UCB adds website for its Facebook-based Parkinson's community

May 11, 2017

Says the site forms the next chapter for More than Motion

UCB has launched a website for the More than Motion Facebook-based community it set up in 2012 for people living with Parkinson’s disease.

The firm says the new online destination, which includes a new desktop and mobile-responsive website, forms the next chapter in its work on the community as it looks to encourage to share their stories.

In its original incarnation the More than Motion Facebook page featured patient videos, including and a reality television style series on how patients and their families are affected by Parkinson’s disease.

They could also register to receive the More than Motion magazine that UCB publishes.

The firm says its new desktop and mobile-responsive website will help bring that magazine’s content to a wider audience, including via a downloadable digital edition.

Patients can also upload their own photos to the site, which UCB said will “bring them into an active support and information group”.

Commenting on the changes Erica Puntel, senior manager of communications and social media at UCB, said: “We look forward to seeing how this community grows as it enters a new phase of its maturity.”

http://www.pmlive.com/blogs/digital_intelligence/archive/2017/may/ucb_adds_website_for_its_facebook-based_parkinsons_community_1192671

International Stem Cell’s Trial in Parkinson’s Can Continue, Board Says

MAY 10, 2017  BY DANIELA SEMEDO, PHD

International Stem Cell’s clinical trial testing its ISC-hpNSC neural cells for the treatment of Parkinson’s disease (PD) can move forward, the company said.

The announcement comes after an evaluation from experts from a Data Safety Monitoring Board (DSMB), who looked at the safety data from the first group of patients enrolled in the trial.

The DSMB said the study can continue with accelerated enrollment and a dose escalation in a second group of patients. The company is now recruiting the second cohort of Parkinson’s patients, who will be receiving a higher dose of 50,000,000 of ISC-hpNSC neural cells.

The open-label, single center, uncontrolled Phase 1 trial (NCT02452723) expects to recruit 12 patients with moderate Parkinson’s. Patients are divided into three groups of four patients each. The groups are receiving increasing doses ranging from 30,000,000 to 70,000,000 neural stem cells transplanted intracranially. The main goal of the trial is to assess the safety of the treatment, with patients followed for 12 months after the transplants.

All patients undergo a positron emission tomography (PET) scan when they enter the study, and then at six and 12 months after surgical intervention. The clinical responses of participants compared to baseline after the administration of ISC-hpNSC are evaluated using the Unified Parkinson Disease Rating Scale (UPDRS) and other tools.

Last month, the company said that the fourth and last patient with Parkinson’s of the first group had successfully received the neural stem cell transplant. To date, trial investigators have not recorded any adverse events among the four patients who had the stem cells inserted into their brains.

“The DSMB approval represents an important step in the clinical development of ISC-hpNSC,” Andrey Semechkin, co-chairman and CEO of the company, said in a recent press release. “In the second cohort we will begin to evaluate the higher cell dose that we believe will have the most likely favorable outcomes and potential to benefit patients.”

ISC-hpNSC cells are derived from unfertilized human eggs, so while they retain all the advantages of embryonic cells, they cannot generate a human being. In this manner, these cells are safe from any ethical issues associated with the use or destruction of viable human embryos.

https://parkinsonsnewstoday.com/2017/05/10/international-stem-cells-trial-in-parkinsons-disease-can-continue-board-says/

Stress Hormone Could Help Treat Parkinson’s Disease, Study Reports

 MAY 9, 2017 BY JOANA FERNANDES, PHD IN NEWS.

The stress hormone cortisol prevents dopaminergic neurons from dying by promoting the expression of parkin, a protein that is in short supply in the brains of Parkinson’s disease patients, a study indicates.

The research, “Hydrocortisone-Induced Parkin Prevents Dopaminergic Cell Death Via CREB Pathway In Parkinson’s Disease Model,” was published in the journal Scientific Reports.

