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Monday, January 11, 2016

Early Weight Loss With Parkinson's May Be a Red Flag

MONDAY Jan. 11, 2016, 2016 -- 

People who lose weight in the early stages of Parkinson's disease may have a more serious form of the movement disorder, according to a new study.
Parkinson's is a chronic and progressive disease marked by tremors, impaired coordination, and slowness and/or stiffness. The cause and cure are unknown.
Weight loss is common in Parkinson's patients, according to background information from the study. But the study findings, published online Jan. 11 in the journal JAMA Neurology, suggest that weight loss in the early stages of the disease could be a red flag for doctors.
"I suspect we may be looking at several subtypes of this disease," study lead author Dr. Anne-Marie Wills, of Massachusetts General Hospital's neurological clinical research institute, said in a hospital news release.
"The patients who experience early weight loss appear to have a more severe, systemic form of the disease, possibly due to involvement of the neuroendocrine system or the gastrointestinal nervous system, while those who gained weight may have a milder form of the disease," she explained.
For the study, conducted between 2007 and 2013, the researchers examined data from more than 1,600 people who had been diagnosed with Parkinson's within the previous five years.
Weight remained stable among 77 percent of the patients, while 9 percent lost weight and 14 percent gained weight during the study period.
Compared to those whose weight remained stable, patients who lost weight had faster worsening of symptoms, the study found. Worsening of symptoms was slowest among patients who gained weight. Rates of survival were similar for all three groups, but that may be because all were in the early stages of the disease, the researchers said.
It's not known if maintaining or increasing weight could slow the progression of Parkinson's.
Also, the study only found an association between early weight loss and worsening symptoms, not a cause-and-effect relationship.
"Since this is just the first observation of this association in Parkinson's, we cannot recommend any changes to standard clinical care right now," said Wills, who's also an assistant professor of neurology at Harvard Medical School.
"But in my own practice, I try to prevent weight loss in patients, and I would recommend providers to be attentive to weight changes in their patients, even early in the disease," she said.
More information
The Parkinson's Disease Foundation has more about Parkinson's disease.
http://health.einnews.com/article/305811983/Bt4tLpFfhu0VEZGH

Blue Sky Science: Can stem cells be used to repair brain damage, help so...




Published on Jan 8, 2016

Blue Sky Science is a collaboration of the Wisconsin State Journal and the Morgridge Institute for Research. The questions are posed by visitors to Saturday Science events at the Discovery Building, a monthly series that features interactive exploration stations centered around a particular topic. The Blue Sky Science team then sets out to find an expert to answer the questions. To view other videos in the series, see http://go.madison.com/bluesky. For more on the Morgridge Institute, see http://morgridge.org/.

http://host.madison.com/wsj/news/local/science/blue-sky-science-video-can-stem-cells-be-used-to/youtube_468087ea-dcc8-5b4b-a20d-b174a66b2a42.html

Researchers describe three cleaning procedures that effectively remove, disassemble α-Syn fibrils

Published on January 11, 2016 at 8:40 AM 




Lewy bodies and Lewy neurites are found in the brains of Parkinson's disease (PD) patients. They consist primarily of fibrils of the protein alpha-synuclein (α-Syn), which self-assembles into fibrils in vitro. If introduced into the human body, these seeds can act as prions and trigger the formation of toxic protein deposits. Because α-Syn fibrils are often used in research, it is important that they are not accidentally transferred to humans or cell cultures. Researchers reporting in the Journal of Parkinson's Disease describe three cleaning procedures that effectively remove and disassemble these α-synuclein seeds.
α-Syn is purified and assembled in test tubes into fibrils that are used to investigate/mimic PD pathogenesis in model animals ranging from worms (c. elegans) to rodents and non-human primates in a large number of laboratories. These laboratories typically contain surfaces and non-disposable items made from plastic, glass, aluminum, or stainless steel. These items are often rough, with areas that cannot be completely cleaned by wiping. Therefore, it is important to minimize contamination through effective cleaning procedures.
"Several teams, including ours, demonstrated that fibrillar α-Syn propagate from one cell, including neurons, to another and amplify during this propagation process mimicking prion particle behavior. These observations suggest that fibrillar α-Syn is not innocuous," explained lead investigator Ronald Melki, PhD, Director of Research at the Paris-Saclay Institute of Neurosciences, CNRS, Gif-sur-Yvette, France.
Researchers applied a solution of fluorescently-labeled fibrils and ribbons of α-Syn to roughened surfaces mimicking laboratory conditions. The droplets were easily visible to the eye and could be assessed by their fluorescence.
Five cleaning solutions were tested: 1) sodium hypochlorite (20,000 ppm); 2) sodium hydroxide (1N), 3) sodium dodecyl sulfate (SDS, 1%, W/V); 4) Hellmanex (1%, V/V); and 5) TFD4 (1%, V/V). As a control, the surfaces were washed with just commercially prepared pure water. After cleaning, the amount of small assemblies, fibrils, and ribbons of α-Syn remaining on the surfaces was measured by fluorescence. To evaluate whether the α-Syn fibrils that were washed off the surfaces were destroyed, fibrils and ribbons were incubated in the various cleaning solutions for one hour and the amount of remaining fibrils was measured.

