Race raises $56,000 for those affected by Parkinson’s

Aug. 27, 2016

The eighth annual Speedy PD Race for Parkinson's Disease drew in over 800 runners to Tuttle Creek State Park Saturday.

The eighth annual Speedy PD Race for Parkinson's Disease drew in over 800 runners to Tuttle Creek State Park Saturday.

The Speedy PD raises money for the Meadowlark Hills Parkinson Fund aimed at helping people affected by PD in the Flint Hills region. 

The annual fundraiser helps people like Allen Sylvester of Wamego, who was diagnosed with Parkinson’s in 2008.

“If you can imagine like being frozen and when you’re on the medication you unfreeze and you can do your regular life tasks. But it sneaks up on you and freezes you solid,” said Sylvester. 

This year’s Speedy PD runners raised $56,000 for Parkinson’s programs in the Flint Hills. 

“All of the money that we raise today stays here in the Flint Hills to help pay for programs, exercise classes and equipment people might need to help live better with the disease. We bring in speakers so that we can provide more education to people,” said Michelle Haub, Meadowlark Hills Parkinson’s Program Director.

Video:

http://www.wibw.com/content/news/Runners-raise-56000-for-people-affected-by-Parkinsons-391497471.html

http://www.wibw.com/content/news/Runners-raise-56000-for-people-affected-by-Parkinsons-391497471.html

Breakthrough in understanding Parkinson’s disease

27 August 2016

Research from The University of Queensland could lead to a new treatment for Parkinson’s disease, with future potential applications to nearly 50 other disorders.

In Parkinson's disease – which affects about eight million people worldwide – vital nerve cells (neurons) in the brain malfunction or die.

Researchers from UQ’s Institute for Molecular Bioscience examined a genetic mutation that interrupts the traffic of materials within neurons and allows waste products to accumulate, causing Parkinson’s disease.

Associate Professor Rohan Teasdale said previous studies showed that dysfunctions in retromer (a protein machine responsible for transporting biological material within a cell) were linked to Parkinson’s disease, but the biological reasons behind this were unclear until now.

“It has been identified that one of these proteins (Vps35) is mutated in some Parkinson’s patients, which creates congestion in the transport network inside cells,” Associate Professor Teasdale said.

“As a result, it appears that the workers responsible for recycling material within these neurons are not getting to their correct work place and without their assistance the cells within the brain cannot rid themselves of waste materials, which increases the likelihood of cell death.

“It’s this cell death that then causes the symptoms of Parkinson’s disease, such as tremors and muscle stiffness,” he said.

Associate Professor Teasdale said the research was in very early stages, but the team’s discovery had potential to improve treatments that now address symptoms rather than the cause of the disease.

“As part of this study we expanded the transport network within these cells which reinstated traffic flow so the neurons could rid themselves of waste,” he said.

“We believe that expanding the cells’ recycling capacity could halt or drastically slow the progression of the disease.”

Associate Professor Teasdale said the same treatment principle could be applied in nearly 50 other disorders that are caused by the build-up of waste materials within cells.

These diseases, known as lysosomal diseases, affect different parts of the body, including the skeleton, brain, skin, heart, and central nervous system, and are especially prevalent in young children.

The work is published in the Journal of Biological Chemistry.

Media: Heidi Jones, heidi.jones@uq.edu.au, +61 7 3346 2134.

https://www.uq.edu.au/news/article/2016/08/breakthrough-understanding-parkinson’s-disease

Brainjacking – A New Cyber-Security Threat

Aug. 23, 2016

We live in an interconnected age where wirelessly controlled computing devices make almost every aspect of our lives easier, but they also make us vulnerable to cyber-security attacks. Today, nearly everything can be hacked, from cars to lightbulbs. But perhaps the most concerning threat is the one posed by implanted medical devices. Experts have demonstrated the ease with which security on pacemakers and insulin pumps can be breached, potentially resulting in lethal consequences.