“Our results showed that [cortisol] could stimulate parkin expression via [a survival] pathway and the induced parkin expression was accountable for its neuroprotective effect,” researchers wrote. Expression is the process by which information from a gene is used to create a functional product, like a protein.

“Since glucocorticoid [corticoid] is a physiological hormone, maintaining optimal levels of glucocorticoid might be a potential therapeutic or preventive strategy for Parkinson’s disease,” the researchers added.

Symptoms of Parkinson’s, such as tremors and movement problems, result from the death of dopaminergic neurons in the brain, particularly in a region called the substantia nigra. Mutations in the parkin protein are known to contribute to this effect.

Previous studies have shown that promoting parkin expression protects against cell stress and prevents dopamine cell loss. The research was done in several animal models of Parkinson’s.

In the latest study, researchers used molecular screening to identify chemicals that increase parkin expression. They found that cortisol can trigger parkin expression and protect cells against oxidative stress, or damage to cell molecules from high levels of oxidant molecules.

Cortisol increased parkin levels in the brains of mice and prevented dopamine cell loss after four days.

An obstacle to using cortisol to prevent neuron loss is its side effects, researchers said. They include suppression of the immune system, high levels of blood glucose and amino acids, a rise in blood pressure, and psychosis, a mental disorder that actually may damage the brain.

“The dosage of hydrocortisone used to provide complete protection to dopaminergic neurons in our study was low compared to its dosage used to suppress immune response (0.4 mg/kg in our study vs. 20–100 mg/kg for anti-inflammatory effects in other studies),” the researchers wrote. “Based on our findings, it would be critical to have sufficient physiological supply of cortisol hormone … for protection of the brain. In this respect, hydrocortisone treatment could be considered as a supplementary measure to maintain parkin expression without causing serious side effects.”

“The significance of this study is that it has identified that the expression of parkin protein induced by a moderate level of the stress hormone cortisol could be an important factor in maintaining the viability of dopaminergic neurons,” Yoon-Il Lee, the study’s senior author, said in a news release. “We will continue to conduct follow-up studies such as clinical studies so that Parkinson’s disease will be curable in the future.”

https://parkinsonsnewstoday.com/2017/05/09/study-reports-stress-hormone-could-be-used-to-treat-parkinsons-disease/

Sage highlights ‘signal of activity’ in Parkinson’s data, but questions linger

By  Ben Adams

May 10, 2017

Sage Therapeutics posted phase 2 results from its Parkinson’s disease study yesterday in which it said its experimental med could help tremors, but the top-line data were met with confusion by Bio Twitter, and its shares fell more than 3% in normal hours trading.

The data, released alongside its financials, showed lightly detailed results from its “exploratory” Part A open-label portion of a small, 12-person phase 2 test for SAGE-217 in Parkinson’s.

The dozen patients with a moderate form of the disease were all on stable doses of the antiparkinson agent levodopa/carbidopa prior to the study, with patients withdrawn from maintenance therapy and given a morning dose only of levodopa/carbidopa for three days, followed by a single morning dose of SAGE-217 on its own for four days.

For the overall population in the trial, levodopa/carbidopa activity was primarily focused on the motor symptoms of bradykinesia and rigidity, while SAGE-217 activity as a monotherapy was primarily focused on tremor symptoms.

In the five subjects with overt tremor (tremor score over 5 at baseline), 20% to 30% saw an improvement in tremor symptoms during the four days of SAGE-217 open-label treatment, the biotech said.

“This improvement in tremor score during the SAGE-217 dosing phase was longer-lasting than the effect on tremor observed in these subjects during the levodopa/carbidopa-only phase,” it added.  

The test was set up to see whether it was worth continuing on with further trials, and the company said it saw enough hints of activity to proceed on to an open-label Part B, which will be designed as an adjunctive treatment to antiparkinson agents in tremor-predominant patients. It also plans to assess nonmotor symptoms of Parkinson’s disease, including depression, anxiety, cognition and sleep.

