Research

Artificial intelligence to monitor Parkinson’s symptoms

Researchers at Massachusetts Institute of Technology, US have developed an artificial intelligence system that can monitor Parkinson’s symptoms from the other side of a solid wall.

The x-ray technology – named RF-Pose – will use radio signals to sense individuals’ posture and movement. This will help medical professionals track the development of Parkinson’s and provide more effective care.

Dina Katabi, professor of electrical engineering and computer science at Massachusetts Institute of Technology, said: “We’ve seen that monitoring patients’ walking speed and ability to do basic activities on their own gives healthcare providers a window into their lives that they didn’t have before.

“A key advantage of our approach is that patients do not have to wear sensors or remember to charge their devices.”

 

Article from EPDA.

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New Reports Measure Parkinson’s Motor Progression

Two recent papers outline the progression of Parkinson’s disease (PD) movement or motor symptoms in distinct study populations. While these findings do not provide an absolute picture of how one person will progress with PD, the results may help researchers design smaller, faster and less expensive clinical trials of new treatments.

Changes in Early Parkinson’s and with Dopamine Therapy

The Parkinson’s Progression Markers Initiative study, sponsored by The Michael J. Fox Foundation (MJFF), reported on changes in motor symptoms over five years from people who joined the study early in their disease (within two years of diagnosis). The largest change (as measured by the Unified Parkinson’s Disease Rating Scale or UPDRS) came in the first year, then symptoms plateaued as people began taking dopamine medication.

Many studies of therapies that aim to slow or stop disease progression recruit people in similar early stage of disease. Understanding what to expect over the first year and as those study participants begin dopamine medication can help drug developers design their trials.

Read the full paper.

Slower Progression in G2019S LRRK2 Mutation Carriers

Analysis from the LRRK2 Ashkenazi Jewish Consortium — part of the MJFF-supported LRRK2 Cohort Consortium — compared progression in people who carry the G2019S mutation in the LRRK2 gene, a leading genetic cause of Parkinson’s disease, to progression in people without a known cause of their disease (so-called sporadic PD).

People in the study who carried a G2019S LRRK2 mutation advanced 30 percent more slowly on the UPDRS than people with sporadic PD. The authors from Mount Sinai Beth Israel Medical Center in New York noted, though, that they could not confirm whether those results were from a subgroup with less severe disease bringing down the average or if most G2019S LRRK2 mutation carriers have less aggressive disease.

It is not to say, either, that if you do not carry this genetic mutation you will definitely progress quickly; Parkinson’s is a highly variable disease.

The results are already helping companies testing therapies against LRRK2 dysfunction. Carole Ho of Denali Therapeutics, which brought the first LRRK2 drug into clinical trials late last year, told research news website AlzForum, “We are using the new data to design trials to test LRRK2 inhibitors. Knowing the natural course of disease is very important.”

Read more on these results.

PPMI is recruiting people of Ashkenazi Jewish descent with a Parkinson’s or Gaucher disease connection. Learn more about the study.

 

Article from Michael J. Fox Foundation for Parkinson’s Research.

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Storming the Hill

By: Samantha Barbian

We came. We saw. We conquered. From March 19-21st my dad, Craig, and I attended the Parkinson’s Policy Forum in Washington DC. We were joined by approximately 300 other Parkinson’s advocates from around the country. The feeling of being one community and truly supporting each other was undeniable. I found it interesting hearing all the different stories how Parkinson’s has affected each persons life. No two stories in the room were exactly alike just like the disease does not effect each person’s body and mind the same.

One speaker who was so inspirational that I will never forget was New Jersey Senator Cory Booker. He told stories about his life growing up and the stories his father would tell. Near the end of his speech he revealed that his father had Parkinson’s. This quote from Senator Booker hit home with many of us:

“My dad showed me what courage was about, as he struggled with this foe of Parkinson’s, and more than that, he showed me what the power of the community is about. About people who were there for him, who counseled him, who laughed with him. About folks who understood the complexities of the challenges.”

Parkinson’s patients need that community to help them keep pushing forward and to never give up.