In a recent paper that I and several of my colleagues at Oxford Functional Neurosurgery wrote, we discussed a new frontier of security threat: brain implants. Unauthorised control of brain implants, or “brainjacking”, has been discussed in science fiction for decades but with advances in implant technology it is now starting to become possible.

Deep brain stimulation

The most common type of brain implant is the deep brain stimulation (DBS) system. It consists of implanted electrodes positioned deep inside the brain connected to wires running under the skin, which carry signals from an implanted stimulator. The stimulator consists of a battery, a small processor, and a wireless communication antenna that allows doctors to program it. In essence, it functions much like a cardiac pacemaker, with the main distinction being that it directly interfaces with the brain.

DBS is a fantastic tool for treating a wide range of disorders. It is most widely used to treat Parkinson’s disease, often with dramatic results (see video below), but it is also used to treat dystonia (muscle spasms), essential tremor and severe chronic pain. It is also being trialled for conditions such as depression and Tourette’s syndrome.

Targeting different brain regions with different stimulation parameters gives neurosurgeons increasingly precise control over the human brain, allowing them to alleviate distressing symptoms. However, this precise control of the brain, coupled with the wireless control of stimulators, also opens an opportunity for malicious attackers to go beyond the more straightforward harms that could come with controlling insulin pumps or cardiac implants, into a realm of deeply troubling attacks.

Remote control

Examples of possible attacks include altering stimulation settings so that patients with chronic pain are caused even greater pain than they would experience without stimulation. Or a Parkinson’s patient could have their ability to move inhibited. A sophisticated attacker could potentially even induce behavioural changes such as hypersexuality or pathological gambling, or even exert a limited form of control over the patient’s behaviour by stimulating parts of the brain involved with reward learning in order to reinforce certain actions. Although these hacks would be difficult to achieve as they would require a high level of technological competence and the ability to monitor the victim, a sufficiently determined attacker could manage it.

There are proposed solutions to making implants more resistant to cyber-attacks, but makers of these devices are in a difficult position when trying to implement security features. There’s a trade off between designing a system with perfect security and a system that is actually usable in the real world.

Implants are heavily constrained by physical size and battery capacity, making many designs unfeasible. These devices must be easily accessible to medical staff in an emergency, meaning that some form of “back-door” control is almost a necessity. New and exciting features, such as being able to control implants using a smartphone or over the internet, have to be balanced against the increased risk that such features can provide.

Brain implants are becoming more common. As they get approved for treating more diseases, become cheaper, and get more features, increasing numbers of patients will be implanted with them. This is a good thing overall but, just as a more complex and interconnected internet resulted in greater cyber-security risks, more advanced and widespread brain implants will pose tempting targets to criminals. Consider what a terrorist could do with access to a politician’s mind or how coercive blackmail would be if someone could alter how you act and think. These are scenarios that are unlikely to remain purely in the realm of science fiction for much longer.

It’s important to note that there’s no evidence to suggest that any of these implants has been subjected to such a cyber-attack in the real world, nor that patients with them currently implanted should be afraid. Still, this is an issue that device makers, regulators, scientists, engineers and clinicians all need to consider before they become a reality. The future of neurological implants is bright, but even a single high-profile incident could irreparably damage public confidence in the safety of these devices, so the risk of brainjacking should be taken seriously before it’s too late.

https://theconversation.com/brainjacking-a-new-cyber-security-threat-64315

Next Steps in Understanding Brain Function

NEUROSCIENCE NEWSAUGUST 26, 2016

Summary: A new paper reports on how understanding brain function has become more than a brain science.

Source: Frontiers.

Designing an approach that tackles brain complexity has challenged scientists to rethink some of the most fundamental aspects of their work and to innovate. NeuroscienceNews.com image is for illustrative purposes only.

How understanding brain function has become more than brain science.

