treatment

Stress Linked to Harsher Parkinson’s Symptoms, but Mindfulness May Help

People with Parkinson’s disease experience more stress than those without this disease, and high stress levels associate with a worsening of symptoms, research based on a patient survey reported.

Mindfulness, a practice of maintaining a heightened state of awareness of thoughts and feelings, may help to lower stress in people with Parkinson’s, especially anxiety and depressive feelings, it also reported.

These findings were in the study “Stress and mindfulness in Parkinson’s disease – a survey in 5000 patients,” published in npj Parkinson’s Disease.

A team led by researchers in the Netherlands sent out a survey through The Michael J. Fox Foundation’s Fox Insight program. The survey asked a variety of questions about stress, Parkinson’s, and related factors.

Survey answers were returned by 5,000 patients and by 1,292 controls, mostly relatives, spouses, or friends of patients who did not have Parkinson’s. Patients’ mean age was 67.3, their average disease duration was 5.9 years, and 48.6% were women. Among controls, the mean age was 60.8 years, and 78.0% were women.

Most survey respondents (93%) were white, and most (82.6%) lived in the U.S. Of note, not all survey respondents answered every question; the researchers analyzed data that were available.

Analyses demonstrated that perceived stress was generally higher in people with Parkinson’s than in controls. This effect was also “much larger for men than for women,” the researchers wrote.

Parkinson’s patients also scored higher than controls on measurements of anxiety and depression, and lower on dispositional mindfulness (a trait that allows a person to be aware of the present moment, even during ordinary tasks). These differences were all independent of age or sex.

Among patients, higher stress scores associated with worse symptoms for all symptoms assessed (including sleeping problems, depression, involuntary movement, and slowness of movement.)

The symptom most affected by stress was tremor: 81.8% of patients reported a worsening in tremor during periods of stress.

“It should be noted, however, that PD [Parkinson’s disease] patients may perceive externally observable symptoms such as tremor more easily than slowness of movement or muscle stiffness, which could (partly) explain the difference between tremor and other motor symptoms,” the researchers wrote.

Patients who reported higher stress levels were also found to be more likely to report lower scores related to quality of life, self-compassion, and dispositional mindfulness. Stressed patients were also more likely to show high scores related to rumination (continuously thinking about the same thoughts, which are often sad or dark).

In free-text portions of the survey, patients commonly stated that stress worsened their cognitive and communication difficulties, and heightened emotional symptoms like anxiety.

Physical exercise was the most commonly reported stress-reducing strategy in the survey, mentioned by 83.1% of patients. Other frequent approaches to lessen stress included religion, music, art, reading, taking anti-anxiety or antidepressant medication, and looking for social support (e.g., talking to a friend).

Over a third (38.7%) of Parkinson’s patients reported practicing mindfulness — which involves focusing on the present moment, rather than fixating on the past or worrying about the future.

Of note, patients who were mindfulness users reported significantly higher dispositional mindfulness, and also higher perceptions of stress and anxiety. The researchers noted that it is difficult to tease out cause-and-effect relationships from this data. For example, people who are more stressed might be more likely to seek out mindfulness, or mindfulness practitioners may be more in touch with feelings of stress or anxiety and so recognize them to a greater degree.

Mindfulness also was associated with less severe symptoms across all motor and nonmotor symptoms measured.

“Patients perceived a positive effect of mindfulness on their symptoms,” the researchers wrote.

“Highest effects were seen for depression and anxiety, for which, respectively, 60.2% and 64.7% noticed improvement,” they added.

About half of mindfulness users (53.2%) practiced this technique once a week or more, while over a fifth (21.5%) practiced mindfulness once a month or less. Broadly, individuals who practiced mindfulness more frequently reported a greater easing of their symptoms, but consistent benefits were seen among all mindfulness users regardless of frequency.

The researchers speculated that, even when people aren’t actively practicing mindfulness, they may incorporate it into their lives more informally, through subtle changes to lifestyle or thought patterns.

These findings “[support] the idea that mindfulness is effective in reducing PD symptoms,” the researchers wrote, though they again noted they could not determine cause-and-effect from these data. Rather, “people for whom mindfulness is most effective might consequently practice it more.”

The researchers called for further studies, particularly in larger and more diverse groups, to better understand the effects of stress on Parkinson’s patients, as well as the potential benefits of practicing mindfulness.

“The significant beneficial effects that patients experienced from self-management strategies such as mindfulness and physical exercise encourages future trials into the clinical effects and underlying mechanisms of these therapies,” they concluded.

