Early Parkinson's patients waiting too long to seek medical evaluation

Figure 1. Relationship between time of diagnosis, need for symptomatic therapy and the opportunity for a patient to participate in an early PD disease modifying therapy trial. Credit: University of South Florida

The time between diagnosis and the institution of symptomatic treatment is critical in the effort to find a cure for Parkinson's Disease (PD). A paper published in Nature Partner Journal: Parkinson's Disease notes too many early PD patients wait too long before seeking medical attention, or start taking symptomatic medications before they are required, thereby dramatically shrinking the pool of candidates for clinical trials.

28 sept 2018--Parkinson's disease is a disorder of the central nervous system that affects movement. Symptoms include tremors, stiffness, and slow and small movement. The pace of progression varies among patients, making the months following diagnosis crucial to researchers studying the disease's progression.
"The critical time of about one year from when the patient can be diagnosed with early PD based on mild classic motor features until they truly require symptomatic therapy can be considered the Golden Year," said lead author Robert A. Hauser, MD, director of the Parkinson's & Movement Disorder Center at the University of South Florida. "It is during this early, untreated phase, that progression of clinical symptoms reflects the progression of the underlying disease."
Hauser says that in order to determine whether or not a potential disease slowing therapy is actually working, they must be able to compare the therapy to a placebo without interference from symptomatic treatment. Otherwise, they won't know if the therapy is slowing the disease's progression or if they are just seeing the effects of symptomatic treatment.
This requires patients to seek assessment soon after they notice the onset of tremor or slow movement. In addition, physicians should consider referring patients to clinical trials soon after diagnosis and delay prescribing symptomatic medication until it's necessary. If a patient waits until symptomatic treatment is necessary, the opportunity to participate in these crucial clinical trialsis lost.

More information: Robert A. Hauser. Help cure Parkinson's disease: please don't waste the Golden Year, npj Parkinson's Disease (2018). DOI: 10.1038/s41531-018-0065-1


Provided by University of South Florida

Effects of deep brain stimulation in patients with Parkinson's disease

The implantation of DBS electrodes enables researchers to gain insights into the functional roles of both the basal ganglia and their associated nerve tracts (structures and nerve tracts inside the orange circle). Basal ganglia are areas of the brain that are involved in movement and motor control. Credit: Neumann/Charit

Researchers at Universitätsmedizin Berlin have studied motor and cognitive effects of deep brain stimulation in patients with Parkinson's disease. Their results show that the adverse cognitive effects of deep brain stimulation are linked to a different neural pathway than that responsible for the treatment's desired motor effects. This finding will help optimize treatments for patients with Parkinson's disease. Results from this research have been published in Brain.

04 sept 2018--Deep brain stimulation (DBS) is an effective treatment alternative for Parkinson's disease patients with an inadequate response to drug treatments. DBS targets the subthalamic nucleus, which forms part of the diencephalon, a division of the forebrain. The subthalamic nucleus integrates information from different neurons and is primarily responsible for motor processes, but also plays an important role in cognitive processes, such as decision-making and response modulation.
Researchers from Charité's Department of Neurology on Campus Charité Mitte have studied the effect of DBS on both cognitive and motor pathways. By combining behavioral experiments with brain mapping and computational modeling, the researchers were able to show that effects on motor function—such as improvements in motor control—are mediated by different neural pathways to those responsible for unwanted cognitive effects, such as premature actions in situations involving a decision-making process.
These findings enhance our understanding of the neuronal networks affected by Parkinson's disease, deliver insights into the pathophysiology of Parkinson's disease, and enable us to draw conclusions regarding the mechanism of action of DBS. "Only an improved understanding of the treatment's mechanism of action will allow us to make deep brain stimulation more effective, thus enabling us to improve the quality of life of patients with Parkinson's disease through a reduction in the side effects of treatment," explains the study's first author, Dr. Wolf-Julian Neumann, a researcher at the Department of Neurology.
As a next step, the researchers from the Movement Disorders Working Group are hoping to use measurements of neural activity to differentiate between disease-specific patterns of neural activity and patterns found in healthy individuals. "This will allow us to adapt brain stimulation treatments according to the needs of the individual patient and in real time. "It is an important step on the way to developing an intelligent, personalized and demand-adapted treatment," says Working Group Leader Prof. Dr. Andrea A. Kühn of the Department of Neurology.

More information: Wolf-Julian Neumann et al, Functional segregation of basal ganglia pathways in Parkinson's disease, Brain (2018). DOI: 10.1093/brain/awy206


Provided by Charité - Universitätsmedizin Berlin

Augmented reality app may aid patients with Parkinson's

Rice engineering students have designed an iPhone app to help patients overcome a symptom known as “freezing,” in which the legs temporarily refuse to follow the brain’s command to lift and move forward. In visual mode, the app places a circle or other object over what the camera sees in front of users and encourages them to step into the graphic. Credit: Jeff Fitlow

15 april 2018--It's appropriate that during Parkinson's Awareness Month, a team of Rice University seniors will show how augmented reality may help patients with the disease.
Six Rice engineering students have designed an iPhone app to help patients overcome a symptom known as "freezing," in which the legs temporarily refuse to follow the brain's command to lift and move forward.
For many of these patients, researchers have found that visual, audio or vibratory cues can help them overcome freezing. The Rice app may be the most elegant and comprehensive way to date to provide those cues, according to the students.
The app takes advantage of new programming tools that allow for the incorporation of augmented reality. In this case, the user can point the phone at the floor or sidewalk and trigger it to place the image of a block, circle or other object where his or her foot should land. That visual cue is often enough to allow patients to initiate their gait.
The app can also provide audio or sensory cues through the phone's sound and vibration capabilities. It should be adaptable to Android phones as well, according to the students.
"This is for patients who, in their day-to-day lives, experience freezing episodes," said team member Gaby Perez. "There are a couple of devices on the market to help them, but none of them incorporate all three kinds of cues."

