness of breath, walking problems and falls. This symptom typically resolves upon lying down, but of course that’s a temporary solution. Treatment options include physical therapy, oral medications, botulinum toxin injections, and, in some patients, spinal fusion or DBS. Canes and walkers can help to correct posture and decrease the risk of falls.

Dystonia and Levodopa

Dystonia also has a complex relationship with levodopa, the most commonly used medication to treat Parkinson’s motor symptoms.

Later in their disease course, people taking levodopa may experience motor fluctuations, when the medication wears off before it’s time for the next dose. Dystonia can come as part of these “off” periods. If this happens, the doctor may increase the dose or frequency of the levodopa prescription, or suggest another therapy. Extended-release formulations of carbidopa/levodopa (including Rytary and Duopa) and other drug classes (dopamine agonists, COMT-inhibitors and MAO-B inhibitors) aim to shorten or eliminate “off” periods.

Even during periods when levodopa is working well to control other symptoms such as tremor and stiffness, a person may still experience dystonia. In these cases, the doctor may recommend smaller, more frequent doses of levodopa, or try an extended-release formulation of levodopa or another drug class.

There’s no one-size-fits-all medication regimen; it’s a trial and error process to find what works best for every person. Each drug has potential side effects that need to be balanced against the benefits. Ultimately, if motor complications are severe and disabling and the medication adjustments are not effective, DBS may be a consideration.

https://www.michaeljfox.org/foundation/news-detail.php?ask-the-md-dystonia-and-parkinson&os_cid=fb-a30U00000004i0l&s_src=MJFFfb&s_subsrc=askmd_dystonia#prclt-4s21TSgk

Great Lakes NeuroTech Secures $1.9M for Closed-Loop Programming of Deep Brain Stimulation in Parkinson's with Wearable Sensors

CLEVELAND, Sept. 21, 2015 /PRNewswire/ -- 

Great Lakes NeuroTechnologies (GLNT), announced they have received $1.9M from the National Institutes of Health to improve the efficacy of deep brain stimulation (DBS) programming for Parkinson's disease (PD) and minimize time required by a clinician to optimize settings. The technology development and commercialization will combine wearable motor symptom sensing and a DBS platform into a single integrated system.  Intelligent algorithms for searching settings and selecting optimal parameters will be validated using real-time closed-loop feedback from sensors to adjust DBS.  The validated closed-loop system for efficiently programming DBS can improve patient care and expand access to underserved populations.

Parkinson's disease is a movement disorder in which affected individuals may experience tremor, slowness of movements, stiff joints, and impaired gait.  DBS therapy can provide effective motor symptom relief. However, challenges exist with respect to programming the system after the electrode and pulse generator have been implanted.  Expert clinicians must manually adjust settings such as stimulation contact, amplitude, pulse width, and frequency to determine the combination that provides the most symptom relief at the lowest battery power. As DBS systems are providing more targeted control through an increased parameter set of amplitude, pulse width, frequency, and contacts, the number of potential combinations and required programming time grow exponentially.  

GLNT has previously commercialized Kinesia [ http://glneurotech.com/kinesia/ ], a system of wearable sensors and mobile apps for assessing PD and other movement disorders.  The company will use this Phase II SBIR funding to target their core technology to programming DBS, building upon successful Phase I pilot studies [ http://glneurotech.com/kinesia/validation/dbs-pilot-study/ ]. "We demonstrated in two studies that intelligent algorithms using sensor feedback could successfully identify optimal stimulation parameters that significantly improved motor symptoms or maintained therapeutic benefits while reducing stimulation amplitude by an average of 50% to decrease battery usage," stated Dustin Heldman, PhD, Biomedical Research Manager.  "One previous limitation was separate systems were used for assessment and programming.  We look forward to this next phase, which will directly integrate the systems to improve clinical workflow and speed programming time."  Once technology integration is complete, the system will be validated in a multi-center clinical trial in collaboration with Dr. Jerrold Vitek at the University of Minnesota.