The most complex piece of matter in the known universe is the brain. Neuroscientists have recently taken on the challenge to understand brain function from its intricate anatomy and structure. There is no sure way to go about it, and Dr. Javier DeFelipe at the Cajal Institute in Madrid proposed a solution, in his Frontiers in Neuroanatomy Grand Challenge article “The anatomical problem posed by brain complexity and size: a potential solution.”

Today, one year after the Challenge was published, DeFelipe and colleagues published a discussion around the actual size of the problem and possible solutions, in the new article “Comments and general discussion on ‘The anatomical problem posed by brain complexity and size: a potential solution’.”

“Rather than attempting to fully reconstruct the whole brain or a particular brain region, the solution seems to lie in realistic computational modelling of the brain,” says DeFelipe. This approach has inspired scientists all over the globe to contribute to large multidisciplinary projects, known as big data projects. The challenge is grand because it goes straight into and beyond the matter of Is there one best way to study brain function?

Designing an approach that tackles brain complexity has challenged scientists to rethink some of the most fundamental aspects of their work and to innovate. “Realist brain models based on biological data obtained in the lab can speed our understanding of brain function, because we expect it to require much less than timely experiments in living tissue,” says DeFelipe, “But as a neuroanatomist, I believe — as do many of my colleagues — that there is a lot of confusion about the anatomy of the brain and that there are frequent misunderstandings and wrong assumptions about many aspects of the brain organization or the use of experimental animals,” he explains.

By uniting many contributors in the discussion, the article resulted in a constructive and thoughtful dialogue from different views on the study of the human brain. “My idea was to present this problem to other neuroscientists and general readers in a simple manner and, try to provide a solution,” he says.

The study of the human brain is challenging, not only because of its complexity and technical difficulties, but also because of ethical limitations. “For obvious reasons, we are not always ethically allowed to collect all the necessary types of data directly from human brains. So, there is a big debate about the range of specific strategies that we should use.” The discussion also touches whether big worldwide projects, like the Human Brain Project based in Europe and the Brain Activity Map based in the United States, are a new and better paradigm to go forward, he says, or “if it is better to just follow the most common and traditional scheme of supporting relatively small groups of researchers.”

This discussion comes at an important moment for neuroscience, with potential impact on the hundred millions of funding devoted to the development of extraordinary technology inspired by biology. “The results of such large efforts can be a true paradigm shift”, says DeFelipe, whose main focus is the study of cortical circuit organization and function, and the history of how we came to our current understanding.

The outlook is inspiring. “By taking on such a grand challenge, this type of work involving hundreds of scientists, will generate results beyond our daily pursuits in the lab”, says DeFelipe.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Michelle Ponto – Frontiers 
Image Source: This NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “The Anatomical Problem Posed by Brain Complexity and Size: A Potential Solution” by Javier DeFelipe, Rodney J. Douglas, Sean L. Hill, Ed S. Lein, Kevan A. C. Martin, Kathleen S. Rockland, Idan Segev, Gordon M. Shepherd and Gábor Tamás in Frontiers in Neuroanatomy. Published online June 10 2016 doi:10.3389/fnana.2016.00060

Abstract

The Anatomical Problem Posed by Brain Complexity and Size: A Potential Solution

This article gathers together different opinions on the current status and future directions of the study of the brain, taking as a working document the article “The anatomical problem posed by brain complexity and size: a potential solution”. These commentaries are followed by a section dedicated to a general discussion of the issues raised, in which all contributors participate. The authors who have contributed to this article are listed in alphabetical order. As the reader will see, there are different points of view and of course there are many other aspects that would need further discussion that have been raised by other scientists who did not participate directly. For example, Peter Somogyi made the following comment (personal communication):

