The magic of dance is to bypass mere thought and speak directly to the heart! And nowhere is this more true than the Argentine Tango. In its birthplace of Buenos Aires, the dance is proving a boon to patients with symptoms of Parkinson's Disease.
On a small dark dance floor in Buenos Aires, a group of men and women are showing it's never too late to Tango.
But dance is never just about the moves. Tango is wonderfully therapeutic in addressing the symptoms of Parkinson's - which can include tremors, problems with balance, and cognitive decline.The magic of dance is to bypass mere thought and speak directly to the heart! And nowhere is this more true than the Argentine Tango.
In its birthplace of Buenos Aires, the dance is proving a boon to patients with symptoms of Parkinson's Disease.The Foundation for Argentine Tango runs these free weekly workshops, and patients are delighted with their progress. Juan Roberto Lopez is 77 years-old."It helps people who have Parkinson's like me. It helps maintain balance. Everything is about balance in Tango," said Juan Roberto Lopez, Parkinson's disease patient.
59-year-old Patricia Ida Frola, a dermatologist with Parkinson's disease, says she's conducted her own research on how the dance can reduce the common symptom of body stiffness.
"What happens to the brain? It decodes. The first stimulus goes to the heart, changes the heart rate, and sends a stimulus back to the brain. From there, it modifies the metrics of the electrical muscle stimulation. I am then filled with joy," said Patricia Ida Frola, Parkinson's disease patient.
This month, Buenos Aires hosted a conference to discuss how the dance can be used therapeutically - this following clinical studies in the U.S., Canada, and the U.K. that show dance classes help with Parkinson's.
A central Indiana patient had tremors that caused her to shake so badly that she couldn't brush her teeth or even hold a cup of water. It was progressing to the point she feared she'd have to quit her job. Then her doctor recommended a new approach to solve her problem.
"When you hear brain surgery, you think, 'oh, my gosh,'" said Rhonda Walls, 46.
The fix for Rhonda Walls' essential tremor was daunting. But so too were the increasing challenges of everyday life despite medication.
Walls took cell phone video snippets showing her shake while writing, holding a coffee cup and even brushing her teeth.
"I was to the point 'Where do I give? What do I do?' I never had a doctor tell me that they could fix this," she said.
But her neurologists at St. Vincent believed a deep brain stimulator implanted while she was asleep instead of the tradition surgery done while the patient is awake could be the fix..
"There is about one percent of neurosurgeons who do this procedure asleep now in the country and I was one of the early trainees in this technique," said Dr. Albert Lee, St. Vincent neurosurgeon, Goodman Campbell Brain & Spine.
Dr. Lee implanted a generator with a battery and small computer in Rhonda's chest. It's similar to a pacemaker, but this device communicates with leads placed in the brain which deliver electrical impulses to stop the tremor signals. It's called Medtronic Deep Brain Stimulation Therapy (DBS), and it's used to treat Parkinson's, essential tremor and cervical dystonia.
While DBS isn't new, the latest development is how doctors are implanting it. Patients were fearful of being awake during the procedure; now it can be done while they're asleep using technology similar to GPS mapping for the brain.
"Once we turned the device on, her life was drastically altered. It's the most rewarding thing I do as a physician is that first time you turn off the tremor," said Dr. Mike Sermersheim.
Rhonda can adjust the device wirelessly with physician guidance to accommodate the daily fluctuations in her tremor strength.
"It's on right now but when I turn it off, you can see that I am already starting to shake," she said. "I can show you it's difficult to hold on to this glass of water and when I turn it back on, my tremor is gone."
The results are impressive. Doctors fear too many patients like Rhonda may be unaware of their options.
"We really feel like there is something we can do to help a lot of folks, not just in Indiana but in the region and feel like there are folks out there just suffering needlessly," said Dr. Lee.
Rhonda is so relieved she is relying on others less.
"It's pretty amazing when you go to work in the morning and write for yourself and pick up a cup of coffee and drink and not worry about shaking, it's amazing. The procedure is similar for Parkinson's patients," she said.
The key: many patients avoided a surgical fix because they feared being awake during frame placement and drilling. This advancement avoids that.