Lewy bodies and Lewy neurites are found in the brains of Parkinson's disease (PD) patients. They consist primarily of fibrils of the protein alpha-synuclein (α-Syn), which self-assembles into fibrils in vitro. If introduced into the human body, these seeds can act as prions and trigger the formation of toxic protein deposits. Because α-Syn fibrils are often used in research, it is important that they are not accidentally transferred to humans or cell cultures. Researchers reporting in the Journal of Parkinson's Disease describe three cleaning procedures that effectively remove and disassemble these α-synuclein seeds.
α-Syn is purified and assembled in test tubes into fibrils that are used to investigate/mimic PD pathogenesis in model animals ranging from worms (c. elegans) to rodents and non-human primates in a large number of laboratories. These laboratories typically contain surfaces and non-disposable items made from plastic, glass, aluminum, or stainless steel. These items are often rough, with areas that cannot be completely cleaned by wiping. Therefore, it is important to minimize contamination through effective cleaning procedures.
"Several teams, including ours, demonstrated that fibrillar α-Syn propagate from one cell, including neurons, to another and amplify during this propagation process mimicking prion particle behavior. These observations suggest that fibrillar α-Syn is not innocuous," explained lead investigator Ronald Melki, PhD, Director of Research at the Paris-Saclay Institute of Neurosciences, CNRS, Gif-sur-Yvette, France.
Researchers applied a solution of fluorescently-labeled fibrils and ribbons of α-Syn to roughened surfaces mimicking laboratory conditions. The droplets were easily visible to the eye and could be assessed by their fluorescence.
Five cleaning solutions were tested: 1) sodium hypochlorite (20,000 ppm); 2) sodium hydroxide (1N), 3) sodium dodecyl sulfate (SDS, 1%, W/V); 4) Hellmanex (1%, V/V); and 5) TFD4 (1%, V/V). As a control, the surfaces were washed with just commercially prepared pure water. After cleaning, the amount of small assemblies, fibrils, and ribbons of α-Syn remaining on the surfaces was measured by fluorescence. To evaluate whether the α-Syn fibrils that were washed off the surfaces were destroyed, fibrils and ribbons were incubated in the various cleaning solutions for one hour and the amount of remaining fibrils was measured.
http://www.news-medical.net/news/20160111/Researchers-describe-three-cleaning-procedures-that-effectively-remove-disassemble-ceb1-Syn-fibrils.aspx

Sublingual Drug for Parkinson’s ‘Off’ Episodes in Phase 3 Study

Cynapsus, Fox Foundation and Intel also use APL-130277 trial to gather data via wearable device