[“Anatomy” is a discipline and not a biological entity that exists in nature. Hence the brain or its cells do not have anatomy; we study them with anatomical methods (usually using microscopes) while we carry out “anatomical analysis.” The brain, its nuclei, cells, and their parts are the biological entities which several disciplines study, preferably together, providing a unified description and explanation of them. We must be clear about this, and avoid terms like “anatomical properties,” “physiological properties,” or “biochemical properties” as if these somehow existed in isolation. The separate disciplines, which developed historically due to the limitation of individual human brain capacity and short life span leading to methodological and conceptual specialization, are based on sets of methods, but study the same indivisible biological entity. E.g., the synaptic current recorded by electrophysiological methods flows through the membrane that we see in the electron microscope or with the help of antibodies to synaptic ion channels in the light microscope. Accordingly, the “anatomical problem” exists because of inadequate scientific rigor in addition to methodological limitations that are often not understood, not because of “brain complexity”.]

This is just an example of the many possible different points of view when dealing with the subject of the anatomy of the brain. Thus, this article is not intended to be comprehensive, and the unavoidable limitations in the selection of comments, data, and their interpretation reflect, in many cases, the personal views and interests of the authors.

“The Anatomical Problem Posed by Brain Complexity and Size: A Potential Solution” by Javier DeFelipe, Rodney J. Douglas, Sean L. Hill, Ed S. Lein, Kevan A. C. Martin, Kathleen S. Rockland, Idan Segev, Gordon M. Shepherd and Gábor Tamás in Frontiers in Neuroanatomy. Published online June 10 2016 doi:10.3389/fnana.2016.00060

http://neurosciencenews.com/neuroscience-brain-function-4914/

Over 1/3 of patients don’t receive enough info about Parkinson’s at diagnosis

Author: Geoffrey Chang 25 August 2016

Parkinson’s UK has outlined key areas for improvement in care, after releasing the results of its Parkinson’s Audit

Leading charity Parkinson’s UK has released the results from what is believed to be the largest and most comprehensive review of Parkinson’s services in the UK.

The ‘2015 UK Parkinson’s Audit’ aimed to measure the quality of care provided for people with Parkinson’s, in comparison to evidence-based guidance on what standard of care they should be receiving.

One of the more alarming results to emerge from the research was that a third of patients feel they don’t receive enough information about Parkinson’s at diagnosis.

The audit evaluated the care provided to 8,846 people with Parkinson’s during the five-month data collection period – more than double the number of patients in the 2012 review.

For the first time, 5,834 people with Parkinson’s and their carers contributed to the Parkinson’s UK Patient Reported Experience Measure (PREM) questionnaire, which allowed patients to voice their own opinions of the care they receive as part of the audit process.

Positive responses

In its findings, the charity showcased evidence of good practice. For example, 73% of respondents felt that the number of times that they were seen by their consultant met their needs. In addition, the majority of comments made about the quality of service received were positive.

Areas for improvement

However, the audit also highlighted the following areas for improvement, along with the evidence to back it up.

1. Integrated services

– Only 13% of services were able to offer access to a full multi-disciplinary team of professionals.

2. Standardised practices

– Around 40% of people were not assessed for blood pressure, pain and bone health in neurology services.

3. Communication and information sharing

– Only 65% of respondents felt they received enough information on initial diagnosis.

4. Inpatient management

– Less than 50% of those admitted to hospital consistently received their Parkinson’s medication on time.

5. Anticipatory care planning

– Only 28% of those with markers of advanced Parkinson’s had any recorded discussion of end-of-life care issues.

Anne-Louise Cunnington, a consultant geriatrician at NHS Greater Glasgow and Clyde and clinical audit lead for the UK Parkinson’s Audit, believes the outcome of the audit is a great opportunity for Parkinson’s services to improve care and really make a difference to people affected by Parkinson’s.

Cunnington said: “This audit presents the most complete picture to date of the state of Parkinson’s care in the UK. The results are not data for the sake of data but are a call to action. We absolutely can’t improve patient care without implementing change.”