Addex Therapeutics a leading company pioneering allosteric modulation-based drug discovery and development announced today that its lead compound dipraglurant, a metabotropic glutamate receptor 5 (mGluR5) negative allosteric modulator (NAM) demonstrated robust efficacy in multiple preclinical models of anxiety and depression.
The studies were conducted in collaboration with the laboratory of Professor Andrzej Pilc of the department of Neurobiology, Institute of Pharmacology at the Polish Academy of Sciences in Krakow, Poland.
Dipraglurant is a novel small molecule inhibitor of the metabotropic glutamate receptor 5 (mGluR5) that has successfully completed Phase II proof-of-concept testing in Parkinson's disease (PD) patients suffering from debilitating levodopa-induced dyskinesia (LID). Dipraglurant given orally showed anxiolytic effects in the elevated plus maze test (EPM) and the stress-induced hyperthermia test (SIH) in mice at the dose of 50 mg/kg, and antidepressant effects in the forced swim test (FST) in rats (at doses of 10 and 30 mg/kg) and mice (at doses of 30 and 50 mg/kg) .
These data will be presented at the XIX International Congress of the Polish Pharmacological Society, 17-19 September 2015 being held in Swinoujscie, Poland. "The consistent effects across a battery of different preclinical models provides further evidence that excessive glutamate activity mediated through mGluR5 can contribute to the development of anxiety and depression symptoms" commented Professor Andrzej Pilc of the department of Neurobiology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland. "There remains a significant unmet medical need for medications to treat the full range of motor and non-motor complications of PD" said Sonia Poli, CSO at Addex, "dipraglurant may represent an attractive approach to treat not only levodopa induced dyskinesia, but also the concomitant non-motor symptoms which are present in almost all PD patients and can have a greater negative impact on the quality of life than motor complications. "The collaboration with Prof. Pilc, a world leader in fundamental research on mGlu receptors is a further demonstration of our strategy to drive forward our research in collaboration with leading academic institutions." said Tim Dyer, CEO at Addex. "While we continue to prioritize the development of dipraglurant for Parkinson's disease levodopa induced dyskinesia and dystonia, these data provide evidence of additional utility for dipraglurant in PD patients."
- See more at: http://www.selectscience.net/commPRDetails.aspx?artID=38363&u=5D04C7F7-61DF-40BC-91EE-FBFA9963B81A#sthash.wLNumy6k.dpuf
Roche said earlier this week that its Pharma Research & Early Development unit has developed a smartphone-based monitoring system to measure the symptoms of Parkinson’s disease.
The app is currently being used in a Phase I trial run by Prothena in collaboration with Roche, in what could be the first time such an app has been used to measure disease and symptom severity in a medicine development program in Parkinson’s disease, the firm noted.
Traditionally, disease disability and impairment are measured in trials by physician assessments using the Unified Parkinson’s Disease Rating Scale, but these are limited to the specific times. The app will enable continuous measurement of PD fluctuation every day and throughout the day.
“Ultimately, we hope the app can be used in future clinical development to enable more objective measures on response to treatment to complement doctor assessments,” said Anirvan Ghosh, Head of Neuroscience Discovery for pRED.
Kills off Heidelberg deal
Meanwhile, the Swiss drug giant is discontinuing its two-year partnership with Wilex subsidiary Heidelberg Pharma, focused on the development of antibody-targeted amanitin conjugates to fight cancer.
The companies signed an agreement in 2013 giving Roche a license to Heidelberg’s ATAC technology, which was subsequently expanded last year to include research on ATACs for various tumour types based on Roche antibodies.
In a statement, Wilex said the collaboration has “progressed well, on schedule, and in a mutually
satisfactory manner”, and that Roche’s decision stemmed from its prioritisation of cancer immunotherapies.
Large Degree of Innovation in Parkinson's Disease Pipeline
The Parkinson's disease (PD) pipeline currently has 302 products in active development across all stages, but a stark contrast between the mechanisms of action employed in the current market and the pipeline is evident. Where the market relies on symptomatic treatments that target neuromodulatory receptors, the pipeline shows a diverse range of neuroprotective therapies targeting dysfunctional disease processes. This diversity is partially due to the presence of 90 first-in-class products, which accounts for 37% of the overall pipeline therapies that disclosed their target. In an industry, market and development landscape that favors first-in-class over non-first-in-class development in many ways, such as through faster approval or greater revenue, this finding has strategic implications for a wide array of market participants, both large and small. Despite their historically high attrition rate, first-in-class therapies that reach the market have the potential to transform and improve the PD treatment landscape.