But Sage's shares dropped yesterday, with some questioning just how positive these results were. Alfredo Fontanini, M.D., Ph.D, associate professor of neurobiology and behavior at Stony Brook University, tweeted: “Ok my first reading of $SAGE results on PD ... unclear signal; 20-30% reduction of UPDRS tremor in subset of patients, not too strong.”

TheStreet columnist Adam Feuerstein added: “$SAGE says ‘217 showed enough 'signal of activity' in Parkinson’s to move forward. Reading data, I have no idea if that’s bullshit or not.”

A few months back, Sage fueled, then dampened, its own M&A rumors after CEO Jeff Jonas was quoted as saying his company was at the top of everyone’s buying list, sending its shares jumping. But a few short hours later (and just before the end of after-hours trading), the chief rowed back on the M&A talk. This came after the biotech posted positive data for SAGE-217 in a small, phase 2 test, that time in major depressive disorder.

On a call with investors yesterday, Jonas said of the Parkinson’s data: “Please recall that this is an open-label trial, designed primarily to help with designing methodology and determining how SAGE-217 might fit into the Parkinson’s disease armamentarium. These initial results, they are open label need to interpret cautiously.

“Overall, the study suggested that as a great monotherapy, given at lower doses in the morning during a short duration of therapy, SAGE-217 did not have an impact on certain Parkinson's disease symptoms in general but did have an impact in reducing tremor.”

http://www.fiercebiotech.com/biotech/sage-highlights-signal-activity-parkinson-s-data-but-questions-linger

Parkinson’s gene mutation discovered in one third of cancers

May 10, 2017

A gene found in a hereditary form of Parkinson’s disease is mutated in a third of all human cancers – and helps regulate one of the disease’s most commonly activated cell signalling mechanisms, a new study reveals.

Scientists at The Institute of Cancer Research, London, analysed nearly 10,000 tumour samples from 28 different types of cancer, and found that the gene PARK2 was altered in over a third of tumours. 

Their study showed how loss of PARK2 can stimulate a crucial network of cancer-driving molecules in cells, called the PI3K/Akt pathway, through a well-researched tumour suppressor gene called PTEN.

The findings reveal a ‘missing link’ in one of the most commonly observed signalling pathways in cancer, showing how the PI3K/Akt pathway can be ramped up in the stressful, energy poor conditions often found inside tumours. 

The study, published in the journal Molecular Cell, was funded in the UK by the Medical Research Council and the ICR, and could help researchers understand how aggressive cancer cells can survive and proliferate in low energy conditions.

Loss of gene in tumours

Mutations in PARK2 have been found in a hereditary form of Parkinson’s disease, a degenerative condition which kills off cells in the brain. When the gene is depleted in cells, mitochondria – the energy factories of cells – become defective. But cancer cells have the ability to withstand the energy stress coming from defective mitochondria by ramping up PI3K/Akt signalling, through deactivating PTEN. 

Importantly, the researchers found that PARK2 was significantly under-expressed across many tumour types. Widespread loss or reduced PARK2 in tumours correlated with poorer survival chances for patients with diseases including brain, breast and lung cancer. 

The research indicates an intriguing link between mutations to PARK2 and the PTEN gene. In mice without working copies of PARK2, mutations to PTEN resulted in a much higher risk of developing tumours and poorer survival outcomes, compared with mice with functional PARK2. 

Study co-author Dr George Poulogiannis, leader of the Signalling and Cancer Metabolism team at the ICR, said: “Our study has highlighted that PARK2 loss is present in around a third of all cancers and has profound implications in understanding how cancer cells may support their proliferation and survival under conditions of nutrient deprivation. 