The audit should be “a driver to improve standards of care for every person living with Parkinson’s,” Cunnington added.

http://parkinsonslife.eu/parkinsons-uk-audit-one-third-of-patients-dont-receive-enough-info-about-parkinsons-at-diagnosis/

SMALL AND LARGE FIBER NEUROPATHY IN PARKINSON'S DISEASE

27th August 2016 - New research

Recent studies have reported that peripheral neuropathy is common in people with Parkinson's Disease and raised the possibility that L-dopa neurotoxicity is the main culprit. Peripheral neuropathy develops when nerves in the body's extremities, such as the hands, feet and arms, are damaged. This can cause numbness and tingling in the feet or hands, burning pain in affected areas, and muscle weakness, especially in the feet. For more information go to : 

http://www.nhs.uk/Conditions/Peripheral-neuropathy/Pages/Symptoms.aspx

In people with Parkinson's Disease, neuropathy screening was carried out, including neurological examination, nerve conduction studies and skin wrinkling tests.

Two of the tests showed that 57% and 42% of people with Parkinson's Disease had abnormal results that indicated polyneuropathy. The prevalence in people with a Parkinsonism was similar to people with Parkinson's Disease but the results were less severe. The results showed that polyneuropathy was more common in Parkinson's Disease than previously assumed, but the cause was not solely attributed to taking L-dopa.

The researchers concluded that large fiber and small fiber polyneuropathy are common in people with Parkinson's Disease. However, instead of concluding that the cause was L-dopa, the cause of the neuropathy was thought to be multifactorial. Neuropathy was previously related to age, vitamin B12 deficiency, serum folate levels, and especially L-dopa use.

Reference : BMC Neurology [2016] 16 : 139 (D.F.de Araújo, A.P.de Melo Neto, I.S. Oliveira, B.S.Brito, I.T.de Araújo, I.S.Barros, J.W.Lima, W.G.Horta, FdeA.Gondim)

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/27530902

http://www.viartis.net/parkinsons.disease/news/160827.pdf mail@viartis.net

©2016 Viartis 

http://www.viartis.net/parkinsons.disease/news/160827.pdf

Delaying Parkinson’s Disease Onset with Statin Therapy

August 27th, 2016

Can statins provide neuroprotective properties in diabetes patients?

Sample of a Statin

The use of statins has been widely implemented in the management of hyperlipidemia, diabetes, and other cardiovascular disease. Studies have shown benefits from the medications that go beyond their ability to inhibit the rate-limiting step in cholesterol biosynthesis. This inhibitory effect has made these agents a pivotal part of maintaining LDL-C levels in patients with type 2 diabetes mellitus. Statins have shown to provide anti-inflammatory and antioxidant effects in the vascular endothelium, which have made this class of medications useful for preventing vascular injury and reducing atherosclerosis risk. Based on these findings, researchers have been studying the use of statins in Parkinson’s Disease (PD). A meta-analysis conducted by Shuang Bai et al., looked in the use of statins and the risk of Parkinson’s Disease. In this study, researchers found that statin use (i.e. lovastatin, simvastatin, pravastatin, atorvastatin, and rosuvastatin) is associated with a reduced risk of Parkinson’s Disease. From the different statins used in this study, it was discovered that simvastatin and atorvastatin provided the most benefit in the risk of developing Parkinson’s Disease due to their lipophilicity and ability to readily cross the blood-brain barrier.

Pravastatin showed least benefit due to its lipophilicity and inability to cross the blood-brain barrier when compared to atorvastatin and simvastatin. Findings from this and other studies show conflicting data, which warranted more research to further highlight the potential benefits from statin therapy in PD patients.

