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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8 Early Parkinson’s Disease Symptoms That Are Too Easy to Miss

This movement disorder is more treatable when caught early, but Parkinson’s disease symptoms can appear quite differently from one person to another. Talk to your doctor if you’re worried about any of these signs.

Changed handwriting

If your handwriting starts to go from big and loopy to small and cramped, this could be one of the earliest Parkinson’s disease symptoms. “Teachers with Parkinson’s will notice students complaining that they can’t read their handwriting when they write on the blackboard,” says Deborah Hall, MD, a neurologist at Rush University Medical Center in Chicago. Look for letters getting smaller and words crowding together. Many patients have slower movement and trouble with repetitive tasks, like handwriting.

Reduced sense of smell

If you’re having trouble smelling pungent foods or no longer pick up your favorite scents, see a doctor. It’s not the most common symptom of Parkinson’s, but Dr. Hall says patients who suffer a loss of smell report it being the earliest sign they experience. The link between reduced sense of smell and Parkinson’s isn’t clear, but one theory is that the clumps of the protein alpha-synuclein, found in the brains of all Parkinson’s patients, may form in the part of the brain responsible for smell before migrating to other areas and affecting motor function.

Trouble sleeping

If you were once a peaceful sleeper, but now toss and turn, flail your limbs, or even fall out of bed, those sleep problems could be Parkinson’s disease symptoms. It’s normal to have an occasional restless night, but talk to your doctor if you or your partner notices extra movement when you’re in a deep sleep, or if you start sleep-talking. More research is needed to discover why disturbed sleep and Parkinson’s are related, but one theory is that the degeneration of specific regions of the brain stem that can cause disordered sleeping may play a role in other Parkinson’s disease symptoms.

Constipation

If you’re not moving your bowels every day, or are increasingly straining, this can be an early sign of Parkinson’s. The disease alters the body’s autonomic nervous system, which controls processes like digestion and bowel function. Constipation on its own isn’t unusual, but if you’re experiencing other symptoms like difficulty sleeping and trouble moving or walking, talk to your doctor.

Depression

Much has been made of the link between the late comedian Robin Williams’ Parkinson’s diagnosis and ongoing battle with depression. Sometimes patients can develop depression after learning they have Parkinson’s, but it’s also common for people to be depressed years before they start to exhibit physical symptoms, says Michele Tagliati, MD, director of the Movement Disorders Program at Cedars-Sinai Medical Center in California. “Parkinson’s is characterized as a movement disorder because of a lack of dopamine in the brain, but there are also low levels of other neurotransmitters like serotonin, which are intimately related to depression,” he says. Parkinson’s patients who are depressed tend to feel apathetic and generally disinterested in things they used to enjoy, compared to feeling intensely sad or helpless, as is common in primary depression. “They lose pleasure in the simple things of life, like waking up in the morning and buying the paper,” says Dr. Tagliati. Treatment for depression includes counseling, antidepressant medication, and in the most extreme cases, electric shock therapy.

Tremors or shaking when relaxed

Shaking can be normal after lots of exercise or if you’re anxious, or as a side effect of some medications. But a slight shake in your finger, thumb, hand, chin, lip, or limbs when your body is at rest and your muscles are relaxed could signal Parkinson’s disease symptoms, according to the National Parkinson Foundation. About 70 percent of people with the disease experience a resting tremor, and it can become more noticeable during stress or excitement. These are the most common symptom and often tip people off to the disease, but when Parkinson’s patients think back they realize they experienced loss of smell, disturbed sleep, or anxiety before the tremors began.

Stiffness and slowed movements

Watch for an abnormal stiffness in your joints along with muscle weakness that doesn’t go away and makes everyday tasks like walking, teeth brushing, buttoning shirts, or cutting food difficult. If you no longer swing your arms when walking, your feet feel “stuck to the floor” (causing you to hesitate before taking a step), or people comment that you look stiff when you haven’t been injured, the National Parkinson Foundation suggests seeing a doctor.

Softer voice, or masked face

Doctors say that a softer voice or masked, expressionless face is a common sign of the disease. Some patients with Parkinson’s disease symptoms may also talk softer without noticing or have excessively fast speech or rapid stammering. Parkinson’s causes disruption of movement, including facial muscles.

Article from Reader’s Digest.

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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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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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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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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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Brain Rewiring in PD May Contribute to Abnormal Movement

The brain’s own mechanisms for dealing with the loss of dopamine neurons in Parkinson’s disease may be a source of the disorder’s abnormal movement, according to a Northwestern Medicine study published in Neuron.

The study suggests the loss of dopamine may cause the brain to rewire in a maladaptive manner, contributing to impaired movement in Parkinson’s disease. These findings also suggest that there are fundamental problems with scientists’ traditional model of Parkinson’s disease, said senior author Mark Bevan, PhD, professor of Physiology.