Rice senior engineering student Jeremy David shows the user interface of an iPhone app intended to help patients with Parkinson’s disease maneuver. Credit: Jeff Fitlow

Perez and her Stairway to Stability teammates, Theresa Sonka, Kristen Smith, Keshav Rao, Jeremy David and Dan Burke, all bioengineering majors, took on the challenge as their capstone design project, required of most Rice engineering seniors. They were advised by bioengineering lecturer Eric Richardson with help from Dr. Eugene Lai, a neurologist at Houston Methodist, and sponsorship by Karen and Richard Whitney. The team said client and partial sponsor Nora Bynum was an influential adviser during development of the app.
Their creation is certainly smaller and cheaper than what they referred to as the state of the art for patients, a cane with a laser attachment. "Every time you place the cane down, the laser line pops up in front of you, cueing the user to step over it," Sonka said. "But a lot of the time, these laser solutions have trouble working outdoors."
"What's cool about our project is that the cheapest solutions available right now are about $200, with some solutions costing as much as $3,000," David said. "Our solution, however, has the potential to work more effectively and at a fraction of the cost."
Because some patients may also experience tremors in their hands, the team created a lanyard phone case a patient can wear to make the phone easier to manipulate.
The team worked with the Houston Area Parkinson Society to recruit patients who are helping them test the app at Rice's Oshman Engineering Design Kitchen, Burke said. "Our goal right now is to prove that the concept of augmented reality can be used in a therapeutic context while maintaining the user-friendly nature of smartphones."
"The patients we've talked to are a little on the milder end and are still able to walk, but each one of them has started to see instances of freezing, whether it be just for a few seconds or on the order of minutes," Rao said. "They've each talked about the mental gymnastics they go through to be able to move their feet again. They're very interested in anything that can reduce that burden."
The students appreciate the irony that their solution for people with Parkinson's would make them look like everybody else who walks down the street staring at a cellphone.
"Another big criterion was social comfort," Smith said. "We wanted it to be a very discreet solution."
The team plans to demonstrate the app at the annual George R. Brown School of Engineering Design Showcase April 12 at Rice's Tudor Fieldhouse. The event opens to the public at 4:30 p.m., with the winners of cash prizes announced at 6:30. As many as 80 teams are expected to compete this year.

More information: Follow the team at oedk.rice.edu/Sys/PublicProfile/41416142/4330110


Provided by Rice University

Singing may be good medicine for Parkinson's patients

15 aug 2017--Singing? To benefit people with Parkinson's disease? It just may help, a researcher says.
"We're not trying to make them better singers, but to help them strengthen the muscles that control swallowing and respiratory function," said Elizabeth Stegemoller, an assistant professor of kinesiology at Iowa State University.
Stegemoller holds a weekly singing therapy class for Parkinson's disease patients. At each session, participants go through a series of vocal exercises and songs.
Singing uses the same muscles as swallowing and breathing control, two functions affected by Parkinson's disease. Singing significantly improves this muscle activity, according to Stegemoller's research.
"We work on proper breath support, posture and how we use the muscles involved with the vocal cords, which requires them to intricately coordinate good, strong muscle activity," she said in a university news release.
Other benefits noted by patients, their families and caregivers include improvements in mood, stress and depression, Stegemoller said.
Her research was published in Complementary Therapies in Medicine.
Parkinson's disease is a chronic and progressive movement disorder. Nearly one million Americans live with the disease. The cause isn't known, and there is no cure at present. But there are treatment options such as medication and surgery to manage symptoms, according to the Parkinson's Disease Foundation.
Symptoms can include tremors of the hands, arms, legs, jaw and face; slowness of movement; limb rigidity; and problems with balance and coordination.

More information: The U.S. National Institute of Neurological Disorders and Stroke has more on Parkinson's disease.

Hand-grip test can indicate decline in physical function of Parkinson's patients

UBC researchers Jenn Jakobi, sitting, and Gareth Jones, right, review results from recent electromyography tests on patients with Parkinson's disease with their student researchers. Credit: UBC Okanagan

12 feb 2017--UBC researchers Jenn Jakobi and Gareth Jones, both Health and Exercise Sciences professors at UBC's Okanagan campus, recently completed a study that examined the methods used to monitor the progressive advancement of Parkinson's disease (PD)—a degenerative disease that affects the central nervous system.
The study compared results from electromyography assessments of leg and arm muscles to basic physical performance tests such as gait speed, balance and hand-grip strength. The results were surprising.
"It became very clear that the hand-grip test was one of the functional tests that proved to be a reliable and valuable test measure," says Jakobi. "The hand-grip test is an easy and conclusive way to test muscle strength decline in this group of people."
The study involved 23 men and women with PD and 14 people without the disease, all 50 years or older living independently in Kelowna. The participants wore a portable monitoring device to measure muscle activity with the device recording electrical activity of muscles in the arms and legs for approximately eight hours. Participants also underwent three physical function tests—hand-grip, gait and balance—each morning and afternoon.
Jones says the data gleaned from the three physical tests was as conclusive and as informative as the lengthy recordings of muscle activity. And the tests were easier for participants and those administering the experiments.
"The hand-grip dynamometer is a tool that is easily accessible, easy to use, and is reliable," says Jones. "In addition they are readily available to health professionals such as family doctors, community therapists and physiotherapists."
"It seems these devices have come full circle and are back being used by clinicians," adds Jakobi. "It's a tool that is ideal for Parkinson's patients as you can easily record a decline in an individual's physical strength and function as the disease progresses."
Patients with PD suffer symptoms like uncontrollable shaking, slowness of movement, and eventually difficulty with balance, coordination and walking. It's important for health care professionals to track early functional decline of Parkinson's patients, says Jakobi. In this way, individual health can be monitored and future falls related to the disease prevented.
According to Statistics Canada more than 67,000 Canadians are living with Parkinson's today, and it is mostly diagnosed in men over the age of 45.
The study was recently published in the journal Archives of Physical Medicine and Rehabilitation.


Provided by University of British Columbia

Skin test may shed new light on Alzheimer's and Parkinson's diseases

Scientists have discovered a skin test that may shed new light on Alzheimer's and Parkinson's diseases, according to a study released today will be presented at the American Academy of Neurology's 67th Annual Meeting in Washington, D.C., April 18 to 25, 2015.