The company has leveraged rapidly growing sales of Kinesia technology in the global clinical trials market to educate and train an engaged clinician and patient market. "Our validated technology, growing customer base, reimbursement, and issued patents uniquely position GLNT to capitalize on two new markets, patient referrals for advanced therapies and closed-loop control of adjusting those therapies," said GLNT president, Joseph P. Giuffrida, PhD. In a separate recently completed European study, the company demonstrated that 36% of advanced patients remotely monitored by wearable technology were referred for and received advanced therapy such as DBS or medication pumps compared to 0% in the standard care group [ http://glneurotech.com/kinesia/therapy-referral/ ]. "Through multiple studies, we have demonstrated our technology can positively impact patient care. Our key market differentiator is not sensors for sensors sake, but targeted applications built around validated and published algorithms," continued Dr. Giuffrida.

Great Lakes NeuroTechnologies thanked the National Institutes of Health and specifically the National Institute of Neurological Disorders and Stroke for this funding (2R44NS081902-02A1).

About Great Lakes NeuroTechnologies 

Great Lakes NeuroTechnologies [ http://www.glneurotech.com ] is committed to pioneering innovative biomedical technologies to serve research, education, and medical communities, improving access to medical technology for diverse populations, and positively impacting quality of life for people around the world. In addition to US Patents No. 8,187,209, No. 8,679,038, No. 8,702,629, No. 8,845,557, the company has numerous pending US and international patents.

Media Contact 

Maureen Phillips, 216-361-5410 – mphillips@GLNeuroTech.com

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/great-lakes-neurotech-secures-19m-for-closed-loop-programming-of-deep-brain-stimulation-in-parkinsons-with-wearable-sensors-300146151.html

SOURCE Great Lakes NeuroTechnologies

http://health.einnews.com/article/287460277/OBM9NWgxZR70tX8r

Parkinson’s Disease Foundation to Increase Investment in Research, Health Care and Patient Leaders

How can we put ourselves out of business? Finding the cure for Parkinson’s disease (PD) has been the goal of the Parkinson’s Disease Foundation (PDF) since 1957. But Parkinson’s is still around. And so are we.

The investments of PDF over the past six decades have done much to advance our understanding of PD. They have improved the lives of millions of people worldwide. But we still don’t have the cure. Nothing that can stop the disease. Nothing that can slow it. That is simply unacceptable. There are seven to 10 million people worldwide living with PD who count on us to move the science and the care forward. We owe it to them to make this happen.

In 2014, under the guidance of our Board of Directors, Scientific Advisory Board and People with Parkinson’s Advisory Council, PDF began a year-long examination of how far we have come, and how we can contribute to solving the puzzle moving forward.

The truth is that no one knows when and from where the cure will come. The reality is that many people hold a piece of the puzzle but lack the tools to realize their contribution. PDF’s strategy is to build a team of people — the best and brightest leaders in science, health care, and the patient community who can move the dial in PD research and care — and then mobilize them to work toward the cure together.

After all, if each member has a piece of the PD puzzle, imagine what can happen when we put them together. Here, we report on our plan.

Investing in Research Leaders

The first urgent question PDF asked was: how can we invest in the innovative ideas of young scientists, while ensuring they have the tools needed to transition into our future leaders?

In years past, a talented young investigator — in his or her late 20s or early 30s — was almost assured federal funding to advance innovative ideas and establish a career. But today most scientists have to wait until their mid-40s for funding.

In the meantime, the field’s future leaders are standing on a precipice facing a “valley of death” between their scientific potential and the funding they need to make it happen. We are losing them from the PD fight before they have a chance to contribute.

PDF’s track record of funding early-career scientists is unparalleled — our funding has nurtured leaders driving today’s new therapies — but it is no longer enough. We need to fund the ideas of young innovators and keep the pipeline of scientists full. And we are doing that by focusing $2 million of our total $4.6 million investment in research on early-career scientists.

As part of PDF’s plan to build research leaders, first we recruit scientists early with ‘small but mighty’ fellowships. These low-cost, high-reward programs motivate students to dedicate their careers to PD, while advancing the research of senior scientists.

Once they graduate, we will help to kickstart their innovative ideas. We will step in with an extensive offering of fellowship opportunities — both our own and other opportunities offered with partners like the American Academy of Neurology and the Howard Hughes Medical Institute — that allow scientists to cultivate creativity and take initial steps to prove the potential of their scientific ideas.