“In the future, tests that look for mutations to PARK2 may help to identify patients who have particularly aggressive forms of cancer that may respond to inhibitors of PI3K/Akt signalling”.

http://www.icr.ac.uk/news-archive/parkinson-s-gene-mutation-discovered-in-one-third-of-cancers

Microsoft Build 2017 live: How Emma Watch a life-changing device helped Emma write again

May 10, 2017   By Ritesh Bendre

The wearable device created by Haiyan Zhang helped a designer with Parkinson’s disease to steady her hand.

At the Build 2017 developer conference, Microsoft made a number of announcements related to cloud computing, Visual Studio for Mac, Intelligent Cloud for IoT devices and more. Microsoft also highlighted a life-changing wearable device created by Haiyan Zhang, innovation director Microsoft Research Cambridge, to help a designer with Parkinson’s disease to stabilize her hands.

Three years ago, graphics designer Emma Lawton was diagnosed with Parkinson’s, a neurological disease at the age of 29. Zhang, created a wearable device to help Emma reclaim her lifelong passion for drawing and sketching. Called ‘Emma Watch,’ the device aims to significantly reduce the constant limb tremors associated with Parkinson’s. 

https://youtu.be/R6rAlFYDffQ

“It was incredibly traumatic but exciting at the same time. There was so much fear and emotion hanging in that moment. I wanted it to work so badly. I was petrified. What if it didn’t work? So when it did work, I thought ‘OK, that’s amazing’. I couldn’t really get my head around it. And then when it carried on working…” Emma said. 

The wearable watch features an interchangeable strap, available in different colors. The device intentionally shakes the user’s arm, which interrupts the feedback loop, thus impending the normal movement. Wearing the device, Emma was able to draw straight lines, and now she wears it on a daily basis. Designed to fit particular needs of Emma, Zhang currently has not plans of developing the watch for commercial use.

ALSO READ: Microsoft Build 2017 Live: After Harman Kardon, HP, Intel join the league of Cortana-powered devices at 

http://www.bgr.in/news/microsoft-build-2017-live-powerpoint-gets-ability-to-translate-presentations-in-real-time/

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http://www.bgr.in/news/microsoft-build-2017-live-how-emma-watch-a-life-changing-device-helped-emma-write-again/

Michael J. Fox puts on lively display at hockey game before Cuba Gooding Jr. reunion

May 10, 2017 By JESSICA EARNSHAW

MICHAEL J. FOX certainly isn’t going to let his Parkinson’s Disease diagnosis stop him doing what he loves, as he proved in New York last might.

Michael J Fox was spotted at an ice hockey match yesterday

The Back To The Future legend looked to be in high spirits as he cheered on his team at the ice hockey at the city’s Madison Square Garden.

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Keeping his Henley Cup baseball cap firmly on, the 55-year-old looked well as he watched the New York Rangers take on the Ottawa Senators alongside his wife Tracy Pollan.

Michael looked engrossed in the match, cheering and clapping as the events unfolded, before catching up with Cuba Gooding Jr.

The actor and his film star pal, 49, were seen going in for a hug in the stands during the sporting event.

Michael J Fox was seen cheering on his team

Michael kept things causal in a leather jacket and a green sweatshirt, while his famous friend looked much smarter in a grey blazer and a crisp white shirt.

Tracy matched her spouse, 56, who she wed back in 1988, in a pale biker jacket and a mostly-black attire.

The producer and activist’s outing comes after her admitted his Parkinson’s made him laugh, following the devastating health news more than two decades ago.

Speaking to the April issue of AARP The Magazine, Michael commented: "The truth is that on most days, there comes a point where I literally can’t stop laughing at my own symptoms."

He continued: "Just the other morning I come into the kitchen. I pour a cup — a little trouble there. Then I put both hands around the cup. She’s [wife, Tracy Pollan] watching.