If you were unable to attend the Parkinson’s Policy Forum there are a few ways you can still get involved. One way is to check out the website www.parkinsonsforum.org for all the information that was shared at the conference. Another way that you can get involved is to contact your legislators and ask them to fund the National Neurological Surveillance System. This program is a database for all neurological diseases to keep track of the occurrences in our society. We are also looking for continued support of Parkinson’s research done on veterans who served in Vietnam by the Department of Defense.

If you would like more information about the forum, please contact me at [email protected].

Samantha with New Jersey Senator Cory Booker

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Exercise Improves Cognition in Parkinson’s Disease

It’s well known that exercise invigorates both body and mind. Exercise studies in Parkinson’s disease (PD) have shown improved mobility and quality of life, and possibly slower rate of disease progression. But what can exercise do for memory and thinking (cognition), which can be affected to different degrees at different points in the course of Parkinson’s?

Recently, a group of researchers answered that question by reviewing exercise and cognition studies conducted in people with Parkinson’s over the past 10 years. They confirmed the benefit of exercise on cognitive function in people living with PD.

For this study, researchers analyzed nine randomized controlled trials from several countries. The participants of these trials were, on average, 60 to 74 years old, diagnosed with Parkinson’s six years prior and living with mild to moderate disease. Exercise programs varied in length, number and duration of sessions, and included studies with a treadmill, stationary bicycle, stretching and strengthening (with and without a Wii Fit exercise program), tai chi and tango. Volunteers’ cognitive function was tested throughout each study to see if the exercise had an effect.

Of the specific exercise programs reviewed, tango, stretching and strengthening with a cognitive component (a Wii Fit exercise program), and treadmill training had benefits on cognition. The latter — walking at a person’s preferred speed or slightly slower for about an hour three times a week for 24 weeks — boosted cognitive function more than the other two exercise programs.

More support for exercise, and treadmill exercise in particular. But this doesn’t mean that treadmill walking is the best exercise for Parkinson’s. Many questions remain about the optimal type, amount and intensity of exercise to keep cognitive (and other) symptoms at bay. Larger, well-designed studies can help provide answers and clarify effects.

Multiple forms of exercise for many symptoms are currently being investigated. Register for Fox Trial Finder to match with recruiting trials. As researchers work to define the ideal exercise for your Parkinson’s, continue regular exercise that you enjoy.

Speak with your physician and physical therapist to design a program that meets your needs and visit our website to learn more.

 

Article from Michael J. Fox Foundation for Parkinson’s Research.

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Could caffeine in the blood help diagnose Parkinson’s?

Blood caffeine levels could be promising diagnostic biomarkers for early-stage Parkinson’s, Japanese researchers reported in the journal ‘Neurology’ earlier this month.

The study found that people with Parkinson’s had lower levels of caffeine and caffeine metabolites in their blood than people without the disease, at the same consumption rate.

Caffeine concentrations also were decreased in Parkinson’s patients with motor fluctuations than in those without Parkinson’s. However, patients in more severe disease stages did not have lower caffeine levels.

The study’s authors, Dr David Munoz, University of Toronto, and Dr Shinsuke Fujioka, Fukuoka University, suggested that the “decrease in caffeine metabolites occurs from the earliest stages of Parkinson’s.”

They added: “If a future study were to demonstrate similar decreases in caffeine in untreated patients with Parkinson’s […] the implications of the current study would take enormous importance.”

 

Article from Parkinson’s Life.

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Shedding a tear may help diagnose Parkinson’s disease

Tears may hold clues to whether someone has Parkinson’s disease, according to a preliminary study released today that will be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018.

“We believe our research is the first to show that tears may be a reliable, inexpensive and noninvasive biological marker of Parkinson’s disease,” said study author Mark Lew, MD, of the Keck School of Medicine of the University of Southern California in Los Angeles and a Fellow of the American Academy of Neurology.

Lew says the research team investigated tears because they contain various proteins produced by the secretory cells of the tear gland, which is stimulated by nerves to secrete these proteins into tears. Because Parkinson’s can affect nerve function outside of the brain, the research team hypothesized that any change in nerve function may be seen in the protein levels in tears.

For the study, tear samples from 55 people with Parkinson’s were compared to tear samples from 27 people who did not have Parkinson’s but who were the same age and gender. Tears were analyzed for the levels of four proteins.