Lastly, we’ll help them cross that “valley of death.” As scientists face pressures that may force them to switch careers and leave their research projects incomplete, PDF will be the bridge to ensure no promising idea is left unstudied. We will invest, through mechanisms like the Stanley Fahn Transition Award (named for PDF’s Scientific Director of 40 years), to keep them in the field and help them potentially find a cure for PD.

Investing in Health Care Leaders

We know from our experience that when people with PD work with a health care team — movement disorder specialists, nurses, and physical, occupational and speech therapists — their lives improve.

PDF has a track record of preparing experts to treat PD on the frontlines. We are the largest private funder of training for early-career neurologists to specialize in Parkinson’s, with more than 150 doctors trained to date.

But all too often, professionals on the frontlines are left without sufficient resources or training in PD. For example, nursing students receive less than one hour of instruction on PD during four years of education! Once in the field, many are left to learn about PD themselves, with few opportunities for continuing education.

We must do more. We will start by investing $600,000 a year in growing and empowering health care leaders of today and tomorrow. PDF is preparing future nurses and health care professionals by reaching those with the greatest impact — their teachers — through initiatives such as our flagship Edmond J. Safra Foundation Visiting Nurse Faculty Program at PDF, which has trained nearly 150 faculty members at nursing schools nationwide. These leaders are, in turn, sharing their knowledge with 9,000 students each year and are influencing national standards for nursing education.

Learning from this success, we are implementing a similar model for the field of physical therapy. We expect that within three years, we will have trained 40 faculty leaders, who will in turn train over 1,800 students.

Second, we are supporting professionals on the frontlines, by arming professionals in the nursing, physical therapy and occupational therapy fields — both in conventional classrooms and online — with the tools they need to stay informed and support their patients. Our offerings include free continuing education opportunities and patient education materials.

Investing in Patient Leaders

As those with the most at stake, people with Parkinson’s disease can help the rest of us get our priorities straight. We have seen this prove true in other health communities, when engaged patient advocates have helped to accelerate new treatments.

This is why PDF has advocated relentlessly to make patient engagement a reality. For us, this means engaging people with PD as partners in every part of our work. While we have seen progress, there is much more to be done to ensure that people with PD are recognized and tapped for their insights and potential to help speed research.

This is why PDF is investing $500,000 a year to expand our work to mobilize the grassroots community.

We will continue to build our groundbreaking Parkinson’s Advocates in Research program, which has provided training to more than 260 Research Advocates, who are now working with 400 research professionals on the frontlines to bring better treatments at a faster pace. And we will take the program even further by proactively seeking and guiding advocate-researcher collaborations at universities, pharmaceutical companies and government agencies.

We are also mobilizing new patient leaders to meet specific unmet needs in the community through programs such as the Women and PD Initiative, which launches this fall with a class of 30 women leaders living with Parkinson’s. Each will return to her community with the tools needed to advocate for other women with PD.

Working Together Towards the Cure

PDF’s investments in leadership lay a foundation for improving science, health care and patient engagement. But our ultimate goal is ending Parkinson’s disease. What comes next?

PDF is not only developing leaders; we are also mobilizing them to work toward the cure — together. After all, science and care are team efforts. To that end, PDF has invested close to $50 million in collaborations since 1957, largely toward teams at PD research centers. Today we are taking the strategy further by expanding the opportunities for research, health care and patient leaders to work together.

For example, at Columbia University Medical Center, where we have long funded collaborative teams within the field of PD, we are currently funding teamwork between PD specialists and bioengineers, who are experimenting with ways to design shoe insoles to ease freezing of gait. And at our research center at Rush University Medical Center, we are funding an interdisciplinary project that may one day help doctors to predict who will get PD as part of routine colonoscopies.

We are also expanding funding for research teams that incorporate insights from people with Parkinson’s through our PAIR Leadership Awards and our Community Choice Research Awards. For the latter, we invite the patient community to identify research priorities and then we engage teams of researchers, health professionals, patients and outside experts (e.g., gastroenterologists and psychiatrists) who can help to address them.

No account of PDF efforts in fostering collaborations would be complete without reference to our work sharing PD science with the entire team. We do this online, in print and most recently, through a new partnership with Nature Publishing Group, the world’s leading publisher of scientific journals. The new journal, npj Parkinson’s Disease, is freely available to all with the click of a button.