27 feb 2015--The study showed that skin biopsies can be used to detect elevated levels of abnormal proteins found in the two diseases.

"Until now, pathological confirmation was not possible without a brain biopsy, so these diseases often go unrecognized until after the disease has progressed," said study author Ildefonso Rodriguez-Leyva, MD, at Central Hospital at the University of San Luis Potosi in San Luis Potosi, Mexico. "We hypothesized that since skin has the same origin as brain tissue while in the embryo that they might also show the same abnormal proteins. This new test offers a potential biomarker that may allow doctors to identify and diagnose these diseases earlier on."

For the study, researchers took skin biopsies from 20 people with Alzheimer's disease, 16 with Parkinson's disease and 17 with dementia caused by other conditions and compared them to 12 healthy people in the same age group. They tested these skin samples to see if specific types of altered proteins were found—ones that indicate a person has Alzheimer's or Parkinson's.

As compared to healthy patients and ones with dementia caused by other conditions, those with both Alzheimer's and Parkinson's had seven times higher levels of the tau protein. People with Parkinson's also had an eight times higher level of alpha-synuclein protein than the healthy control group.

Alzheimer's disease is ranked as the sixth leading cause of death in the United States, and 5.4 million Americans are currently diagnosed with Alzheimer's disease. Parkinson's disease affects one million Americans, with at least 60,000 new cases reported annually each year.

"More research is needed to confirm these results, but the findings are exciting because we could potentially begin to use skin biopsies from living patients to study and learn more about these diseases. This also means tissue will be much more readily available for scientists to study," said Rodriguez-Leyva. "This procedure could be used to study not only Alzheimer's and Parkinson's, but also other neurodegenerative diseases."

Provided by American Academy of Neurology

Simple clinical tests help differentiate Parkinson's disease from atypical parkinsonism

Two simple tests conducted during the neurological exam can help clinicians differentiate between early-stage Parkinson's disease (PD) and atypical parkinsonism. By asking patients to perform a tandem gait test and inquiring whether they are still able to ride a bicycle, clinicians can ascertain whether medio-lateral balance is impaired, a defining characteristic of atypical parkinsonism. These findings are published in the Journal of Parkinson's Disease.

18 nov 2014--This issue of the Journal of Parkinson's Disease also marks the inauguration of a new feature, "How I examine my patient," which is designed to help improve the clinical skills of physicians, allied health professionals, and other professionals involved in the care of patients with PD and other movement disorders.

The occurrence of a sideways or medio-lateral balance impairment is a "red flag" of atypical parkinsonism conditions, such as multiple system atrophy (MSA), progressive supranuclear palsy, or vascular parkinsonism. As the condition progresses, patients with this deficit often compensate by adopting a wide-based walking pattern, probably reflecting widespread pathologic brain involvement of the cerebellum and brain stem, explains Jorik Nonnekes, MD, of the Radboud University Medical Center, Department of Rehabilitation, Nijmegen, the Netherlands.

In contrast, patients with PD develop a shuffling gait, maintaining a narrow distance between their feet. Because medio-lateral balance is preserved, a PD patient may still be able to ride a bicycle even when walking is difficult.

In the first test, 36 patients with PD and 49 patients with atypical parkinsonism were given a tandem gait test. Patients were instructed to take 10 consecutive steps along an imaginary straight, thin line, toe-to-heel. An abnormal tandem gait was scored if one or more side steps were needed to maintain balance. The researchers found that 18% of patients with atypical parkinsonism were able to perform the tandem gait test without a single side step, compared with 92% of patients with PD. The results were similar for patients with only early disease (< 3 years).

Another study included 45 patients with PD and 64 patients with atypical parkinsonism, all of whom said they previously rode bicycles before the onset of motor symptoms. When asked if they still were able to ride a bicycle, 52% of the atypical parkinsonism patients said they had stopped cycling compared to 2% of those with PD.

"Both tests are easy to perform in clinical practice and have a good diagnostic accuracy, even early in the course of the disease," says Dr. Nonnekes. He adds that the tests should always be judged in the clinical context and presence of other red flags or supportive features.

In the new "How I examine my patient," feature researchers and clinicians will contribute practical information about how to conduct good neurological examinations. In many cases, the literature and even neurological textbooks do not include practical descriptions of very common clinical tests.

In the first example, "How I examine my patient: The art of neurological examination for Parkinson's disease and atypical parkinsonism," authors Bastiaan R. Bloem, MD, PhD, Department of Neurology, Radboud University Nijmegen Medical Center, the Netherlands, and Patrik Brundin, MD, PhD, Laboratory of Translational Parkinson's Disease Research, Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, discuss how a well-done examination provides important diagnostic information. They write, "Details about how to perform certain clinical tests can be retrieved from standard neurological textbooks, but many useful clinical tips and tricks have been simply transmitted from teacher to student...such clinical pearls were never laid down in accessible form for a broad readership.

"We hope this new section offers readers a glimpse into the examination room of experienced clinicians who share their clinical pearls," say Dr. Bloem and Dr. Brundin.

Provided by IOS Press

Targeted exercise benefits Parkinson's patients

Can exercise help people with Parkinson's disease? Maureen Gartner, MSN, a nurse practitioner with the University of Cincinnati (UC) Neuroscience Institute's Gardner Family Center for Parkinson's Disease and Movement Disorders, answers with an emphatic "Yes!"

24 auug 2014--"Everyone with Parkinson's disease is encouraged to exercise," Gartner says. "Research strongly suggests that exercise holds significant quality-of-life benefits for people with Parkinson's. Studies show that patients' motor and non-motor scores improve after only three months of targeted exercise." (Motor scores involve muscle strength, mobility, flexibility, balance, walking, swallowing and speaking. Non-motor scores involve depression, apathy, fatigue and constipation.)

"In short, exercise is a win-win for people with Parkinson's," Gartner says. Exercise also reduces the risk of other diseases that may develop, including cardiovascular disease, osteoporosis, cognitive impairment and Alzheimer's disease."