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Therapy Fights Depression for People with PD

Cognitive behavioral therapy is a form of psychotherapy that increases awareness of negative thinking and teaches coping skills.

About 50% of people diagnosed with Parkinson’s disease will experience depression, and up to 40% have an anxiety disorder.

“The psychological complications of Parkinson’s disease have a greater impact on the quality of life and overall functioning than the motor symptoms of the disease,” says lead author Roseanne Dobkin, a professor of psychiatry at Rutgers University’s Robert Wood Johnson Medical School.

“Untreated, depression can accelerate physical and cognitive decline, compromise independence, and make it more difficult for individuals to proactively manage their health, like taking medication, exercising, and visiting the physical therapist.”

Depression in Parkinson’s patients is under-recognized and often goes untreated. Among those who receive treatment, antidepressant medication is the most common approach, though many patients continue to struggle with depressive symptoms.

The researchers investigated how adding cognitive behavioral therapy to the care individuals already received would affect their depression.

Cognitive behavioral therapy sessions helped patients re-examine their usual ways of coping with the daily challenges of Parkinson’s. Researchers individually tailored therapy, targeting negative thoughts—such as “I have no control”—and behaviors including social withdrawal or excessive worrying. Treatment also emphasized strategies for managing the disease, such as exercise, medication adherence, and setting realistic daily goals.

The researchers enrolled 72 people diagnosed with both Parkinson’s and depression. All participants continued their standard treatment. In addition, half the participants (37 people) also received cognitive behavioral therapy over the telephone weekly for three months, then monthly for six months.

By the end of treatment, individuals receiving only standard care showed no change in their mental health status, whereas 40% of the patients receiving cognitive behavioral therapy showed their depression, anxiety, and quality of life to be “much improved.”

The convenience of phone treatment reduced barriers to care, allowing patients access to personalized, evidence-based mental health treatment, without having to leave their homes, Dobkin says.

“A notable proportion of people with Parkinson’s do not receive the much needed mental health treatment to facilitate proactive coping with the daily challenges superimposed by their medical condition,” she says.

“This study suggests that the effects of the cognitive behavioral therapy last long beyond when the treatment stopped and can be used alongside standard neurological care to improve global Parkinson’s disease outcomes.”

The study appears in NeurologySource: Rutgers University. Original Study

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Can We Repair the Brain?

Cell replacement may play an increasing role in alleviating the motor symptoms of Parkinson’s disease (PD) in future. Writing in an open access special supplement to the Journal of Parkinson’s Disease, experts describe how newly developed stem cell technologies could be used to treat the disease and discuss the great promise, as well as the significant challenges, of stem cell treatment.

The most common PD treatment today is based on enhancing the activity of the nigro-striatal pathway in the brain with dopamine-modulating therapies, thereby increasing striatal dopamine levels and improving motor impairment associated with the disease. However, this treatment has significant long-term limitations and side effects. Stem cell technologies show promise for treating PD and may play an increasing role in alleviating at least the motor symptoms, if not others, in the decades to come.

“We are in desperate need of a better way of helping people with PD. It is on the increase worldwide. There is still no cure, and medications only go part way to fully treat incoordination and movement problems,” explained co-authors Claire Henchcliffe, MD, DPhil, from the Department of Neurology, Weill Cornell Medical College, and Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA; and Malin Parmar, PhD, from the Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University, Lund, Sweden. “If successful, using stem cells as a source of transplantable dopamine-producing nerve cells could revolutionize care of the PD patient in the future. A single surgery could potentially provide a transplant that would last throughout a patient’s lifespan, reducing or altogether avoiding the need for dopamine-based medications.”

The authors have analyzed how newly developed stem cell technologies could be used to treat PD, and how clinical researchers are moving very quickly to translate this technology to early clinical trials. In the past, most transplantation studies in PD used human cells from aborted embryos. While these transplants could survive and function for many years, there were scientific and ethical issues: fetal cells are in limited supply, and they are highly variable and hard to quality control. Only some patients benefited, and some developed side effects from the grafts, such as uncontrollable movements called dyskinesias.

Recent strides in stem cell technology mean that quality, consistency, activity, and safety can be assured, and that it is possible to grow essentially unlimited amounts of dopamine-producing nerve cells in the laboratory for transplantation. This approach is now rapidly moving into initial testing in clinical trials. The choice of starting material has also expanded with the availability of multiple human embryonic stem cell lines, as well as the possibilities for producing induced pluripotent cells, or neuronal cells from a patient’s own blood or skin cells. The first systematic clinical transplantation trials using pluripotent stem cells as donor tissue were initiated in Japan in 2018.