January 11, 2016
Cynapsus Therapeutics, Inc., a Toronto-based specialty pharmaceutical company, and The Michael J. Fox Foundation for Parkinson’s Research (MJFF) announced they are collaborating to incorporate wearable device technology and “big data” approaches into Cynapsus’ pivotal Phase 3 clinical study of APL-130277, a fast-dissolving, sublingual formulation of the drug apomorphine to treat “off” episodes in Parkinson’s disease (PD) patients.
Off episodes are a complication of Parkinson’s that leave patients rigid and unable to move and/or communicate.
As PD progresses, the efficacy of dopamine replacement medication (the gold standard treatment for the disease) shortens, and patients experience motor fluctuations known as off episodes. Cynapsus’ product candidate, APL-130277, in development since 2010, is a sublingual (under-the-tongue) thin-film formulation of apomorphine designed to be easy to administer, and to rapidly, safely, and reliably convert a patient from “off” to “on” status in all types of off episodes, including those experienced in the morning.
Cynapsus says its unique packaging would allow most patients, when they begin to experience an off episode or even while in an off state, to simply peel open the packaging, remove and self-administer the thin film by placing it under their tongue. The film dissolves over the course of a few minutes, allowing the apomorphine to quickly enter the bloodstream.
The company’s target market for APL-130277 is PD patients who suffer at least one off episode per day. A 2014 paper by A. Rizos, et al., published in the journal Parkinsonism & Related Disorders (DOI: http://dx.doi.org/10.1016/j.parkreldis.2014.09.013) found that approximately 60 percent of PD patients suffer morning off episodes, and Cynapsus believes that nearly all of these patients also suffer other types of off episodes, although necessarily daily. However, the company estimates that two-thirds of the approximately 600,000 patients who experience off episodes suffer at least one every day.
The Michael J. Fox Foundation says that apomorphine, despite its strong efficacy as a rescue medication for intermittent off episodes in PD, and its rapid action, is an underutilized drug largely because its delivery method — Apokyn (apomorphine hydrochloride) injections — can be painful, and patients are inclined to resist its use until later disease stages. Additionally, the foundation argues that physicians find the dose initiation cumbersome. Eliminating some of these barriers are key objectives for Cynapsus’ APL-130277, designed to achieve pharmacokinetics that mimic an Apokyn injection.
Another objective of a pilot effort involving Cynapsus, the MJFF, and microchip maker Intel is to advance understanding of how clinical studies can harness data science approaches, in order to objectively measure disease progression and speed progress toward breakthroughs in drug development. The project builds on MJFF’s ongoing data science partnership with Intel Corporation, launched in August 2014, to develop platforms for storing large volumes of patient-generated data and algorithms to glean insights from this data.
“This strategic alliance with The Michael J. Fox Foundation and the use of technology-enabled research solutions builds on our standing collaborative relationship as well as our individual commitments to change the lives of people with Parkinson’s disease,” says Anthony Giovinazzo, president and CEO of Cynapsus, in a release. “Employing wearable technology to collect data in clinical trials has enormous potential to improve our understanding of how drugs and other treatments impact patients living with the debilitating symptoms of this disease.”
MJFF chief executive officer Todd Sherer, PhD says: “Clinical studies are the most expensive and time-consuming stages of drug development. Data science approaches hold the potential to accelerate the pace of progress by allowing drug developers to objectively gather and analyze unprecedented volumes of data and more quickly reveal insights about a potential new treatment. We’re optimistic about the potential of this technology to help speed breakthroughs patients need.”
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Eric Dishman, general manager of Health & Life Sciences at Intel, observes: “Amassing valuable objective data and turning it into insightful information can lead to advances in how new therapeutics are developed. This implementation of a consumer wearable and an analytics platform, developed by The Michael J. Fox Foundation and Intel for use in Parkinson’s disease research, is a great example of interdisciplinary collaboration harnessing the power of data to advance disease research while bringing value to patients.”
While the MJFF funded earlier phases of APL-130277 clinical development, neither the Foundation nor Intel is funding the current Phase 3 studies. Phase 3 results on the safety and efficacy of APL-130277 are expected in mid- and late 2016.
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The Cynapsus release explains that a subset of participants in the Phase 3 safety study will take part in a data analytics sub-study. Through a wearable device and the Fox Insight smartphone application (developed jointly by MJFF and Intel), volunteers will contribute data on movement and medication effect. Data will be securely collected, and anonymously evaluated using advanced analytics, then stored in a cloud platform that will enable researchers to potentially gain insights into Parkinson’s disease, off episodes, and APL-130277’s efficacy. The technology platform and algorithms developed by Intel for the foundation are intended as a proof of concept, demonstrating that data science technologies can contribute to the objective measurement of Parkinson’s disease in interventional clinical studies.
“The data analytics capabilities enabled by Intel and The Michael J. Fox Foundation will allow us to better evaluate how APL-130277 is helping patients. As our Phase 3 clinical trials progress and we move toward gaining FDA approval of APL-130277, we plan to work closely with Intel and The Michael J. Fox Foundation to use this technology to improve the lives of patients with Parkinson’s disease,” says Cynapsus’ chief medical officer, Albert Agro, PhD.
Patients interested in participating in Parkinson’s clinical trials, such as Cynapsus’ ongoing APL-130277 study or other technology-enabled studies, are invited to register on the Fox Trial Finder at http://www.foxtrialfinder.org, an online tool that matches individuals to the trials best suited to them, based on factors such as time since diagnosis and medication/surgical status. The MJFF says more than 50,000 individuals have registered with Fox Trial Finder since 2011.
Cynapsus’ Pivotal Phase 3 Clinical Trial Program (CTH-300 and CTH-301)
Cynapsus announced enrollment of the first patient in the CTH-300 clinical trial on June 29, 2015. The CTH-300 trial is a double-blind, placebo-controlled, parallel-design efficacy study in an estimated 126 PD patients, enrolled at 35 centers, who have at least one off episode every 24 hours, with total off time of at least two hours per day. The study’s objective is to evaluate the efficacy and safety of APL-130277 versus a placebo. Participants are being observed for 12 weeks, with dosing both at home and in the clinic. The primary endpoint to be measured at week 12 is the mean change in the MDS-UPDRS Part III score at 30 minutes after dosing. The key secondary endpoint will be the percentage of patients who convert from the off to the on state at or before 30 minutes of dosing with APL-130277 at week 12.
Cynapsus announced enrollment of the first patient in the CTH-301 clinical trial on Sept. 2, 2015. The CTH-301 trial is a six-month, open-label, single-arm safety study in PD patients who have at least one off episode every 24 hours, with total off time of at least two hours per day. The study’s primary endpoint is the safety and tolerability of APL-130277. Secondary endpoints are the examination of efficacy variables, including the change in MDS-UPDRS Part III scores over the six months of treatment. Sites are recruiting patients over several months, with each patient being evaluated for six months. An estimated 226 patients will be enrolled, including up to 126 patients enrolled in the CTH-300 study.
Cynapsus cites National Parkinson’s Foundation metrics estimating that PD — a chronic and progressive neurodegenerative disorder that diminishes motor activity — afflicts more than 1 million people in the U.S., and an estimated 4 million to 6 million people globally.