Gartner will be a panelist at the Parkinson's Disease Symposium and Expo Sept. 6 at the Oasis Conference Center in Loveland, Ohio, part of the 2014 Sunflower Revolution. The Sunflower Revolution Fitness Festival, featuring a 5-kilometer run/walk and 25K, 40K and 100K bike rides, will be held Sept. 7 at Yeatman's Cove on the Ohio River at downtown Cincinnati.

Also appearing at the symposium will be Becky Farley, PT, PhD, founder and chief executive officer of Parkinson's Wellness Recovery, a nonprofit organization based in Tucson, Arizona. Her topic will be "Exercise as Medicine: Essentials for Parkinson's."

With exercise high on the priority list for people who have Parkinson's disease and their families and caregivers, Gartner answered some questions about it:

What is "targeted" exercise?

Targeted exercise for people with Parkinson's is different from simply getting on a treadmill three days a week. Getting on a treadmill will help your fitness, but by itself it will not help your Parkinson's. The goal of "targeted" exercise is to challenge your brain to develop or strengthen a variety of neural connections. You can do this by performing different movements rather than a single, repetitive movement. Exercising in a variety of ways will yield the greatest benefits.

How often should I exercise, and for how long?

Your doctor can recommend a program that is appropriate for you based on your symptoms, fitness level and overall health. Your doctor can recommend how many times a week you should exercise and how long and how intensely you should exercise. Stop exercising if at any time you begin to feel pain or feel sick.

What types of exercise are best?

An ideal exercise program for people with Parkinson's is a "targeted" exercise program that includes stretching, strengthening, walking, balance training and aerobic activities that get your heart pumping. It could include time spent on a treadmill or stationary bike. Water aerobics and swimming are other good options. In addition, there are forms of exercise that we don't always think of as exercise, such as yoga, tai chi and just getting out on the dance floor. You can also exercise your hand muscles and reflexes with the Nintendo Wii, whose games include tennis, bowling, baseball and a balance board. It's important to stick with your exercise program. Keep in mind that exercise is a way to take control of your Parkinson's. You cannot always control your disease, but exercise is part of your health that you can control.

Who can help create an exercise program that's right for me?

There are a growing number of personal trainers who are knowledgeable about Parkinson's disease. The local chapter of the American Parkinson's Disease Association also sponsors multiple exercise classes. These classes are led by personal trainers whose passion is helping people with Parkinson's disease.

Is it safe for me to exercise by myself?

To exercise safely is to exercise with a partner or caregiver. Someone should always be with you in case you fall or freeze in place. Wherever you exercise, you should avoid slippery floors, rooms with poor lighting and throw rugs. If you have balance problems, you should exercise in an environment where you can grab onto something if you begin to fall. Nevertheless, there are a few exercises that you might prefer to do alone in the comfort of your home. These include exercises for your facial muscles. You can smile, yawn, shout, sing, make faces in the mirror and make chewing movements to help keep your facial muscles as strong as possible.

What are cues and what role do they play in exercise?

Cues are hints given by another person, a sound, an image or an object to help you stay balanced or in the right position so that you do not hurt yourself. Cues can be verbal, musical, written (on reminder cards) or visual. For example, if you have freezing of gait, a trainer might put blocks on the floor for you to walk around. The trainer also might also give you verbal cues by saying "BIG STEP" or "BIG STRIDE" to help your brain send that message to your legs.

What should I wear when I exercise?

Wear loose, comfortable clothing and comfortable shoes.

When is the best time to exercise?

Exercise when your medicines are working well, not when they are wearing off.

I have always been a couch potato. How do I begin?

First, be realistic. Check with your doctor and then start slowly. Perhaps you can begin by walking around the block or doing a few crunches while watching TV. Soup cans or soda bottles can be used as simple weights. Next, find an exercise buddy, perhaps your spouse or someone from your support group, neighborhood or church. Be on the lookout for ways to incorporate more activity into your day. Make exercise more enjoyable by listening to music. Remember that exercisecan help you live better with Parkinson's.

Provided by University of Cincinnati

High-intensity strength training shows benefit for Parkinson's patients

29 jan 2014—Researchers at the University of Alabama at Birmingham say that high-intensity strength training produced significant improvements in quality of life, mood and motor function in older patients with Parkinson's disease. The findings were published Jan. 9 online in the Journal of Applied Physiology.

Fifteen subjects with moderate Parkinson's underwent 16 weeks of high-intensity resistance training combined with interval training designed to simultaneously challenge strength, power, endurance, balance and mobility function. Before and after the 16 weeks, the subjects were compared to age-matched controls who did not have Parkinson's and did not undergo the exercise regimen.

"We saw improvements in strength, muscle size and power, which we expected after rigorous weight training; but we also saw improvement in balance and muscle control," said Marcas Bamman, Ph.D., professor in the Department of Cell, Developmental and Integrative Biology and lead author of the study. "We also saw improvement in cognition, mood and sense of well-being."

Parkinson's disease is a debilitating, neurodegenerative disease that dramatically affects mobility function and quality of life. Patients often experience weakness, low muscle power and fatigue.

Bamman, who heads the UAB Center for Exercise Medicine, devised a strenuous exercise regimen for the participants. Subjects performed three sets of eight to 12 repetitions of a variety of strength training exercises, such as leg or overhead presses, with a one-minute interval between sets for high-repetition, bodyweight exercises, such as lunges or pushups.

"We pushed these patients throughout the exercise period," said Neil Kelly, M.A., a graduate student trainee and first author of the study. "We used a heart rate monitor to measure exercise intensity—keeping the heart rate high through the entire 40-minute session."

Bamman says this was the first study of its kind to look at the biology of the muscles. Biopsies of muscle tissue were collected before and after the 16 weeks.

"We found favorable changes in skeletal muscle at the cellular and subcellular levels that are associated with improvements in motor function and physical capacity," Bamman said.

Physicians who treat Parkinson's patients, such as UAB's David Standaert, M.D., Ph.D., chair of the Department of Neurology, say they have long believed that exercise is beneficial to their patients.

"What we do not know is what kind of exercise and how much exercise will prove best for individual patients with Parkinson's," Standaert said. "This study is concrete evidence that patients can benefit from anexercise program and can do so rapidly in only 16 weeks."