The prevailing consensus was that excessive patterning of the subthalamic nucleus (STN), a component of the basal ganglia, by the cerebral cortex was linked to the symptomatic expression of Parkinson’s disease, including muscle rigidity and slowness of movement, according to Bevan.

“When one saw a burst of activity in the cortex that was consistently followed by an abnormal burst of activity in the STN, scientists assumed that the direct connection between the two was responsible,” Bevan said.

Thus, Bevan and his colleagues, including lead author Hong-Yuan Chu, PhD, a post-doctoral fellow in the Bevan Lab, expected to see transmission in the cortex-to-STN pathway increase as dopamine levels dropped. Instead, they found the opposite: the strength of the pathway decreased massively.

“Like most scientists who come across something unexpected, we thought we’d done something wrong,” Bevan joked. “So, we used multiple, complementary approaches but everything pointed to the same conclusion.”

Further investigation suggested abnormal activity in a more indirect pathway from the cortex to the STN, involving the globus pallidus, was responsible. Abnormal activity in the indirect pathway leaves the STN vulnerable to excessive excitation, triggering compensatory plasticity that ultimately proved to be harmful, according to the study.

When the scientists prevented this maladaptive plasticity in late-stage Parkinson’s models, they found the symptoms improved, pointing to a link between compensation and motor dysfunction.

“According to the classic model, these adaptations should be homeostatic and preserve STN function,” Bevan said. “Preventing them should make the symptoms much worse — but it made them better instead.”

While the compensatory mechanisms may initially keep the brain operating normally under conditions of moderate dopamine neuron loss, as the disease progresses and more dopamine neurons die, the adaptations may become so extreme that they impair movement, according to the study.

These results suggest that there are fundamental flaws in our traditional understanding of brain dysfunction in Parkinson’s disease, Bevan said.

For Bevan, the unexpected results in this study served as a reminder that scientists must remain open-minded.

“It’s easy to be emotional and cling to your hypothesis,” Bevan said. “You have to be dispassionate, open-minded, and look at the data ­— if the data is not consistent with the hypothesis then you have to reject it and come up with a new one.”

This study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke grants 2R37 NS041280, P50 NS047085, 5T32 NS041234, and F31 NS090845. Confocal imaging work was performed at the Northwestern University Center for Advanced Microscopy, which was supported by National Cancer Institute Cancer Center Support grant P30 CA060553.

 

Article from Northwestern.edu.

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Scratch-and-Sniff Test Could Predict Parkinson’s Even Earlier

A new study provides further evidence that a simple scratch-and-sniff test could predict Parkinson’s disease even earlier than previously thought.

According to Michigan State University researcher Honglei Chen, lead author and professor of epidemiology, the test could potentially identify certain people who are at an increased risk of developing the disease up to 10 years before they are actually diagnosed. Previous research has shown an association between sense of smell and disease progression of up to four to five years.

The federally funded study, now published online in Neurology, the official publication of the American Academy of Neurology, is also one of the first to follow black people.

“One of the key differences in our study was we followed older white and black participants for an average of about 10 years, much longer than any other previous study,” Chen said. “We found that there was a strong link between smell and disease risk for up to six years. After that, the link remained, but just wasn’t as strong.”

He added that the relationship between smell and Parkinson’s risk in black participants also appeared not as strong as in the white participant group.

“Previous studies have shown that black people are more likely to have a poor sense of smell than whites and yet may be less likely to develop Parkinson’s disease,” said Chen, who is part of MSU’s Global Impact Initiative, an effort to help accelerate research in key areas affecting the world such as health and energy.

“We found no statistical significance for a link between poor sense of smell and Parkinson’s disease in blacks, but that may have been due to the small sample size and more research is needed.”

The study also found that older men with a poor sense of smell were more likely to develop the disease compared to women.

The study included 1,510 white and 952 black participants with an average age of 75. The test asked people to smell 12 common odors including cinnamon, lemon, gasoline, soap and onion, and then select the correct answer from four choices.

Based on their scores, participants were divided into three groups – poor sense of smell, medium and good. Researchers then monitored participant health through clinical visits and phone interviews for more than a decade.

Overall, 42 people developed Parkinson’s during the study including 30 white people and 12 black people.

People with poor sense of smell were nearly five times more likely to develop the disease than people with a good sense of smell. Of the 764 people with a poor sense of smell, 26 people developed the disease, compared to just seven of the 835 people whose sense of smell was good and nine of the 863 people whose sense of smell was categorized as medium.

Researchers also discovered that the results stayed the same after adjusting for other factors that could affect risk including smoking, coffee intake and history of head injury.

“It’s important to note that not everyone with low scores on the smell test will develop Parkinson’s disease,” Chen said. “More research is needed before the smell test can be used as a screening tool for Parkinson’s, but we are definitely on to something and our goal now is to better characterize populations that are at higher risk for the disease and to identify other factors involved.”

The National Institute on Aging, National Institute of Nursing Research and National Institute of Environmental Health Sciences funded the study.

 

Article from Michigan State University.

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