Researchers found differences in the levels of a particular protein, alpha-synuclein, in the tears of people with Parkinson’s compared to controls. Additionally, levels of another form of alpha-synuclein, oligomeric alpha-synuclein, which is alpha-synuclein that has formed aggregates that are implicated in nerve damage in Parkinson’s, were also significantly different compared to controls. It is also possible that the tear gland secretory cells themselves produce these different forms of alpha-synuclein that can be directly secreted into tears.

Total levels of alpha-synuclein were decreased in people with Parkinson’s, with an average of 423 picograms of that protein per milligram (pg/mg) compared to 704 pg/mg in people without Parkinson’s. But levels of oligomeric alpha-synuclein were increased in people with Parkinson’s, with an average of 1.45 nanograms per milligram of tear protein (ng/mg) compared to 0.27 ng/mg in people without the disease. A picogram is 1,000 times smaller than a nanogram.

“Knowing that something as simple as tears could help neurologists differentiate between people who have Parkinson’s disease and those who don’t in a noninvasive manner is exciting,” said Lew. “And because the Parkinson’s disease process can begin years or decades before symptoms appear, a biological marker like this could be useful in diagnosing, or even treating, the disease earlier.”

More research now needs to be done in larger groups of people to investigate whether these protein changes can be detected in tears in the earliest stages of the disease, before symptoms start.

 

Article from American Academy of Neurology.

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LRRK2 Drug Trial Shares Promising Results

In December, Denali Therapeutics announced positive results from its first-in-human LRRK2 inhibitor clinical trial. The experimental treatment is safe, and it lowers LRRK2 protein activity in humans’ body cells. This is a meaningful milestone in the clinical development of a drug with potential to slow or stop Parkinson’s progression (something no currently available treatment can do).

Denali also shared it is testing a second compound in a separate Phase I trial in control volunteers. Following completion of both trials, one of the two compounds will move into studies in people with Parkinson’s carrying a LRRK2 mutation.

In a press release, the company announced its first trial showed greater than 90 percent inhibition of LRRK2 activity at peak drug levels. This is a critical early step in testing a drug — does it do what you want it to do in the cell? Denali used two tests to measure inhibition, including one based on a finding from a Michael J. Fox Foundation-organized consortium linking LRRK2 to another protein.

“Mutations in LRRK2 are a major risk factor for Parkinson’s disease. Targeting this degenogene represents a promising approach to develop disease-modifying medicines,” said Ryan Watts, PhD, Denali CEO.

Read more on the findings and next steps.

Article from Michael J. Fox Foundation for Parkinson’s Research.

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Participate in Research from Home

Researchers from the University of Rochester’s Department of Neurology are conducting a study to identify the needs of people living with Parkinson’s and opinions and knowledge about palliative care. The online survey will take an estimated 20 minutes to complete and ask questions about your Parkinson’s, symptoms and care

The survey will ask questions about your Parkinson disease, your current quality of life, the presence of controlled and uncontrolled symptoms, your thoughts about your own future care, and your opinions and knowledge of palliative care.

WHO IS ELIGIBLE?
People living with Parkinson’s. Begin the survey to complete eligibility requirements.

WHEN
The survey is open now.

WHERE
Online by computer, smartphone, tablet or other electronic device.

TAKE THE SURVEY HERE

 

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Duopa device among newer treatments for Parkinson’s disease

Until August, Kern Jackson avoided going out in public.

Parkinson’s disease had progressed far enough that the levadopa pills he’d taken since 2008 weren’t as reliable to ease the symptom of his muscles freezing up. In the past two years, he had to take the medicine more frequently as it wore off quickly, leaving him unable to move.

“I was taking pills every two hours, and during the night,” said Jackson, 70, a retired physician who lives in Medical Lake. “It would take 20 to 45 minutes to be effective, then I’d be moving normally for about an hour. It was hard to plan to do anything.”

So in August, Jackson chose to get a newer Duopa device through Dr. Jason Aldred, a neurologist at Northwest Neurological. The Spokane clinic partners with Inland Imaging, where patients go in for an outpatient procedure to make a small incision in the stomach wall and insert a tube in the small intestine.

The external Duopa device has a pump for continuous delivery via the tube of a levadopa gel, contained in a medication cartridge that patients reload once a day into the device.