Alignment of First-in-Class Molecular Target with Disease Processes and Genetics
PD is a complex and multifaceted disease with a complex interplay between different pathological processes. Enormous research efforts and significant technological advances have furthered knowledge of the neuroanatomy of the basal ganglia and of the fundamental processes underlying neurodegeneration, helped by the ongoing identification of susceptibility genes and causative genes in familial PD. Although the exact mechanisms that initiate onset remain unclear, these insights have been translated into the pool of novel therapeutic targets, which may potentially become disease-modifying therapies by aligning to the disease processes and some genetic determinants of PD.
GBI Research's proprietary analysis showed substantial variation in how well the functional roles of PD first-in-class targets align to the pathophysiology of PD. Further in-depth analysis identified the most promising first-in-class targets based on various scientific and clinical parameters. Examining scientific and clinical data of promising first-in-class targets showed that first-in-class status is not, in its own right, enough for a successful product; however, the first-in-class products substantiated by scientific and clinical evidence will be exciting future prospects with the potential to transform the PD market.
First-in-Class Products in Licensing and Co-development Deals
Strategic consolidation is relatively uncommon in the PD market. Concerning first-in-class specifically, only nine first-in-class products that are currently in development have been involved in licensing or co-development deals since 2006. Despite the low sample size, it is clear that the first-in-class PD products offer an attractive investment prospect as they command much higher deal values and, on average, deals occur earlier in development compared to non-first-in-class counterparts. Both trends were substantiated by industry-wide data that showed that, particularly in Phase I, first-in-class products would attract larger mean and median total deal values. The data highlight that the first-in-class deals landscape is different and indicates a greater chance of becoming much more lucrative than the deals landscape for addition-to-class or advance-in-class therapies.
A total of 81 first-in-class products that are currently in development have not yet been entered into a licensing or co-development deal. Under a growing unmet need for disease-modifying therapies and increasing understanding of disease processes allowed by technological advances, there are numerous opportunities for strategic alliances to bolster a first-in-class portfolio or fund clinical development. Some of these first-in-class products are supported by promising scientific and clinical data, making them attractive prospects as both therapeutics and investment opportunities.
Scope
The report analyzes innovation in PD in the context of the overall pipeline and current market landscape. It also analyzes the deals landscape surrounding first-in-class products and pinpoints in-licensing opportunities.The report includes -
- A brief introduction to PD, including symptoms, pathophysiology, and an overview of pharmacotherapy and treatment algorithms
- Coverage of the changing molecular target landscape and particular points of innovation in the pipeline
- A comprehensive review of the pipeline for first-in-class therapies, analyzed by stage of development, molecule type and molecular target
- Identification and assessment of first-in-class molecular targets with a particular focus on early-stage programs of which clinical utility has yet to be evaluated, as well as literature reviews of novel molecular targets
- Industry-wide analysis of first-in-class deals compared to non-first-in-class deals
- An assessment of the licensing and co-development deal landscape for PD therapies and benchmarking of deals comparing first-in-class and non-first-in-class-products
Reasons to buy
The report will enable business development and enable marketing executives to strategize their product launches by allowing them to -
- Understand the focal shifts in molecular targets in the PD pipeline
- Understand the distribution of pipeline programs by phase of development, molecule type and molecular target
- Access a scientific and clinical analysis of first-in-class developmental programs for PD, benchmarked against non-first-in-class targets
- Assess the valuations of licensed and co-developed PD treatments
- Access a list of the first-in-class therapies potentially open to deal-making opportunities
Download the full report: https://www.reportbuyer.com/product/2588077/About ReportbuyerReportbuyer is a leading industry intelligence solution that provides all market research reports from top publishershttp://www.reportbuyer.comFor more information: Sarah SmithResearch Advisor at Reportbuyer.com Email: query@reportbuyer.com Tel: +44 208 816 85 48 Website: www.reportbuyer.com
B Dasarath Reddy | HyderabadAugust 12, 2015 Last Updated at 18:12 IST
Dr Reddy's Laboratories Limited announced today that it has launched Pramipexole dihydrochloride extended-release tablets of 0.375 mg, 0.75 mg, 3 mg, 4.5 mg, in the US market on Tuesday, following the approval by the United States Food and Drug Administration (USFDA) .