Sources:
Cynapsus Therapeutics Inc.
The Michael J. Fox Foundation
http://parkinsonsnewstoday.com/2016/01/11/cynapsus-and-michael-j-fox-foundation-collaborate-on-pilot-use-of-wearable-device-and-data-science-approaches-in-phase-3-parkinsons-clinical-study/

Parkinson’s Patients Show Psychological Impact of Disease

Study of reward anticipation, motivation pinpoints importance of dopamine levels in the brain.

Jan. 5, 2016

A recent study shows that patients with Parkinson’s disease (PD) have a dysfunctional brain reward anticipation response — a finding likely linked to the decreased motivational state that can afflict PD patients.
The deficit in dopaminergic signaling that underlies PD affects more than just motor skills. Depression, apathy, and sleep disorders also frequently trouble PD patients. The authors behind the study —  SG Manohar and M Husain from the University of Oxford — hypothesized that dopamine might be involved in motivation related to incentives, in turn regulating emotional states such as apathy.
The study, titled “Reduced pupillary reward sensitivity in Parkinson’s disease” and published in the journal npj Parkinson’s Disease, aimed to explore this idea in PD patients both on and off their usual dopaminergic drugs.
To study the response to reward, the team enrolled 16 PD patients and 22 age-matched healthy controls, and presented them with a visual task. The participants were asked to look at an illuminated disk while they heard a voice stating the amount of money they would win if they performed the task correctly.
After 1,200–1,600 milliseconds (ms), two discs were illuminated: a distraction disc followed 80 ms later by the reward disc. The goal was to look at the reward disk without being distracted by the other disc. The reward sum varied between zero British pennies, 10 pennies and 50 pennies.
During this task, the team measured the diameter of participants’ pupils to obtain an objective measure of reward anticipation. The size of the pupil is regulated by the autonomous nervous system, and the neurotransmitter dopamine — the main player in the brain’s reward system — can dilate the pupil by changing the output of the autonomic nervous system.
The team found that the pupil of the healthy controls dilated more when a bigger reward was offered, while in PD patients currently free of medication that response was blunted. When the patients were back on medication, however, the reward anticipation response registered at the same levels seen in controls.
These results indicate that dopamine is crucial both for evaluating reward and for motivating effortful activities. Researchers believe that dopamine also influences apathy and impulsivity in PD by changing the incentive processing in the brain.
http://parkinsonsnewstoday.com/2016/01/05/parkinsons-disease-patients-show-reduced-reward-anticipation-response/?utm_source=PAR+E-mail+List&utm_campaign=238ccfca3a-RSS_WEEKLY_EMAIL_CAMPAIGN&utm_medium=email&utm_term=0_62dd4fb5e3-238ccfca3a-71459285