According to Aldred, the Duopa device first became available in 2015 after U.S. Food & Drug Administration approval, and it’s among a couple of newer developments for Parkinson’s treatment. The clinic also is participating in two clinical research trials that are attempting to slow disease progression.

The day after his outpatient procedure, Jackson saw Aldred at Northwest Neurological to program the system’s medicine dosage. Clinic staff observed Jackson’s movements for a day during office hours to make sure the new system was syncing correctly for his ability to get around.

Jackson now wears the device in a belted pack around his waist, and he said it’s helped him be more active. He and his wife, Diana, have since traveled by airplane and walked on the Centennial Trail.

“I feel much more confident going somewhere,” Jackson said. “I just went to a men’s retreat in Idaho with my son-in-law, and things went well.”

Although estimates vary, about 1 million people in the U.S. live with the disease, according to the Parkinson’s Foundation. Symptoms include tremor, rigidity, extreme slowness of movement and impaired balance.

Levadopa, now used for more than 50 years to treat Parkinson’s, is often considered the most effective for treatment of motor symptoms.

“Levadopa is turned into dopamine in the brain and replaces dopamine,” Aldred said “That’s huge because dopamine is the natural chemical in the brain that’s low in Parkinson’s patients, so we literally have the ability to replace something that’s low to bring about remarkable improvement in movement, stiffness and tremor.

“However, it doesn’t slow the progression. It treats symptoms remarkably for years or decades. Parkinson’s progresses slowly, but it does progress, and it can cause horrible quality of life issues.”

The Duopa device is offered as a choice for some patients with moderate to advanced Parkinson’s if levadopa in a pill form becomes less reliable, Aldred said. Other patients might be candidates for deep brain stimulation, a therapy that’s been around since 1997, he said.

“As the disease advances for moderate to advanced Parkinson’s, the medicine kicks in and wears off,” said Aldred, adding that also long-term, the disease affects other nerves outside of the brain including in the stomach, so medicine is less effectively moved into the small intestine for absorption.

“We call it dose failure,” he said. “That’s actually a big problem; the medicine is sitting in the stomach and doesn’t move. With the Duopa device, the tube mechanically bypasses the stomach and goes into the small intestine, and the medicine is released physically past the stomach.”

Aldred said the Duopa device is new enough that, so far, just over 30 of its clinic patients have one.

“This is a very new treatment and largely people are slow to warm up to it,” he said, adding that some people might have a stigma about having a tube inserted, a procedure that’s sometimes associated with end-of-life issues.

The small amount of tubing that’s external is flexible, Aldred said, and it’s hidden often under clothing. It can be disconnect for up to two hours if needed.

However, Aldred said current treatments, including Duopa, only partially relieve symptoms, so the two research trials are attempting approaches that might slow or stop the disease’s progression.

Both trials are seeking to stem what is thought to damage cells in the brain that regulate behavior, cognition and movement. A main research focus is finding a way to stop or clear out Lewy bodies, which are abnormal aggregates of protein that develop inside nerve cells in Parkinson’s.

“We have some interesting, cutting-edge NIH, Michael J. Fox Foundation-affiliated clinical research trials,” Aldred said.

One is a vaccine trial using anti-bodies in an attempt that might prevent the spread of Lewy bodies in the brain. A second phase of that study started this month involving a handful of clinic patients.

The other trial will test Nilotinib, a FDA-approved medicine used in treatment for a form of leukemia, but with a fraction of the dose applied for patients with mild Parkinson’s.

“This is a medication that may enhance the clearing of Lewy Bodies from the brain that we think is destructive,” Aldred added.

“We’re trying to get to the point before it spreads,” he said. “That’s a novel way of treating Parkinson’s. These two trials if they’re proven to work, which they haven’t been yet, may be safe and effective ways to slow the disease progression or potentially halt the disease progression.”

There’s also a new device that came out this year for deep brain stimulation, Aldred said. “It was developed by St. Jude’s Medical (since acquired by Abbott). We can aim the electrical current more precisely in the brain to get better effect.”

The DBS treatment requires surgery to implant a wire with four electrodes that deliver an electrical current in the brain to regulate abnormal impulses and smooth out “on time” and “off time” experienced by patients as the impact of medication rises and falls.