The drug is a therapeutic equivalent generic version of Mirapex ER owned by Boehringer Ingelheim company. The product is used to treat symptoms of Parkinson's disease.
Mirapex ER brand and generic had US sales of approximately $ 48.3 million for the most recent twelve months ending in June, 2015, the company said quoting the IMS Health data
Subtle changes in white matter (WM) integrity are detectable in patients with Parkinson’s disease (PD) and are associated with early impairments in cognition, say researchers.
They therefore suggest that imaging of WM could be used as a biomarker for mild cognitive impairment in PD patients.
Early identification of PD patients at risk of developing dementia “is of prognostic importance”, they say, adding that imaging could potentially facilitate therapeutic intervention “early in the disease process before extensive neuronal loss.”
Diffusion tensor imaging revealed significantly increased mean diffusivity among 125 PD patients compared with 50 controls, indicating degeneration of WM. This occurred bilaterally in frontal and parietal subcortical tracts, affecting the forceps minor, cingulum, superior longitudinal fasciculus, inferior longitudinal fasciculus and inferior fronto-occipital fasciculus tracts, the corticospinal tract, the corpus callosum and the internal capsule.
WM degeneration was most marked in PD patients with significant impairments in tests of semantic fluency; they had significantly increased mean diffusivity relative to PD patients with normal cognition, as well as versus controls, which the researchers describe as “a novel finding”.
The PD patients overall had slight but statistically significant impairments in cognition, relative to the controls. For example, the median scores on the Mini-Mental State Examination were 29 versus 30.
Patients with impaired semantic fluency also had reduced grey matter volume in frontal and parietal areas relative both to PD patients with normal cognition and controls, and the same was true for patients with impaired executive function in the Tower of London task. But there were no differences in grey matter volumes between the overall PD group and controls.
Gordon Duncan (Western General Hospital, Edinburgh, UK) and co-researchers stress that reduced mean diffusivity was detectable despite no overall changes in grey matter volume or the directionality of fluid flow in brain matter, assessed via fractional anisotropy.
“Together, these results indicate that degeneration of central WM tracts occurs early in PD and may underlie early cognitive dysfunction”, the team writes in Movement Disorders.
Researchers grappling to understand what happens inside brain cells of people with Parkinson's disease are baffled by a mystery that plays out as the disease progresses. Why is it that one group of neurons decays while a similar group nearby remains unscathed?
Published: New research discovers two proteins that appear to protect the brain cells most affected by Parkinson's disease.
Answering this question could lead to new ways of treating a devastating - and currently incurable - brain-wasting disease that gradually erodes the ability to walk, talk, and live an independent life.
One answer is offered in a study published in Nature Neuroscience. There, a team from The Rockefeller University and Columbia University, both in New York, NY, describes finding two proteins that may play a key role in the progression of Parkinson's disease.
The two proteins - SATB1 and ZDHHC2 - appear to protect the brain cells most affected by Parkinson's disease. When the proteins become less active, the disease sets in.
Scientists believe the causes of Parkinson's disease center around what are called dopaminergic neurons. These cells release the messenger molecule dopamine, a chemical that is important for control of movement.
The dopamine-releasing cells most affected by Parkinson's disease are located in a midbrain region called the substantia nigra pars compacta (SNpc). As the disease progresses, these cells gradually deteriorate and die.
The researchers - whose study focuses on molecular changes in dopamine-releasing cells - suggest their discovery could lead to new targets for drugs that slow the progression of Parkinson's disease.
Researchers searched 'translatome' as opposed to genome
The study is also significant for another reason - the molecular searching method that the team used to find the two proteins.
Usually, when scientists want to look for molecular changes that affect disease, they use genetic sequencing to create a profile of the variations in gene expression.