Hepatitis C virus linked to increased risk of Parkinson's disease, studies show


Hepatitis C

Liz Highleyman

People with hepatitis C virus (HCV) infection may be more likely to develop Parkinson's disease, especially when combined with other risk factors, though the reason for the association is not fully understood, according to a pair of recently published studies from Taiwan.
While hepatitis C is primarily a disease of the liver, chronic HCV infection has also been linked to manifestations throughout the body. Numerous studies have found associations between HCV infection and various neuropsychological and cognitive symptoms.
As described in the December 23, 2015, edition of Neurology, Hsin-Hsi Tsai of National Taiwan University Hospital and colleagues assessed whether HCV infection is a risk factor for developing Parkinson's disease.
Parkinson's disease is a progressive neurodegenerative disorder – the second most common after Alzheimer's disease – characterised by the early death of dopaminergic neurons in the substantia nigra region of the brain, leading to movement disorders including tremors, muscular rigidity and gait impairment.
This nationwide population-based cohort study looked at data from 49,967 people with viral hepatitis – hepatitis B virus (71%), hepatitis C (21%) or HBV/HCV co-infection (8%) – in the Taiwan National Health Insurance Research Database, which covers almost all Taiwanese residents, during the period 2000 to 2010. More than half (57%) were men and the mean age was about 46 years; blood transfusion was the most common risk factor for HCV infection. Another 199,868 people without viral hepatitis served as a control group.
The analysis found that over an average follow-up period of 12 years, people with hepatitis C were more than twice as likely to develop Parkinson's disease, with a crude hazard ratio (HR) of 2.50. 
After adjusting for age, sex and co-morbidities including heart disease, stroke, head injury and cirrhosis, the adjusted HR was 1.29 – about a 30% increased risk – and was statistically significant. The strongest association was seen in men, people under age 65 and those with multiple co-morbidities. 
In contrast, there was no significant association between hepatitis B virus infection and Parkinson's (crude HR 0.66), while people with HBV/HCV co-infection fell in between (crude HR 1.28).
"Many factors clearly play a role in the development of Parkinson's disease, including environmental factors," said senior author Chia-Hung Kao of China Medical University. "This nationwide study, using the National Health Insurance Research Database of Taiwan, suggests that hepatitis caused specifically by the hepatitis C virus may increase the risk of developing the disease. More research is needed to investigate this link."
Lead author Tsai suggested that HCV may breach the blood-brain barrier and enter the central nervous system, where it triggers inflammation that can cause neuronal injury, possibly including damage to dopaminergic neurons that characterises Parkinson's disease. Prior studies have suggested that other viruses may also elicit inflammatory responses in people with Parkinson's. Many experts believe multiple 'hits' or causal factors combine to cause the disease.
"While these results are intriguing, it is too early to suggest that people living with hepatitis C should be concerned about their risk of developing Parkinson's," cautioned Beth Vernaleo of the Parkinson's Disease Foundation. "That said, this study highlights one potential risk factor, which should be further investigated."
But another study done in Taiwan, published in the October 2015 Journal of Viral Hepatitis, found a similar link between HCV infection and increased risk of Parkinson's disease.
In this study the researchers analysed data from a community-based screening programme that included 62,276 participants. They investigated the association between HCV infection and Parkinson's and also assessed the neurotoxicity of HCV in a rat midbrain neuron-glial cell culture model.
This analysis saw odds ratios similar to the hazard ratios in Tsai's study: 0.62 for hepatitis B and 1.91 for hepatitis C. After controlling for potential confounding factors, the association with Parkinson's disease again remained statistically significant for hepatitis C (adjusted OR 1.39), but not for hepatitis B. 
The researchers also found that exposure to HCV – but not HBV – led to the death of 60% of dopaminergic neurons in the rat midbrain. Levels of inflammatory chemokines such as sICAM-1, LIX/CXCL-5 and RANTES were increased, while the neuro-protective TIMP-1 was down-regulated in the HCV-infected midbrain.
In summary, the authors wrote, "our study not only demonstrated a significantly positive association between HCV infection and Parkinson's disease from a large population-based epidemiological study, but also proved the dopaminergic neuronal toxicity by HCV in vitro at the molecular level through an increase in cytokines induced by HCV." 