Conclusions

PDF’s goal is to put itself out of business by ending PD. Until the day comes when we close our doors, please know that they are open to you. Take advantage of our free educational materials, webinars and toll-free HelpLine to find answers, support and resources to help you take charge of PD. Join our team. Get involved as a patient advocate, apply for research funding or take our professional courses. Know that each day, our promise to you is to do everything in our power to accelerate new treatments and end Parkinson’s disease.

And when the day comes to close our doors forever, we can all remember that PDF will not have done it alone: we will have done it as a team.

http://www.pdf.org/fall15_investment_leaders?utm_source=newsletter&utm_medium=email&utm_campaign=general

UVa researchers testing focused ultrasound to treat Parkinson's symptoms

Posted: Saturday, September 19, 2015 1:00 pm

The University of Virginia is leading the first effort to use noninvasive focused ultrasound to treat symptoms of Parkinson’s disease.

Since 2011, UVa has been a center for research in focused ultrasound, the use of high-intensity sound energy to destroy damaged or diseased tissue. It has proved safe and effective for patients with essential tremor, officials said, providing an alternative to risky brain surgery.

-Now researchers say they’re confident it could help treat a range of symptoms in Parkinson’s patients sometimes known as dyskinesia, including tremors and involuntary movements.

“Everybody wants a cure for Parkinson’s, but for the time being, this could be a big breakthrough in symptom management,” said Dr. W. Jeffrey Elias, who has headed several major studies in focused ultrasound.

UVa is collaborating with the University of Maryland — along with centers in Canada and South Korea — to test the effectiveness of the treatment on dozens of patients. Earlier this summer, UVa conducted the first focused ultrasound session on a Parkinson’s patient in the U.S.

Researchers at the University of Maryland conducted another trial one week later, said Dr. Howard M. Eisenberg, chair of the university’s department of neurosurgery.

Patients in the trials will go through several sessions between now and next year, Elias said. Typically, the patients are subjected to focused ultrasound beams for about 10 to 15 seconds at a time. The treatment is essentially painless, though patients have reported discomfort during long sessions.

The point is to interrupt an “abnormal circuit” that forms in Parkinson’s patients, Elias said. Doctors do this by directing more than 1,000 beams of sound deep inside the skull to a part of the brain smaller than a grain of rice.

 “We’re able to do the type of treatment that would usually require making a hole in the head and inserting a probe,” Elias said. “We’re able to do this without making an incision in the head.”

Interrupting these abnormal circuits can relieve rigidity and tremors in patients, Eisenberg said.

“When you have Parkinson’s, some cells in the brain degenerate — that is one of the major pathologies,” he said. “If you perturb the system, you can relieve some of those symptoms.”

The focused ultrasound procedure produces nearly the same results as the invasive brain surgery used on patients until the late 1960s. After that era, doctors began using the drug levodopa — L-dopa for short — to treat symptoms. L-dopa has allowed doctors to treat symptoms without surgery since then, but patients often reach a “ceiling,” Elias said. The longer they take it, the less effective it becomes.

When the drug has become completely ineffective, doctors sometimes resort to deep brain stimulation, a risky surgical procedure that involves implanting electrodes into the brain. When the batteries powering the device run out, patients could need another procedure.

“Over the years, it became clear patients needed more L-dopa as time went on and there were side effects,” Eisenberg said. “The possible place of focused ultrasound is to be another step. … This could replace [deep brain stimulation].”

Like anything else, the ultrasound treatment carries risks, Elias said, including “neurological events” such as a stroke or a hemorrhage. But researchers believe the risk should be significantly lower than the risk associated with deep brain stimulation, he said.

“We’re in the process of figuring out what is the perfect amount of treatment to balance the risk of side effects with the durability of the treatment,” Elias said.

The study, funded by a partnership between the Focused Ultrasound Foundation and The Michael J. Fox Foundation for Parkinson’s Research, is still searching for volunteers. Patients whose medication has failed to satisfactorily control dyskinesia are eligible.