But gene expression profiling is not a very useful tool when you are trying to identify the molecular changes that occur in a particular type of cell and focus on the really important ones.
Also, genes do not act in a straightforward manner - they also regulate each other. There are master regulator genes that act as control dials, turning other genes on and off, or up and down. Gene expression profiling does not easily tell you about the molecular changes that arise from gene expression.
To overcome this difficulty, the team adapted a method that some of the members had already been working on - one that searches the "translatome" as opposed to the genome - to find the proteins involved in communicating changes arising from master regulator genes.
The translatome is the complete collection of messenger molecules that are involved with translating genetic information from DNA and carrying it to sites where proteins are made inside cells.
With genetically engineered mice, the team captured the genetic messages being translated into proteins in dopaminergic neurons in the mice's midbrain region.
They then compared the interactions of regulator genes with their target genes in the mouse brain, and used this map to interpret the changes they found between normal mice and those with Parkinson's-like symptoms.
Senior author Paul Greengard, a neuroscience professor who heads a Rockefeller lab that specializes in investigating molecular activity in nerve cells, says:
"Within a dying nerve cell, the levels of hundreds of proteins change. Some of these shifts are consequences, others are causes. We set out to find which cause cell death among neurons."
Discovery explains why one group of dopamine cells is more affected
Their new approach helped the team find two of the so-called master regulatory molecules. Prof. Greengard says the discovery offers an "unexpected explanation as to why one population of neurons degenerates in Parkinson's, while similar neighbors do not suffer from the same degree of degeneration."
While the dopamine-producing neurons of the SNpc are the ones most affected by Parkinson's disease, there is another group of dopamine-producing neurons in another region called the ventral tegmental area (VTA) that is less affected.
The team found that the two proteins SATB1 and ZDHHC2 are more abundant in the dopaminergic neurons in the SNpc than in the VTA.
When the researchers reduced the abundance of these molecules in the brains of normal mice, they observed it was followed by rapid degeneration like that seen in Parkinson's disease.
The team believes conventional gene expression profiling would not have been able to identify the two proteins as key protective factors. Even though they continue to be expressed in the neurons, their regulatory activity drops off and they no longer stimulate their target genes, says first author Lars Brichta, a senior research associate in Greengard's lab, who adds:
"We later found similar changes in activity in the brains of Parkinson's patients, particularly those in the early stages."
The findings also challenge current thinking about the molecular origins of Parkinson's disease, where it is thought that the VTA neurons are protected in some way by the decay seen in neurons of the SNpc. But, Greengard asserts:
"In an unexpected contradiction to current models, the proteins we found protect the SNpc. Because dopamine and its metabolites can be toxic, we can speculate that, in the course of evolution, SATB1 and ZDHHC2 arose to protect this particular set of sensitive neurons from cell death."
As well as opening a route to new treatments for Parkinson's disease, the team believes their translatome approach may also be useful in the study of other neurodegenerative diseases such as Alzheimer's disease, amyotrophic lateral sclerosis (ALS), spinal muscular atrophy, and Huntington's disease.
Could daily chocolate supplements reduce symptoms of Parkinson's disease? That's the thinking behind a new trial at Dresden University of Technology in Germany.
Around 30 patients will be given 50g of either white chocolate, which contains no cocoa, or dark chocolate (85 per cent cocoa) twice daily for a week. They'll then receive the other type of chocolate in a second week. The differences in their symptoms will be compared.
Parkinson's disease is caused by a loss of nerve cells in the part of the brain that produces dopamine, which helps co-ordinate body movement. Low levels of the hormone have been linked to symptoms of Parkinson's disease, such as shaking.
The cocoa in chocolate contains phenylethylamine, which has been shown to increase the release of dopamine.
IMAGE: PARKINSON'S DISEASE IS CAUSED BY THE LOSS OF DOPAMINE-PRODUCING NEURONS IN A MIDBRAIN REGION CALLED THE SUBSTANTIA NIGRA PARS COMPACTA (SNPC). ABOVE, THE SNPC DOPAMINE NEURONS OF A MOUSE BRAIN appear in yellow.