Standaert says he hopes this study will open the door to a more complete understanding of the role of exercise in this patient population.

"My patients who participated in the study told me that they enjoyed the exercise regimen and that they saw distinct improvement in their health and physical condition," he said. "Future studies should be able to help answer questions such as optimal frequency, intensity and type of exercise."

Study participants showed significant improvement of six points on average on a measure called the Unified Parkinson's Disease Rating Scale. On another measure, a seven-point fatigue scale, the group improved from a score above the clinical threshold for undue fatigue to a score below this threshold.

A sit-to-stand test showed that, after strength training, participants dropped from requiring 90 percent of maximum muscle recruitment to rise to a standing position to just 60 percent, which put them on par with their same-age, non-Parkinson's peers.

"These are all indications that strength training produced a major improvement in the ability to activate muscles, to generate power and to produce energy," Bamman said, "all of which can contribute to improved quality of life and reduction of injury risk from falls."

The study was funded by the UAB School of Medicine and the Department of Neurology, along with the UAB Center for Exercise Medicine. Bamman hopes the findings will pave the way for larger studies to define optimal exercise doses for Parkinson's patients across the disease spectrum.

"This is the first step in an important direction to maximize the therapeutic benefits of exercise training for people with Parkinson's disease," he said.

Provided by University of Alabama at Birmingham

PARKINSON: Unleashing the watchdog protein

McGill University researchers have unlocked a new door to developing drugs to slow the progression of Parkinson's disease. Collaborating teams led by Dr. Edward A. Fon at the Montreal Neurological Institute and Hospital -The Neuro, and Dr. Kalle Gehring in the Department of Biochemistry at the Faculty of Medicine, have discovered the three-dimensional structure of the protein Parkin.

11 may 2013--Mutations in Parkin cause a rare hereditary form of Parkinson's disease and are likely to also be involved in more commonly occurring forms of Parkinson's disease. The Parkin protein protects neurons from cell death due to an accumulation of defective mitochondria. Mitochondria are the batteries in cells, providing the power for cell functions. This new knowledge of Parkin's structure has allowed the scientists to design mutations in Parkin that make it better at recognizing damaged mitochondria and therefore possibly provide better protection for nerve cells.

The research will be published online May 9 in the leading journal Science.

"The majority of Parkinson's patients suffer from a sporadic form of the disease that occurs from a complex interplay of genetic and environmental factors which are still not fully understood, explains Dr. Fon, neurologist at The Neuro and head of the McGill Parkinson Program, a National Parkinson Foundation Centre of Excellence. "A minority of patients have genetic mutations in genes such as Parkin that cause the disease. Although there are differences between the genetic and sporadic forms, there is good reason to believe that understanding one will inform us about the other. It's known that toxins that poison mitochondria can lead to Parkinson's-like symptoms in humans and animals. Recently, Parkin was shown to be a key player in the cell's system for identifying and removing damaged mitochondria."

Researchers have unlocked a new door to developing drugs to slow the progression of Parkinson's disease. They have discovered the 3-D structure of the protein Parkin. Mutations in Parkin cause a rare hereditary form of Parkinson's disease and are likely to also be involved in more commonly occurring forms of Parkinson's disease. This new knowledge of Parkin's structure has allowed the scientists to design mutations in Parkin that make it better at recognizing damaged mitochondria and therefore possibly provide better protection for nerve cells. Credit: Montreal Neurological Institute and Hospital

Dr. Gehring, head of McGill's structural biology centre, GRASP, likens Parkin to a watchdog for damaged mitochondria. "Our structural studies show that Parkin is normally kept in check by a part of the protein that acts as a leash to restrict Parkin activity. When we made mutations in this specific 'leash' region in the protein, we found that Parkin recognized damaged mitochondria more quickly. If we can reproduce this response with a drug rather than mutations, we might be able to slow the progression of disease in Parkinson's patients."

Parkin is an enzyme in cells that attaches a small protein, ubiquitin, to other proteins to mark them for degradation. For example, when mitochondria are damaged, Parkin is switched on which leads to the clearing of the dysfunctional mitochondria. This is an important process because damaged mitochondria are a major source of cellular stress and thought to play a central role in the death of neurons in neurodegenerative diseases.

Husband and wife team, Drs. Jean-François Trempe and Véronique Sauvé, are lead authors on the paper. Dr. Sauvé led the Gehring team that used X-ray crystallography to determine the structure of Parkin. Dr. Trempe in the Fon laboratory directed the functional studies of Parkin.

"We are proud to invest in scientific excellence and to fund discovery stage research so that investigators like Dr. Gehring and Fon in Canada can test new theories and pursue promising new leads. We believe that our National Research Program plays an important role in the global search for better treatments and a cure for Parkinson's disease," says Joyce Gordon, President and CEO, Parkinson Society Canada.

More information: www.sciencemag.org… ence.1237908

Provided by McGill University

Head injury + pesticide exposure = Triple the risk of Parkinson's disease

A new study shows that people who have had a head injury and have lived or worked near areas where the pesticide paraquat was used may be three times more likely to develop Parkinson's disease. The study is published in the November 13, 2012, print issue ofNeurology, the medical journal of the American Academy of Neurology. Paraquat is a herbicide commonly used on crops to control weeds. It can be deadly to humans and animals.

13 nov 2012--"While each of these two factors is associated with an increased risk of Parkinson's on their own, the combination is associated with greater risk than just adding the two factors together," said study author Beate Ritz, MD, PhD, of UCLA's Fielding School of Public Health. "This study suggests that the physiological process that is triggered by a head injury may increase brain cells' vulnerability to attacks from pesticides that can be toxic to the brain or the other way around, for example, chronic low dose exposure to pesticides may increase the risk of Parkinson's after a head injury."

The study involved 357 people with Parkinson's disease and 754 people without the disease, all of whom lived in an agricultural area in central California. The participants reported any head injuries they had ever received with a loss of consciousness for more than five minutes.

The researchers determined participants' exposure to the weed killer based on a 500-meter area around their home and work addresses, using a geographic information system (GIS) that combined data on paraquat use collected by the state of California's Pesticide Use Reporting system with land use maps.