References

Tsai, HH et al. Hepatitis C virus infection as a risk factor for Parkinson disease: A nationwide cohort study. Neurology. December 23, 2015 (online before print). 
Wu, WY et al. Hepatitis C virus infection: a risk factor for Parkinson's disease. Journal of Viral Hepatitis 22:784-791, 2015.

http://health.einnews.com/article/305737302/7JSx8OC1JtBSrXt5

Cholesterol Drug Being Tested In Parkinson's - New Use For Old Drug?


Parkinson's disease, which is the second most common neurodegenerative disorder after Alzheimer's disease, is characterized by loss of certain nerve cells in the brain. It is estimated that 6.3 million people worldwide have Parkinson's disease. Although the available medications for Parkinson's can provide relief from the symptoms, there is no cure yet. 

The Holy Grail of Parkinson's treatment is finding a drug that is capable of slowing or stopping the loss of nerve cells in the brain. But that wonder drug has been elusive so far. However, all hope is not lost among scientific community, and the quest for finding a possible cure has never dimmed.
Statins, like Simvastatin, which are prescribed by doctors to help lower cholesterol levels in the blood, have been reported to protect nerve cells in the brain from injury or loss. Based on this neuroprotective evidence of statins, Plymouth University Peninsula Schools of Medicine and Dentistry is conducting a clinical trial to see whether or not *Simvastatin has the potential to slow or halt the progression of Parkinson's disease. (*Simvastatin is sold under the brand name Zocor).

The trial will involve 198 Parkinson's disease patients, and will be conducted in 21 centers in the UK including Plymouth Hospitals NHS Trust.



Commenting on the study, the trial's chief investigator Camille Carroll said: "It is encouraging to see new compounds that are already approved as being safe for use in man being trialled for use in Parkinson's. There have been few innovations in the treatment of Parkinson's for over 40 years and for the more than 127,000 people living with the condition in the UK, the results of this trials programme could lead to new and highly effective treatments in the armoury of medications to tackle Parkinson's. 
by RTT Staff Writer

http://health.einnews.com/article/305729569/3C_NGwcAfUxvnIWQ

Review: Anchorage author's graphic novel describes coping with Parkinson's disease with intellect, humor