CREDIT: LABORATORY OF MOLECULAR AND CELLULAR NEUROSCIENCE AT THE ROCKEFELLER UNIVERSITY/NATURE NEUROSCIENCE
PUBLIC RELEASE:
ROCKEFELLER UNIVERSITY
As Parkinson's disease progresses in patients, a puzzling dichotomy plays out in their brains. One set of neurons degenerates, while a similar population nearby is spared the same degree of damage. Why the difference? An answer to this question could clear the way for preventions and treatments for this disease, which impairs movement.
Using a new strategy they have devised to identify the molecular changes that drive the loss of neurons, researchers at The Rockefeller University and colleagues at Columbia University have identified two proteins they report may be important to Parkinson's. These two gene-regulating molecules appear to have a protective effect in the set of neurons most affected by the disease, and when their activity wanes, disease sets in. This discovery, described online in Nature Neuroscience on July 27, suggests new avenues by which the disease might be prevented or treated.
"Within a dying nerve cell, the levels of hundreds of proteins change," says study author Paul Greengard, Vincent Astor Professor and head of Laboratory of Molecular and Cellular Neuroscience. "Some of these shifts are consequences, others are causes. We set out to find which cause cell death among neurons."
"Using a new combination of techniques," Greengard adds, "we identified two of these so-called master regulatory molecules -- a discovery that offers an unexpected explanation as to why one population of neurons degenerates in Parkinson's, while similar neighbors do not suffer from the same degree of degeneration."
Parkinson's disease often first shows up as a slight tremor of the hands, and progresses to affect speech, facial muscles, and other movements. This deterioration is caused by the progressive loss of neurons located in a midbrain region called the substantia nigra pars compacta (SNpc). These neurons produce dopamine, a molecule that transmits signals between neurons, and it is the loss of dopamine that causes the loss of motor control associated with Parkinson's.
Some deterioration also occurs in the dopamine-producing neurons of a neighboring brain region, the ventral tegmental area (VTA), but the VTA neurons are much less affected than those of the SNpc.
Typically, when scientists want to look for molecular changes associated with a condition they use genetic sequencing to create a profile of variations in gene expression. But with conventional profiling approaches it is difficult to pick out the changes that occur in a particular type of cell, and distinguish those that are truly important. It is also very hard to tell which changes arise from the master regulator genes, which can act as control dials turning their target genes up or down.
To overcome these issues, the team led by first author Lars Brichta, a senior research associate in Greengard's lab, adapted a technique previously developed in Greengard's and Nathaniel Heintz's labs, which involves genetically engineering mice to capture the genetic messages being translated into proteins in a specific population of cells. They then mapped the interactions of regulator genes with their target genes in the mouse brain, and used this new tool to interpret the changes they documented between normal mice and those suffering from Parkinson's-like degeneration.
This led them to two molecules: the proteins SATB1 and ZDHHC2, which are more abundant in the dopaminergic neurons in the SNpc versus the VTA. When the researchers reduced the abundance of these molecules in the brains of normal mice, rapid degeneration like that seen in Parkinson's disease followed.
"Conventional gene activity profiling approaches would not have been able to identify SATB1 and ZDHHC2 as key protective factors because the levels of these proteins do not change. But even though they continue to be expressed within the neurons, it appears that their regulatory activity drops off and they no longer stimulate their target genes," Brichta says. "We later found similar changes in activity in the brains of Parkinson's patients, particularly those in the early stages."
Their findings also challenge the prevailing thought as to the molecular origins of Parkinson's: that VTA neurons had some sort of factor protecting them against the kind of degeneration seen in the SNpc.
"In an unexpected contradiction to current models, the proteins we found protect the SNpc. Because dopamine and its metabolites can be toxic, we can speculate that, in the course of evolution, SATB1 and ZDHHC2 arose to protect this particular set of sensitive neurons from cell death," Greengard says. "The discovery of these two molecules' role in Parkinson's may assist in the development of treatments, because they are potential new targets for drugs."
The researchers believe their new strategy may also be useful in studies of other neurodegenerative diseases, including Alzheimer's, spinal muscular atrophy, Huntington's disease and amyotrophic lateral sclerosis.