"'Can I get that for you, dear?' 'Nah, I got it!' Then I begin this trek across the kitchen. It starts off bad [and] only gets worse. Hot java’s sloshing onto my hands."

http://www.express.co.uk/celebrity-news/802598/Michael-J-Fox-Cuba-Gooding-Jr-Parkinson-s-Disease-wife-hockey-game

Penn expert probes possible reasons for loss of smell

May 10, 2017   UNIVERSITY OF PENNSYLVANIA SCHOOL OF MEDICINE

     Review seeks neurological link for symptom commonly tied to Alzheimer's, Parkinson's

PHILADELPHIA - Studies have shown that loss of the sense of smell can be among the first warning signs of diseases such as Alzheimer's and Parkinson's. Now a researcher at the Perelman School of Medicine at the University of Pennsylvania wants to shift the search for clues about this process back even further, to find out if there is a common factor responsible for the loss of smell that may also serve as an early warning signal for a number of neurodegenerative diseases. In a review published online in Lancet Neurology, Richard L. Doty, PhD, a professor of Otorhinolaryngology and director of the Smell and Taste Center, cites evidence that the common link could be damage to neurotransmitter and neuromodulator receptors in the forebrain - the front part of the brain.

"We need to retrace the steps of the development of these diseases," Doty said. "We know loss of smell is an early sign of their onset, so finding common factors associated with the smell loss could provide clues as to the pre-existing processes that initiate the first stages of a number of neurodegenerative diseases. An understanding of such processes could provide novel approaches to their treatment, including ways to slow down or stop their development before irreversible damage has occurred." 

Currently, it's is generally believed that the smell loss of various neurodegenerative diseases is caused by disease-specific pathology. In other words, different diseases can bring about the same loss of smell for different reasons. Doty's review - the first of its kind - looked at many neurodegenerative diseases with varying degrees of smell loss and sought to find a common link that may explain such losses. He considered physiological factors as well as environmental factors like air pollution, viruses, and exposure to pesticides. 

"Ultimately, as each possibility was evaluated, there were cases where these factors didn't show up, which ruled them out as potential universal biomarkers."

Doty did find compelling evidence for a neurological solution: Damage to the neurotransmitter and neuromodulator receptors in the forebrain - most notably, a system employing the neurochemical acetylcholine. Neurotransmitters are the chemicals that send signals throughout the brain. Neuromodulators influence the activity of neurons in the brain. The receptors receive the signals, and if they are damaged, it hurts the brain's ability to process smells normally.

"The good news is we can assess damage to some of the systems by evaluating their function in living humans using radioactive neurochemicals and brain imaging processes such as positron emission tomography (PET)," Doty said. "Unfortunately, few data are currently available, and the historical data of damage to neurotransmitter/neuromodulator systems, including cell counts from autopsy studies, are limited to just a few diseases. Moreover, quantitative data on a patient's olfactory status is rarely available, especially prior to disease diagnosis." 

Doty said the lack of early data is a problem across the board in the search for factors that may explain smell loss. 

"Smell testing isn't part of a standard check-up, and people don't recognize a smell problem themselves until it's already severe," Doty said. "Research now starting in Japan will be testing thousands of people over the course of the next few years that will better define associations between changes in smell and a wide variety of physiological measures in older populations." 

"If a universal factor does exist, the benefits for patients would be obvious," Doty said. "Damage to the neurotransmitter and neuromodulator receptors shows promise as one possibility, but we need more research in this area to truly answer the question. It could be the key to unlocking better understanding of neurological disease."

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Editor's Note: Doty receives funding from the Michael J. Fox Foundation for Parkinson's Research. He is a consultant to Acorda Therapeutics, Eisai Co., Ltd., and Johnson & Johnson. He is president of and major shareholder in Sensonics International, which manufactures and distributes smell and taste tests.

Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. 

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2017-05/uops-pep051017.php

Parkinson's patient pours creative efforts into children's book

May 9, 2017

Video:http://www.fox13news.com/health/253566553-story#

TAMPA (FOX 13) - The walls inside Jacquie Hoblit's home tell her story, including her painting of a woman in Paris on a background of street maps.