People with Parkinson's disease were twice as likely to have had a head injury with loss of consciousness for more than five minutes as people who did not have the disease. Of the 357 people with Parkinson's disease, 42, or 12 percent, reported ever having had such a head injury, compared to 50 of the 754 people without the disease, or 7 percent.

People with Parkinson's disease were 36 percent more likely to have exposure to paraquat than those who did not have the disease. Of those with Parkinson's, 169 had exposure to the weed killer, or 47 percent, compared to 291 of those without the disease, or 39 percent.

Provided by American Academy of Neurology

Focused ultrasound for treating Parkinson's disease to be tested

Dr. Jeff Elias, left,is the principal investigator of a a new study to investigate the scalpel-free technology’s safety and effectiveness in reducing tremor related to Parkinson’s disease. 

15 oct 2012—After a promising clinical trial of focused ultrasound as a potential treatment for essential tremor, the University of Virginia Health System is launching a new study to investigate the scalpel-free technology's safety and effectiveness in reducing tremor related to Parkinson's disease.

The phase 1 clinical trial has been approved by the U.S. Food and Drug Administration and is expected to enroll 30 subjects with medication-resistant Parkinson's disease. The subjects will undergo an investigational procedure using focused sound waves delivered within a magnetic resonance scanner to target a small area deep in the brain. Unlike traditional brain surgery, there is no need to cut into the skull.

"We are very encouraged by our initial experience with MRI-guided focused ultrasound. There is a tremendous amount of enthusiasm from our patients and the public for treatments without incisions," Dr. Jeff Elias, the trial's principal investigator, said. "Parkinson's disease is the next logical step on our roadmap of investigation."

Elias previously conducted the first focused ultrasound trial for treatment of essential tremor. All 15 trial participants were discharged the day after their procedures, and tremor improvement has been seen throughout follow-up.

"The technology allowed us to safely perform the procedure in all 15 of the patients, and none of them received any anesthesia," Elias said. "They got a similar degree of tremor control that we see with other surgical procedures like deep brain stimulation."

Elias is preparing the full findings of the essential tremor trial, and he expects to proceed to a larger, multicenter and international trial. Because the trial was the first of its kind, more work needs to be done to determine the long-term effectiveness of the procedure in treating essential tremor. As such, it remains investigational and is not yet available as a treatment outside a clinical trial.

The new Parkinson's trial will test focused ultrasound's safety and efficacy in treating tremor related to Parkinson's disease, an incurable, neurodegenerative condition characterized by tremor and uncontrollable movements. Surgery can, in some cases, alleviate symptoms when medications have become ineffective. The current frontline surgical option is deep brain stimulation, which involves drilling holes in the skull and implanting a pacemaker system in the brain.

U.Va.'s new Parkinson's trial is sponsored jointly by the Focused Ultrasound Foundation, the Heller Foundation, the Commonwealth of Virginia and InSightec, the maker of the ultrasound device. Trial participants must have Parkinson's disease with tremor that is resistant to standard medical therapy.

More information: To learn more about focused ultrasound at U.Va., visit uvahealth.com/focusedultrasound. The site includes a link to a database where those interested in being considered for the Parkinson's trial should submit their information.

Provided by University of Virginia

Study investigates genetic variants' role in increasing Parkinson's disease risk

Boston University School of Medicine (BUSM) investigators have led the first genome-wide evaluation of genetic variants associated with Parkinson's disease (PD). The study, which is published online in PLOS ONE, points to the involvement of specific genes and alterations in their expression as influencing the risk for developing PD.

07 oct 2012--Jeanne Latourelle, DSc, assistant professor of neurology at BUSM, served as the study's lead author and Richard H. Myers, PhD, professor of neurology at BUSM, served as the study's principal investigator and senior author.

A recent paper by the PD Genome Wide Association Study Consortium (PDGC) confirmed that an increased risk for PD was seen in individuals with genetic variants in or near the genes SNCA, MAPT, GAK/DGKQ, HLA and RIT2, but the mechanism behind the increased risk was not determined.

"One possible effect of the variants would be to change the manner in which a gene is expressed in the brains, leading to increased risk of PD," said Latourelle.

To investigate the theory, the researchers examined the relationship between PD-associated genetic variants and levels of gene expression in brain samples from the frontal cortex of 26 samples with known PD and 24 neurologically healthy control samples. Gene expression was determined using a microarray that screened effects of genetic variants on the expression of genes located very close to the variant, called cis-effects, and genes that are far from the variant, such as those on a completely different chromosome, called trans-effects.

An analysis of the cis-effects showed that several genetic variants in the MAPT region showed a significant association to the expression of multiple nearby genes, including gene LOC644246, the duplicated genes LRRC37A and LRRC37A2 and the gene DCAKD. Significant cis-effects were also observed between variants in the HLA region on chromosome 6 and two nearby genes HLA-DQA1 and HLA-DQA1. An examination of trans-effects revealed 23 DNA sequence variations that reached statistical significance involving variants from the SNCA, MAPT and RIT2 genes.

"The identification of the specific altered genes in PD opens opportunities to further study them in model organisms or cell lines with the goal of identifying drugs which may rectify the defects as treatment for PD," said Myers.

More information: dx.plos.org/10.137… pone.0046199

Provided by Boston University Medical Center

Freezing Parkinson's in its tracks

Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

07 may 2012--The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.
Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.
Guarding dopamine levels
As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.
The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.
In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.
Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.
Filling an urgent need
According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson's disease. "Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease," she says. "Until now, we have lacked tools for neuroprotection."
The researchers also note the potential for the peptides to be used preventatively. In some cases, Parkinson's can be diagnosed before motor symptoms begin with the help of brain scans, explains Dr. Lev, and patients who have a genetic link to the disease might opt for early testing. A preventative therapy could help many potential Parkinson's patients live a normal life.
Provided by Tel Aviv University

How Parkinson's disease starts and spreads

Injection of a small amount of clumped protein triggers a cascade of events leading to a Parkinson's-like disease in mice, according to an article published online this week in the Journal of Experimental Medicine.