What do tandem bicycles, exoskeletons and ARM processors have in common? They're all helping in the fight against Parkinson's.
The effects of Parkinson's are destructive: muscle tremors take hold, and the ravages of the disease render them stiff and slow. Now, a chance discovery by a US doctor has led to a breakthrough treatment which combines cycling with a cutting-edge robotic exoskeleton.
About 1 in 350 Australians live with the disease, and there are up to a million more sufferers living in the US. The disease progressively damages parts of the brain, with symptoms arising when the levels of a chemical messenger in the brain, dopamine, drop below normal levels. Medication can help, as can physiotherapy, but this unusual development delivers a surprising, two-wheeled twist.
To prepare, his friend trained for the trip on an exercise bike, pedalling at a steady rate of 60rpm. However, the trip provided her with an unexpected challenge: the tandem's shared drive chain forced her to pedal roughly 40% faster in order to match Alberts' swifter 85 rpm. Just two days into the trip, they were both surprised to notice that her symptoms had improved.
Amazingly, it wasn't just her legs that showed fewer symptoms – her handwriting was better, too. Alberts decided to investigate.
He recruited 10 patients to take part in sessions on a tandem exercise bike. A qualified trainer sat on the front, as "captain", and the patients sat behind, as "stoker". The patients had to pedal as quickly as the fully-fit trainer for an hour each time, three times a week for two months.
The results were extraordinary and supported Jay's suspicions. They showed a remarkable 35% improvement in motor functions and the effects persisted even four weeks after the tandem sessions had ended.
Significantly, the improvements were evident in the upper body, not just in the muscles that had done the pedalling. This was evidence that the assisted exercise had led to beneficial changes in the brain.
All this would be excellent news, if only tandem exercise bikes were common and easily accessible to Parkinson's patients. Unfortunately, they are very rare. What's more, it becomes increasingly costly if the sessions are one-to-one and require the services of a trainer to lead each workout.
"Sensors in the electro-mechanical legs detect the how hard the wearer is pushing on the pedals, and automatically adjust how much assistance to give."
The concept involves strapping robotic exoskeletal limbs to a rider's own legs. These act as a stabilising force, making sure the wearer uses their own muscles in the right way to maximise the benefit of the exercise, and assisting them by adding power from in-built motors. Sensors in the electro-mechanical legs detect the how hard the wearer is pushing on the pedals, and automatically adjust how much assistance to give.
This frees the patient to ride on a common, single-saddle, static exercise bicycle on their own – no tandem required. What's more, a personal trainer wouldn't be tied to a single person during the session, and could attend to other patients at the same time.
It's an ingenious solution. Instead of a tandem captain expertly regulating the forces and cadence, the robotic legs would be programmed to make sure the wearer is exerting enough effort during the exercise session to help alleviate their condition for weeks to come.
The results provide a ray of hope for sufferers worldwide. It's thought that intense cycling can improve a variety of muscle functions, not just in the legs, if practiced in the early stages of the condition. By helping patients pedal more quickly, and smoothly, than they could unaided, the symptoms of Parkinson's can be reduced.
It's not about the bike
Building a powered machine that interacts intimately with the movement of a human being isn't easy. The motorised limbs have to accurately track and mimic the kinematics of the hip, knee and ankle joints, so sensitive control mechanisms must be in place. After all, nobody will want to wear the device if it could manipulate their legs in an unsafe way.
"The exoskeleton has sensors to measure the loads, angles and pitch at each joint, and to constantly monitor the pressure bearing down on each pedal."
It's an immensely complex undertaking. The exoskeleton has sensors to measure the loads, angles and pitch at each joint, and to constantly monitor the pressure bearing down on each pedal. The data is analysed by the controlling computer, a 32-bit ARM Cortex chip. Commands are then sent to the 90W motors at the hips and more powerful 120W motors at the knees.
The first flush of experiments have confirmed that the system design is robust, but more work needs to be done to refine the design. The prototype will need more modifications and better sensors in order for the motion of the exoskeleton to conform more closely to the movement of human legs while pedalling.
There's still a long way to go with this exceptional project but, when complete, it will offer hope of a better quality of life to Parkinson's sufferers across the globe.