"I did this with acrylic polymer and crushed charcoal and painted it because we walked everywhere," she explained. 

But these days, creating works of art is tough.  That's because 10 years ago Jacquie was diagnosed with Parkinson's disease, or PD for short.

"It was just a little tremor in my little finger but eventually it took over my right hand and my right side. And I'm right-handed, so it was, of course, terribly frustrating doing art,” she said as she tried to decrease the uncontrolled movements of her right arm. “I went through a period of depression, I suppose; it took me a long time to accept it.”

Part of that acceptance came in the form of photography and textured art using materials like computer pieces and jewelry. 

Now, this former art teacher is turning yet another page in her career by releasing her first children's book called 'Ms. O'Keeffe and Her Three Talented Cats.' 

"Took me a year; took me a good year to do that," she offered.

During that year, Jacquie was gaining strength in a boxing class for patients with PD. Studies show exercise helps manage or even delay Parkinson’s symptoms and the visual arts can help, too. 

           

But there's another way PD may affect artists.  According to a French study, medications used to treat PD enhanced creativity in people who were artistic before their diagnosis.  The creativity was lost in almost all patients when medications were stopped after a deep brain stimulator was implanted.  

A Japanese patient switched from impressionist paintings to realism even before his tremors began.As for Jacquie, she's recently completed a video for her boxing class and plans to hand illustrate her next book -- work she'll tackle during quiet times in her day, when the shakiness subsides.

"I only do this jerky stuff when I’m anxious or nervous or tired,” she added.  “When I'm left alone and I'm calm, I'm great. I can do really well."

http://www.fox13news.com/health/253566553-story

New App Adjusts Brain Stimulators For Parkinson’s Patients

MAY 8, 2017

NEW YORK (CBSNewYork) — You’ve heard it before – there’s an app for that.

But how about an app that a patient can use to adjust their own brain stimulator?

As CBS2’s Dr. Max Gomez reported, an iPod app is helping patients with Parkinson’s disease. People with Parkinson’s can have deep brain stimulators implanted, called DBS, to ease many of the motor symptoms of Parkinson’s such as tremors.

But that electrical stimulation often has to be tweaked to get the best result. That is where an app comes in handy.

Paul Detlefsen was only 36 when the Parkinson’s tremor in his right hand became so noticeable that he started avoiding going out in public.

“It was like a public thing – a little depression. You know, my friends, ‘Let’s go out.’ I’m like, ‘Naw,’” Detlefsen said.

Detlefsen had read about the side effects of Parkinson’s medications, so he instead opted for deep brain stimulation.

“Two probes put into the brain, and runs down to a generator,” Detlefsen said.

It sounds simple enough, but as neurosurgeon Dr. Asif Bashir points out: “Every patient is different. Every patient requires different parameters to program them.”

That used to mean multiple trips to the doctor to have the stimulation adjusted. But now, Detlefsen can call up an app on his phone.

When he turns on the app, his tremors disappear.

And should his stimulator need adjustment, Detlefsen takes a phone video of his tremor and emails it to neurologist Dr. Philip Hanna.

As amazing as the app’s ability to turn tremors on and off is, Detlefsen still cannot freelance his own brain stimulation.

“They are given certain parameters which they have no ability to move above,” said Jacqueline Cristini of the JFK Neuroscience Institute.

Detlefsen is the first patient in the U.S. to receive the new controller system, so he has become a bit of an educator – showing another Parkinson’s patient and prospective DBS user how it works.

“It’s quality of life changing,” he said.

Detlefsen said he feels only a slight, momentary tingle all over his body when he turns on the DBS, but normally, the stimulator is on all the time.

The app connects to his electrode generator via a secure Bluetooth link so that others cannot meddle with his DBS, and he cannot fool with someone else’s.

Video:

http://cbsloc.al/2peDk4L

http://newyork.cbslocal.com/2017/05/08/parkinsons-stimulator-app/