Progressive accumulation of clumps of the protein alpha-synuclein in the brains of patients with Parkinson's disease coincides with the onset of motor dysfunction. However, whether these clumps are sufficient to trigger neurodegeneration, and how these clumps spread throughout the brain, remained unclear.
To answer these questions, a team led by Virginia M.Y. Lee at the University of Pennsylvania School of Medicine studied mice expressing a mutated form of alpha-synuclein found in patients with Parkinson's disease. These mice show symptoms of disease around one year of age but not earlier.
Lee and colleagues found that injecting preformed clumps of human alpha-synuclein into the brains of young mice accelerated disease onset and severity. These clumps seemed to act as "seeds" that recruited even the mouse version of alpha-synuclein into new clumps, which then spread throughout the brain. The pattern of spreading from neuron to neuron suggests that the clumps may hijack the highway traveled by normal brain signals.
These findings suggest that Parkinson's disease, like other neurodegenerative diseases including Alzheimer's, may start and progress due to abnormal aggregation and accumulation of proteins within the brain. What gets these clumps going in the first place remains unclear.
More information: Hung, L.W., et al. 2012. J. Exp. Med. doi:10.1084/jem.20112285
Provided by Rockefeller University

Curcumin shows promise in attacking Parkinson's disease

Curcumin, a compound found in the spice turmeric, is proving effective at preventing clumping of a protein involved in Parkinson's disease, says a Michigan State University researcher.

26 march 2012--A team of researchers led by Basir Ahmad, an MSU postdoctoral researcher, demonstrated earlier this year that slow-wriggling alpha-synuclein proteins are the cause of clumping, or aggregation, which is the first step of diseases such as Parkinson's. A new study led by Ahmad, which appears in the current issue of the Journal of Biological Chemistry, shows that curcumin can help prevent clumping.

"Our research shows that curcumin can rescue proteins from aggregation, the first steps of many debilitating diseases," said Lisa Lapidus, MSU associate professor of physics and astronomy who co-authored the paper with Ahmad. "More specifically, curcumin binds strongly to alpha-synuclein and prevents aggregation at body temperatures."

Lapidus' lab uses lasers to study protein folding. Proteins are chains of amino acids that do most of the work in cells. Scientists understand protein structure, but they don't know how they are built – a process known as folding. Lapidus' team is shedding light on the process by correlating the speed at which protein folds with its tendency to clump or bind with other proteins.

When curcumin attaches to alpha-synuclein it not only stops clumping, but it also raises the protein's folding or reconfiguration rate. By bumping up the speed, curcumin moves the protein out of a dangerous speed zone allowing it to avoid clumping with other proteins.

Finding a compound that can fix a protein when it first begins to misfold can lead scientists to identify drugs that can treat certain diseases. Doctors won't be prescribing curcumin pills any time soon, though, Lapidus said.

"Curcumin's usefulness as an actual drug may be pretty limited since it doesn't go into the brain easily where this misfolding is taking place," she said. "But this kind of study showcases the technique of measuring reconfiguration and opens the door for developing drug treatments."

Provided by Michigan State University

Study: Weight training improves Parkinson's symptoms

New research suggests weight training for two years significantly improves the motor symptoms of Parkinson's disease compared to other forms of exercise such as stretching and balance exercises. The clinical trial, which compared two forms of exercise for Parkinson's disease, was released today and will be presented at the American Academy of Neurology's 64th Annual Meeting in New Orleans April 21 to April 28, 2012.

17 feb 2012--"While we have known that many different types of exercise can benefit Parkinson's patients over short time periods, we did not know whether exercise improves the motor symptoms of Parkinson's over the long term," said study author Daniel Corcos, PhD, with the University of Illinois at Chicago.

For the study, 48 people with Parkinson's disease were randomized to progressive resistance exercise, known as weight training, or they were assigned to the exercise known as fitness counts, which includes flexibility, balance and strengthening exercises. The groups exercised for one hour, twice a week for two years.

The severity of motor symptoms, including tremors, was measured using the Unified Parkinson's Disease Rating Scale (UPDRS) after six, 12, 18 and 24 months of exercise. Scores were taken when the participants were not taking their medication.

While both forms of exercise reduced motor symptoms at six months of exercise, participants who did weight training saw a 7.3 point improvement in their UPRDS score after two years while the fitness counts group returned to the same scores they had at the start of the study.

"Our results suggest that long-term weight training could be considered by patients and doctors as an important component in managing Parkinson's disease," said Corcos.

Provided by American Academy of Neurology

Tai Chi program helps Parkinson's disease patients

An Oregon Research Institute (ORI) exercise study conducted in four Oregon cities has shown significant benefits for patients with mild-to-moderate Parkinson's disease. In an original article published in the February 9, 2012 issue of the New England Journal of Medicine (NEJM), ORI scientist Fuzhong Li, Ph.D. and colleagues report that a tailored program of twice-weekly Tai Chi training resulted in improved postural stability and walking ability, and reduced falls in the participants.

09 feb 2012--"These results are clinically significant because they suggest that Tai Chi, a low-to-moderate impact exercise, may be used, as an add-on to current physical therapies, to address some of the key clinical problems in Parkinson's disease, such as postural and gait instability. Since many training features in the program are functionally oriented, the improvements in the balance and gait measures that we demonstrated highlight the potential of Tai Chi-based movements in rehabilitating patients with these types of problems and, consequently, easing cardinal symptoms of Parkinson's disease and improving mobility, flexibility, balance, and range of motion," noted Dr. Li.

In the 4-year project funded by the National Institute of Neurological Disorders and Stroke, the investigators randomly assigned 195 patients to one of three exercise groups: Tai Chi, resistance training, or stretching. The patients participated in 60-minute exercise sessions twice weekly for 24 weeks.

The results of the study showed that the Tai Chi group performed consistently better than the stretching group in how far they could lean in any direction without losing balance as well as demonstrating better levels of directional control of the body and walking ability (i.e., longer stride length). Tai Chi participants also outperformed those in the resistance training group on the balance and stride length measures. Finally, Tai Chi training was shown to significantly lower the incidence of falls compared to stretching and to be as equally effective as resistance training in reducing falls.