Peter Dunlap-Shohl is the author and illustrator of the graphic novel "My Degeneration: A Journey Through Parkinson's." He signed copies of the book at the Blue Hollomon Gallery on Wednesday, December 2, 2015.Marc Lester / ADN
January 10,2016
My Degeneration: A Journey Through Parkinson’s
By Peter Dunlap-Shohl; The Pennsylvania State University Press; 2015; $29.95
When Peter Dunlap-Shohl, the former editorial cartoonist for the Anchorage Daily News, received a diagnosis of Parkinson’s disease at age 43, he saw his whole world collapsing.Thirteen years later, he has delivered to us an astounding work in the form of a graphic narrative that documents — in a formidable blend of intellect, emotion and humor — the experience of living with Parkinson’s.
Parkinson’s, a treatable but incurable and progressive disease, afflicts as many as 1 million Americans. Thought to be caused by a combination of genetic and environmental factors and exhibited differently in different people, it’s a disorder of  nervous system that affects movement.
We learn basic facts and so much more from Dunlap-Shohl’s honest and honestly engaging account, from his initial depression through all of his learning and experience with the disease to his final chapter. Most of us likely know at least one person with Parkinson’s, and to now have this incredibly informative text allows us to understand the disease in a fresh, bold, visual and visceral way. Those who may find themselves with the unfortunate diagnosis will have a helpful guide to understanding and coping.
In chapter two, “Learning to Speak Parkinson’s,” we do indeed learn a new language. Festination is a difficult way of walking, not at all festive. Emotional incontinence is an unfortunate term for a form of depression involving emotional responses far out of proportion to situations. Then there’s logorrhea, extreme talkativeness that can be a side effect of drug treatments. Akathesia, dystonia, postural instability, dopamine, Sinemet (this last a brand name for a common drug): These are all words and terms we come to be familiar with. In the process we learn just how complicated Parkinson’s can be, and that a person must adjust to both the illness and the side effects of drugs used to treat it.  

Interview with a Killer

In another chapter, "Interview with a Killer," the character representing Dunlap-Shohl interviews a green-headed, red-eyed monster who comes to his house in a suit and tie to explain how the disease will go down. “(I am) the thug who is going to kick your pathetic ass and leave it for the crows!” the Parkinson’s monster shouts at his terrified host.
Elsewhere, Dunlap-Shohl shares the strategies he learned to cope, including maintaining an exercise regimen, managing medications and trying different ways of walking to “trick” his brain into performing its motor duties. Eventually, he takes us through the experience of receiving deep brain stimulation surgery.For a cartoonist to face Parkinson’s seems like a particularly cruel injustice. The loss of hand motor skills would seem to be career-ending. But in one chapter, we learn how the author transitioned from drawing with a pen and ink to learning computer skills that allowed him to recreate his old style with new technologies. In one panel we read, “The computer not only saved my aching body, it opened the creative floodgates.” An editor replies, “Damn, Pete, we should have computerized you years ago.”
And what about those cartoons? The colored drawings here are simply outstanding, showing just how powerful graphic narratives can be when artful illustration combines with a compelling story. Whether the drawing is of a wrinkled brain reacting to a drug, the author looking like a character from Monty Python’s Ministry of Silly Walks (because of dyskinesia, a drug side effect), a snickering red devil stabbing the author in the back or a landscape that falls away from Mountains of Denial to Sea of Acceptance panel invites and rewards close study.
The medical profession gets an ample critique here. Dunlap-Shohl details how a doctor first delivered his diagnosis, when he could only focus on the words progressive, disabling and incurable. He then devotes several panels to examples of other doctors (“paraphrased from first-hand sources”) being callous and insensitive. (Dr. Doom, answering a patient’s question about adjusting to a new medication: “You will be dead before your body gets used to it.”) The author then gives over a couple of pages to offer examples of language more kindly medical people might employ.

Life is tenuous

There are many feel-good moments in this book, too, related to family and community support. In the chapter, “Island of the Caring and Competent,” Dunlap-Shohl tells us (as he sails a sea in a boat made of a folded newspaper with depressing political headlines), “I didn’t realize that a hazard of editorial cartooning was misanthropy. Who’d have guessed that a run-in with a catastrophic disease would restore a more nuanced view of humanity?”
In the end, Dunlap-Shohl comes back to his diagnosis, re-examining that first dark day and then the path of his journey. In his drawings, he carries a heavy pack, negotiates a washed-out route and battles stinging insects. As friends and family stumble along with him, he finds much to celebrate, and the final images serve to remind us that life — for all of us — is both tenuous and best held with gratitude.
http://health.einnews.com/article/305660717/_Z5y-WTTOE2AH5tF

Sunday, January 10, 2016

Smart bottles remind patients to take their meds when doses are missed

Failure to take prescriptions as directed is blamed for an annual death rate of more than 125,000 people.