The DBS treatment and the Duopa device haven’t been studied head to head on whether one is more effective than the other, Aldred said.

“If someone has moderate cognitive issues, we’d never want to do DBS,” he said.

Alternatively, he added that the Duopa device might be a choice for some patients who aren’t comfortable with DBS.

“I tell patients this is a heavy diagnosis, but there is lot we can do, and one of the things is exercise, ” said Aldred, who encourages physical therapy and regular exercise to maintain better movement and quality of life.

 

Article from The Spokesman-Review.

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New smell test could aid early detection of Alzheimer’s and Parkinson’s

Nisha Pradhan was seven when she began to suspect she was missing out on something. Her sister seemed to have an uncanny knack for predicting what their mother was making for dinner. Pradhan, meanwhile, never had a clue.

“I would just stare at her,” Pradhan says. “She’s younger than me—how does she know more than I do?”

Now 21, Pradhan knows she has a limited ability to detect odor—including the smell of dinner cooking. Her situation is not unique: The sense of smell is often taken for granted, until it malfunctions.

As a patient in a clinical trial being conducted at Rockefeller University, Pradhan is helping scientists develop new smell tests, which promise to help improve diagnosis because they can be used reliably for anyone, anywhere. Because smell disorders can be linked to a variety of health conditions—interfering with appetite, as well as social interaction and sometimes leading to isolation, anxiety, and depression.

“People have their vision and hearing tested throughout their lives, but smell testing is exceedingly rare,” says neuroscientist Leslie Vosshall.

The new tests, developed by Vosshall along with Julien Hsieh, a Rockefeller clinical scholar, and their colleagues could even aid the early detection of neurological disorders that have been linked to problems with olfaction.

An underappreciated skill

People suffer from smell loss for various reasons—a head trauma or sinus infection, for example, or even a common cold—and the cause can be as hard to pinpoint as the condition itself. In Pradhan’s case, she believes she lost much of her sense of smell as a young child, although she’s not sure how. She brought the issue up with her pediatrician, but never received any testing or guidance.

Both the medical community and the people affected by smell loss can be prone to overlook it. “Olfies,” says Pradhan, referring to people with a normal sense of smell, “think not having a sense of smell just affects our ability to detect gas leaks, smoke, and bad body odor. But it deprives us of so much more, including emotions and memories that are so intimate and integral to the human experience.”

A handful of tests already exist for diagnosing people like her. One problem with these tests is that they rely on a patient’s ability to detect and identify single types of odor molecules, such as rose-scented phenylethyl alcohol. However, the ability to detect odors and to recognize them can vary greatly between people. So, someone with an otherwise normal sense of smell may not be able to detect the rose molecule. Meanwhile, another person who can smell roses but is from an area where these flowers are scarce may struggle to put a name to the scent. In either case, there is the potential for misdiagnosis, particularly when testing across different populations and countries.

The problem of smell

Hsieh and colleagues set out to eliminate these potential biases with the help of “white smells,” made by mixing many odors together to produce something unfamiliar. Just as a combination of wavelengths of light produces white light, and many frequencies of sound make up white noise, the team generated white smells from assortments of 30 different odor molecules. Their two new tests ask patients to distinguish white smells with overlapping ingredients and to detect white smells at increasingly lower concentrations.

If a person is unable to detect a single component of the test scent, this has little effect on the outcome, and test takers don’t need to identify the odor at all. “We’re really excited about these new tests,” says Vosshall, who is Robin Chemers Neustein Professor and a Howard Hughes Medical Institute investigator. “They focus on the problem of smell itself, because they don’t force people to match smells to words.”

Clinical trials conducted at The Rockefeller University Hospital and Taichung Veterans General Hospital in Taiwan showed that the new tests detected smell loss more reliably than conventional options. The results, published in Proceedings of the National Academy of Sciences, open up the possibility of a new means to detect smell loss worldwide. It could be used for detection of Alzheimer’s and Parkinson’s diseases, says Hsieh, now a resident at the Geneva University Hospitals in Switzerland.

“The goal is to use changes in the sense of smell, along with other biomarkers, to identify underlying causes of these neurological disorders very early, and so potentially improve treatment,” he says.

 

Article from The Rockefeller University.

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