Impaired movement, especially the loss of ability to maintain standing balance, adversely affects function and quality of life in patients with Parkinson's disease. With progression of the disease, patients lose stability and have trouble walking, difficulty managing activities of daily living, and experience frequent falls. Exercise is an important part of the management of Parkinson's disease because physical activity has been shown to retard the deterioration of motor function and to prolong functional independence. However, research on alternative forms of exercise, such as Tai Chi, that could improve balance, gait, and function in patients with Parkinson's disease is scarce.

The Tai Chi program developed by Dr. Li consisted of six Tai Chi movements integrated into an eight-form routine that focused on weight-shifting, controlled-displacement of the center of gravity over the base of support, ankle sway, and front-to-back and sideways stepping. Natural breathing was integrated into the training routine.

"There are a number of practical advantages to using Tai Chi to improve motor dysfunction of Parkinson's disease - it is a low cost activity that does not require equipment, it can be done anywhere, at any time, and the movements can be easily learned. It can also be incorporated into a rehabilitation setting as part of existing treatment. Similarly, because of its simplicity, certain aspects of this Tai Chi program can also be prescribed to patients as a self-care/home activity," Dr. Li added.

Provided by Oregon Research Institute

New study supports view that Lewy bodies are not the primary cause of cell death in Parkinson's Disease

The pathology of Parkinson's disease is characterized by a loss of dopamine-producing neurons in the pars compacta of the substantia nigra (SN), an area of the brain associated with motor control, along with the development of α-synuclein (αS) protein in the form of Lewy bodies (LB) in the neurons that survive. The spread of LB pathology is thought to progress along with the clinical course of Parkinson's disease, although recent studies suggest that they are not the toxic cause of cell death. A new study published in The Journal of Parkinson's Disease finds no support for a primary pathogenic role of LBs, as neither their distribution nor density was associated with the severity of nigral cell loss.

12 jan 2011--"We investigated the relationship between nigral dopaminergic cell loss, distribution and density of α-synuclein immunoreactive LBs, and the duration of motor symptoms in 97 patients with Parkinson's disease," explains lead investigator Andrew J. Lees, MD, of Queen Square Brain Bank for Neurological Disorders and the Reta Lila Weston Institute for Neurological Studies, UCL Institute of Neurology, London, UK. "Despite the reasonably close correlation between neuronal density in SN and severity of bradykinesia and rigidity in Parkinson's disease, our results suggest that nigral cell loss is gradual and there is considerable variability, which may explain the clinical heterogeneity."

Researchers confirmed that both neuronal number and density in SN in Parkinson's disease decrease over time. The density of nigral neurons was estimated to decrease by 2% each year after confirmation of the clinical diagnosis of Parkinson's disease, but showed marked heterogeneity across patients. Some patients with longer duration of illness still had a significant number of preserved nigral neurons at the time of death. An average of 15% of surviving nigral neurons contained LBs and the age-adjusted proportion of LB-bearing neurons appeared relatively stable through the disease duration. "This could be explained by a passive 'one-pass' phenomenon where the LBs appear at the beginning of the disease and then decrease at the same rate as nigral neurons are lost, or alternatively that a dynamic 'turnover' occurs with some LBs continuously produced and destroyed at the same rate," explains Dr. Lees.

Nigral neuron density was unrelated to the Braak PD stage of the disease (i.e. distribution of LBs in the brain) or to cortical LB densities. "In our view, the fact that neither the widespread regional distribution of LBs nor increased cortical LB densities were found directly linked with pars compacta nigral cell loss lends support to the view that they are not the primary cause of the pathological process leading to cell death in vulnerable regions in the brain in Parkinson's disease," concludes Dr. Lees.

More information: The article is "Disentangling the Relationship between Lewy Bodies and Nigral Neuronal Loss in Parkinson's Disease" by Laura Parkkinen, Sean S O'Sullivan, Catherine Collins, Aviva Petrie, Janice L. Holton, Tamas Revesz, and Andrew J. Lees. Journal of Parkinson's Disease. 1(2011) 277-286. DOI 10.3233/JPD-2011-11046

Provided by IOS Press

Abnormal oscillation in the brain causes motor deficits in Parkinson's disease

The research group headed by Professor Atsushi Nambu (The National Institute for Physiological Sciences) and Professor Masahiko Takada (Primate Research Institute, Kyoto University) has shown that the 'oscillatory' nature of electrical signals in subcortical nuclei, the basal ganglia, causes severe motor deficits in Parkinson's disease, by disturbing the information flow of motor commands. The group also found that chemical inactivation of the subthalamic nucleus (a structure of the basal ganglia) in parkinsonian monkeys improved the motor impairments by reducing the 'oscillations.' The results of this study were reported in European Journal of Neuroscience, November 2011 issue.

02 nov 2011--A member of the research group, Assistant Professor Yoshihisa Tachibana, succeeded to record electrical signals in monkey basal ganglia neurons under unanesthetized conditions. The group found that neurons in the parkinsonian basal ganglia showed abnormal 'oscillatory' activity, which was rarely seen in normal subjects. The abnormal rhythm was completely eliminated by systemic administration of a dopamine precursor (L-DOPA), which is clinically used for human parkinsonian patients. The group considered that loss of dopamine induced the 'oscillations' in the basal ganglia and that the following disturbances in information flow of motor commands impaired motor performances. Abnormal neuronal oscillations were already reported in parkinsonian patients and animal models, but this report has provided the direct evidence that 'oscillations' are associated with motor abnormalities. Moreover, it was also shown that the injection of a chemical inhibitor, muscimol, into the subthalamic nucleus silenced the oscillatory signals, and eventually reversed parkinsonian motor signs.

Professor Nambu claims, "By investigating the 'oscillatory' nature of electrical signals in the basal ganglia, we can advance our understanding of the pathophysiology of Parkinson's disease. We improved motor deficits by means of infusion of the chemical inhibitor (muscimol) into the subthalamic nucleus to silence the 'oscillatory' signals in the brain structure. This may provide us important clues to developing new treatments for Parkinson's disease."

Provided by National Institute for Physiological Sciences