Recently, K.D. Lin and colleagues expanded on this topic and looked at the association between the use of statins and onset of Parkinson’s Disease in diabetes patients. A total of 50,432 patients were enrolled in the study. Diagnosis of diabetes was established by the use of ICD-9-CM codes. Those patients who had 3 outpatient visits within the follow-up year were assigned to the diabetes group. The study took into consideration other comorbidities, such as hypertension, hyperlipidemia, ischemic heart disease, and stroke. Patients were followed for 7.84 ± 3.79 years. From the study subjects, 76.28% were diagnosed with hypertension, out of which 54.02% were statin users. A total of 69.13% were diagnosed with hyperlipidemia and only 64.23% were statin users. Subsequently, stroke was the diagnosis for 28.14% of patients and an ischemic heart disease diagnosis was established for 39.59% of patients, out of which 53.29% and 56.91% were on statin therapy, respectively.

Results from this research study show a lower incidence rate of Parkinson’s Disease in those patients receiving statin therapy (crude HR: 0.63; 95% CI 0.57-0.69; p<0.001 based on dose-dependent trends). A regression analysis showed a higher RR in the incidence of PD in patients diagnosed with stroke (crude HR: 1.78; 95% CI 1.60-2.00). This can be explained by the neurological damages a stroke can cause in the patient.  It was also found that older patients, those with low socioeconomic status, and patients with hyperlipidemia and no statin use were at an increased risk for Parkinson’s Disease. Another finding from this study shows that all statins except lovastatin demonstrated protective effects on PD incidence, which may be attributed to their pharmacological properties.

These findings can support the use of statins in diabetes patients who are at risk for PD. Even though there is evidence supporting the use of statins in Parkinson’s Disease, some of the results seem inconclusive. Some limitations from this study include the fact it did not take into consideration confounding factors, such as nutrition status, alcohol use, and smoking/nicotine levels. Additionally, the study did not look into specific laboratory values for lipid levels, which have been shown to be inversely proportional with the incidence of Parkinson’s Disease. These characteristics can help guide future studies in a more diverse population, which includes all of these variables, therefore making it more applicable to our patient population. Nonetheless, the current evidence shows that statin therapy can have protective effects in the substantia nigra, in addition to attenuating glial activation, inhibiting neuronal inflammatory process, promoting antioxidant pathways, and providing protection to dopaminergic neurons.

Practice Pearls:

• Statins have the potential of decreasing the onset of Parkinson’s Disease in diabetes patients through neuroprotective effects.
• Statin therapy with lovastatin provides least benefit in delaying the onset of Parkinson’s Disease in diabetes patients when compared to other statins.
• More studies are needed in order to establish the exact response from statins in patients with Parkinson’s Disease

References:

Bai, Shuang, Yi Song, Xin Huang, Lidan Peng, Jie Jia, Yu Liu, and Hong Lu. “Statin Use and the Risk of Parkinson’s Disease: An Updated Meta-Analysis.” PLOS ONE PLoS ONE 11.3 (2016): n. pag. Web

Lin KD, Yang CY, Lee MY, Ho SC, Liu CK, Shin SJ. “Statin Therapy Prevents the Onset of Parkinson Disease in Patients with Diabetes” Ann Neurol. (2016). Web. doi: 10.1002/ana.24751. [Epub ahead of print]

http://www.diabetesincontrol.com/delaying-parkinsons-disease-onset-with-statin-therapy/

Here’s What We’re Looking At From Neuroderm Ltd (NASDAQ:NDRM)’s Parkinson’s Trial

Aug. 26, 2016

Neuroderm Ltd (NASDAQ:NDRM) just announced the kicking off of a pivotal trial in its lead Parkinson’s disease (PD) candidate, and the company has taken a bit of a dive on the news. Parkinson’s is notoriously difficult to go after in the biotech space, and very few pivotal trials come out in favor of the drugs they are studying. Neuroderm’s candidate has performed well in trials to date, however, and if it can carry its performance through to the phase III, it’s got a good chance of hitting commercialization. Ahead of completion and topline, therefore, let’s take a look at the drug in an attempt to figure out what its chances of success are, and what an approval might mean for Neuroderm.