Anyone interested in the trials can contact the Focused Ultrasound Foundation at (434) 220-4993.

http://www.dailyprogress.com/starexponent/uva-researchers-testing-focused-ultrasound-to-treat-parkinson-s-symptoms/article_a65a6b9c-5f24-11e5-9e39-8fe4e739e335.html

Technology used to tag prisoners is now helping doctors measure sleep spasms of Parkinson's sufferers

The buddi bracelet has identified a previously unknown symptom, that sufferers experience spasms in their sleep

• Devices to help better understand disease and lead to improved treatments
• Tracker has recorded sleep spasms doctors were previously unaware of 
• Spasms do not wake sufferer and therefore were unreported to medics
• Only clue for medics was patients feeling unwell the next day 
•  

By SAM MATTHEW FOR MAILONLINE

PUBLISHED: 09:43 EST, 20 September 2015 | UPDATED: 09:56 EST, 20 September 2015

The breakthrough was made by the technology firm, which is owned by businesswoman Sara Murray, and provides monitoring alarm bracelets for the NHS, local authorities and Ministry of Defence. 

'It is very early days but we will be presenting our data to the medical establishment because it seems quite clear that this discovery has great potential for doctors to learn more about this awful disease,' said Buddi's chief executive Ms Murray, the founder of Confused.com and a member of the Government's Technology Strategy Board.

'It may even form the basis of new forms of treatments depending on the findings of doctors.'

The data was recorded on the wristbands as sufferers slept. 

The Buddi system works as 24/7 monitoring and personal emergency response service. It not only tracks the user's whereabouts using GPS, but alerts their next of kin or carers if the person appears to be in trouble.

It comes in three parts, the wristband, a clip which is attached to a lanyard or key ring and the dock.

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The buddi was created by entrepreneur Sara Murray

The wristband goes everywhere with the user and traces movements and can raise the alarm if it detects a fall.

Unlike many personal alarm systems which are taken off at night, the Buddi wristband is designed to be worn during sleep incase of falls on the way to the bathroom and this is how the spasms were detected.

Falls are detected automatically and the device immediately sends an alarm call but the wristband also monitors activity levels during sleep and can detect restless sleep.

The graphs from these movement logs on 3,000 wristbands were analysed by Buddi which lead to the discovery of the sleeping spasms.

The Parkinson's findings became clear with the analysis of six months of data per individual.

Ms Murray added: 'The data from the Buddi is unequivocal in that is shows Parkinson's sufferers are experiencing previously undiscovered spasms in their sleep.

'Often they report to their doctor feeling very unwell the next day and doctors have not been able to explain this.

'At the very least our discovery will help patients manage their medication better because one possible cause of the spasms could be because the patient is not taking tablets at the right time.

'However, that is only part of the story. The fact that these spasms are happening gives a whole new area of investigation for the medical profession.

'We will do everything we can to help and make all our data available.'

Parkinson's afflicts about 127,000 people in the UK and there is no cure though there are a range of treatments to manage the condition.

It is a progressive neurological illness which usually affects people over the age of 50 and the three main symptoms are tremors, muscle stiffness and slowness of movement.

The condition is triggered because there is a shortage of chemical called dopamine because specific nerve cells in the brain have died.

No-one is immune from the disease which has struck down the former heavyweight boxer Muhammad Ali, Hollywood star Michael J Fox, the late country singer Johnny Cash and the evangelist Billy Graham.

Closer to home the Scottish comedian and actor Billy Connolly has been diagnosed as a sufferer. Roger Bannister, the first man to run a four-minute mile was among its sufferers as well as Ray Kennedy the former Arsenal, Liverpool and England footballer.

Buddi operates an emergency monitoring centre in the UK which is manned 24/7 365 days a year to react to emergencies.

The firm works with over 100 local authorities and NHS Trusts to help protect vulnerable people.

Murray, who has forged a reputation as one of Britain's top innovators and was named entrepreneur of the year in 2009, was in the headlines last year when one of her tracking devices helped convict criminal Darren Girling, 38, who tried to dodge a speeding ticket while on bail.

His tracking device, worn as part of his bail conditions, was using GPS technology and put him at the scene of the crime.

Girling was caught riding a scooter at 41mph in a 30mph zone on the A13 in Leigh, Essex. He claimed someone else had 'cloned' his bike and it wasn't him on the scooter.

But the Buddi tracker - dubbed 'ChavNav' - proved he was lying.

Murray created Buddi in 2005 after the horror she felt when her young daughter temporarily disappeared in a supermarket. 

http://health.einnews.com/article/287319359/BQSmg6FjUoLsGx7a