January 6, 2016

New “smart” pill bottles are now in production thanks to collaboration between Manhattan start-up Adhere Tech Inc., and Hauppauge (Long Island) based Intelligent Product Solutions. The bottles employ built in sensors to compare how often they are used to what the patient should be doing and are designed to issue reminders via flashing lights, sounds or automated text and phone calls when a dose is missed. According to the CDC failure to adhere to prescription directives results in approximately 125,000 deaths each year, and carries a “direct economic cost estimated to be close to $289 billion annually.”
“The whole idea is that this product can leverage analyzed data to improve the lives of users,” stated Adhere Tech co-founder and CEO Josh Stein.
He also added that while the first generation of smart bottles succeeded in improving medical dosage adherence by 20%, the companies have had to retool the design to make it more practical for mass production on automated manufacturing equipment, as well as to increase the battery life from 45-days to 6-months. In addition, they have had to make sure that the bottles meet FCC and cellular carrier regulations.
“The biggest challenge was fitting very complicated dense electronics into a very small footprint,” added IPS founders Mitch Maiman and Paul Servino.
Adhere Tech plans to manufacture 10,000 of its smart bottles by the end of the year. In the meantime, they have already distributed a limited number of them to a few pharmaceutical companies, as well as a limited number of medical facilities, including Walter Reed National Medical Center and Cincinnati Children’s Hospital.
http://www.examiner.com/article/smart-bottles-remind-patients-to-take-their-meds-when-doses-are-missed

Under tongue device to provide valuable data for treating Parkinson's disease

Therapeutics Inc. and The Michael J. Fox Foundation for Parkinson’s Research are working together to incorporate wearable device technology and “big data” approaches into Cynapsus’ pivotal Phase 3 clinical study of APL-130277, an under-the-tongue formulation of apomorphine to treat (“OFF”) episodes in Parkinson’s disease patients. The project expands upon MJFF’s ongoing data science partnership with Intel Corporation, launched in August 2014, to develop platforms for the storage of large volumes of patient-generated data and algorithms to amass insights from this data.
As Parkinson’s progresses, the efficacy window of dopamine replacement medication shortens, and patients experience motor fluctuations known as OFF episodes. Apomorphine is a “rescue” therapy, approved in subcutaneous formulation, to quickly bring patients back to “ON.” Cynapsus has been developing APL-130277, its fast acting, easy-to-use sublingual thin film formulation of apomorphine since 2010. While the Michael J. Fox Foundation funded earlier phases of clinical development, neither the Foundation, nor Intel, is funding these APL-130277 Phase 3 studies. Phase 3 results on the safety and efficacy of APL-130277 are expected in 2016.
“Employing wearable technology to collect data in clinical trials has enormous potential to improve our understanding of how drugs and other treatments impact patients living with the debilitating symptoms of this disease,” stated Todd Sherer, Ph.D., chief executive officer of MJFF. “Clinical studies are the most expensive and time-consuming stages of drug development. Data science approaches hold the potential to accelerate the pace of progress by allowing drug developers to objectively gather and analyze unprecedented volumes of data and more quickly reveal insights about a potential new treatment. We’re optimistic about the potential of this technology to help speed breakthroughs patients need.”
The Michael J. Fox Foundation is dedicated to accelerating a cure for Parkinson’s disease and improved therapies for those living with the condition today. The Foundation pursues its goals through an aggressively funded, highly targeted research program coupled with active global engagement of scientists, Parkinson’s patients, business leaders, clinical trial participants, donors and volunteers. In addition to funding more than $525 million in research to date, the Foundation has fundamentally altered the trajectory of progress toward a cure.
Participants in the Phase 3 safety study will contribute data on movement and medication effect via a wearable device and the Fox Insight smartphone application (developed jointly by MJFF and Intel). The information will be securely collected, "de-identified" and evaluated using advanced analytics, then stored in a cloud platform that will allow researchers to potentially gain insights into Parkinson’s disease, OFF episodes, and the efficacy of APL-130277
“The data analytics capabilities enabled by Intel and The Michael J. Fox Foundation will allow us to better evaluate how APL-130277 is helping patients," stated Albert Agro, Ph.D., chief medical officer of Cynapsus. "As our Phase 3 clinical trials progress and we move toward gaining FDA approval of APL-130277, we plan to work closely with Intel and The Michael J. Fox Foundation to use this technology to improve the lives of patients with Parkinson’s disease.”
http://www.examiner.com/article/under-tongue-device-to-provide-valuable-data-for-treating-parkinson-s-disease