So, the drug. It’s called ND0612L, and it’s targeting moderate PD – i.e. patients that who can no longer effectively control their motor complications with the current SOC in the space, oral levodopa. It’s a continuous dosing product, available in two administration types – patch pump and belt pump.

Levodopa is pretty much the only widely used drug right now, and it is designed to help replenish the dopamine levels in PD patients, which as a result of the disease, are low, causing the motor difficulties and other symptoms. However, as the condition progresses, the single dose administration isn’t effective enough, and patients can find themselves having longer and more severe OFF periods, during which the symptoms are almost impossible to control and can be debilitating.

ND0612L is designed to continuously dose a patient so that he or she can receive a steady, full time dose, and in turn, control their symptoms much more effectively. The drug is a combination of carbidopa and levodopa. Carbidopa is designed to inhibit the natural metabolism of levodopa, so as to increase the levels that become active in controlling symptoms. It also helps with the nausea side effect that is associated with levodopa.

It’s a pretty simple concept, but might be a great solution for patients that find standard administration ineffective. So how has it performed so far?

The company completed a phase II trial back in 2014, looking at safety and efficacy in patients with motor complications. It was placebo controlled and double blinded, with the goal of showing that this type of administration could improve motor function in a group of 30 patients compared to placebo. It was primarily a safety trial, so tolerability was the primary endpoint. Secondary, and more interesting, was the fluctuations in plasma levodopa across the dosing period. The assumption is that a reduction in fluctuations would result in a reduction in OFF time.

The trial showed that the patients that received continuous, subcutaneous doses of the active drug exhibited stat sig reduction in fluctuations of plasma levodopa concentrations compared to patients receiving placebo. Further, those in the active arm exhibited a corresponding in-clinic two-hour reduction over placebo in OFF time, and a host of other quality of life benefits including better sleep, no increase in dyskensia, etc. In simple terms, the drug performed very well.

So what are we looking for from the pivotal?

This one’s an efficacy study, with an endpoint of the change from Baseline to Week 16 in the mean percentage of OFF time during waking hours, based on patient’s home diary assessments. It’s targeting a 150 patient enrollment, and they will be split down the middle and double blinded to receive either a continuous placebo or continuous levodopa/carbidopa infusion.

We’re basing the endpoint on the data from the phase II, so we would like to see a minimum of two hours’ improvement from baseline. The trial is looking at waking hour percentage, so assuming sixteen hours of waking hours, and a 50 50 split in OFF ON, this translates to a min 25% improvement.

The trial is running through to August next year, and full completion is slated for November 2017. We expect topline, therefore, before the close of 2017.

http://marketexclusive.com/heres-looking-neuroderm-ltd-nasdaqndrms-parkinsons-trial/25000/

Qld breakthrough in Parkinson's treatment

Aug. 27, 2016

breaking news

Australian Associated Press

Queensland researchers have made a breakthrough that could help treat tremors and muscle stiffness caused by Parkinson's disease.

The study from the University of Queensland's Institute for Molecular Bioscience examined a genetic mutation the biological cause of which has not been understood - until now.

Their study showed that dysfunctions in retromer - in a type of protein responsible for transporting biological material within a cell - creates congestion in the transport network inside cells.

That disrupts the ability of recycling cells to get to the right place, which means cells in the brain can't get rid of waste material, leading to cell death.

"It's this cell death that then causes the symptoms of Parkinson's disease, such as tremors and muscle stiffness," says Associate Professor Rohan Teasdale.

He says the team's discovery has the potential to improve treatments that address the symptoms of Parkinson's disease.

The same treatment principle could also apply to nearly 50 other disorders caused by the build-up of waste materials within cells.

Those disorders, known as lysosomal diseases, are especially prevalent in young children.

The study by the Institute for Molecular Bioscience has been published in the Journal of Biological Chemistry.

http://www.news.com.au/national/breaking-news/qld-breakthrough-in-parkinsons-treatment/news-story/8445361d0b16d1cdde4beed9779b9d25