“We are moving into a very exciting era for stem cell therapy,” commented Dr. Parmar. “The first-generation cells are now being trialed and new advances in stem cell biology and genetic engineering promise even better cells and therapies in the future. There is a long road ahead in demonstrating how well stem cell-based reparative therapies will work, and much to understand about what, where, and how to deliver the cells, and to whom. But the massive strides in technology over recent years make it tempting to speculate that cell replacement may play an increasing role in alleviating at least the motor symptoms, if not others, in the decades to come.”

“With several research groups, including our own centers, quickly moving towards testing of stem cell therapies for PD, there is not only a drive to improve what is possible for our patients, but also a realization that our best chance is harmonizing efforts across groups,” added Dr. Henchcliffe. “Right now, we are just talking about the first logical step in using cell therapies in PD. Importantly, it could open the way to being able to engineer the cells to provide superior treatment, possibly using different types of cells to treat different symptoms of PD like movement problems and memory loss.”

“This approach to brain repair in PD definitely has major potential, and the coming two decades might also see even greater advances in stem cell engineering with stem cells that are tailor-made for specific patients or patient groups,” commented Patrik Brundin, MD, PhD, Van Andel Research Institute, Grand Rapids, MI, USA, and J. William Langston, MD, Stanford Udall Center, Department of Pathology, Stanford University, Palo Alto, CA, USA, Editors-in-Chief of the Journal of Parkinson’s Disease. “At the same time, there are several biological, practical, and commercial hurdles that need circumventing for this to become a routine therapy.”

Article from IOS Press.

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Radical PD treatment tested in patients

A radical Parkinson’s treatment that delivers a drug directly to the brain has been tested in people.

Patients in the trial were either given the drug, which is administered via a “port” in the side of the head, or a dummy treatment (placebo). Both groups showed improved symptoms, meaning it was not clear if the drug was responsible for the benefits. However, scans did find visual evidence of improvements to affected areas of the brain in those given the drug. The study’s authors say it hints at the possibility of “reawakening” brain cells damaged by the condition.

Other experts, though, say it is too early to know whether this finding might result in improvements in Parkinson’s symptoms. Researchers believe the port implant could also be used to administer chemotherapy to those with brain tumours or to test new drugs for Alzheimer’s and stroke patients.

Parkinson’s causes parts of the brain to become progressively damaged, resulting in a range of symptoms, such as involuntary shaking and stiff, inflexible muscles. About 145,000 people in the UK have been diagnosed with the degenerative condition, which cannot be slowed down or reversed.

For this new study, scientists gave patients an experimental treatment called glial cell line-derived neurotrophic factor (GDNF), in the hope it could regenerate dying brain cells and even reverse the condition. Participants underwent robot-assisted surgery to have four tubes placed into their brains, which allowed GDNF to be infused directly to the affected areas with pinpoint accuracy, via a port in their head.

After an initial safety study of six people, 35 patients took part in a nine-month “blinded” trial, where half were randomly assigned to receive monthly infusions of GDNF and the other half dummy infusions.

Dr Alan Whone, principal investigator, said patients in the trial had, on average, been diagnosed eight years previously, but brain scans of those given the drug showed images that would be expected just two years after diagnosis.

He said: “We’ve shown with the Pet [positron emission tomography] scans that, having arrived, the drug then engages with its target, dopamine nerve endings, and appears to help damaged cells regenerate or have a biological response.”

Tom Phipps, 63, from Bristol, said he had noticed an improvement during the trial and had been able to reduce the drugs he takes for his condition. Since it ended, he has slowly increased his medication but is continuing to ride his bike, dig his allotment and chair his local branch of Parkinson’s UK.

“My outcome was as positive as I could have wished for,” he said. “I feel the trial brought me some time and has delayed the progress of my condition. The best part was absolutely being part of a group of people who’ve got a similar goal – not only the team of consultants and nurses but also the participants.

“You can’t have expectations – you can only have hope.”

Following the initial nine months on GDNF or placebo, all participants had the opportunity to receive GDNF for a further nine months.

By 18 months, when all participants had received GDNF, both groups showed moderate to large improvements in symptoms compared with their scores before they started the study. But the authors say the results need to be treated with caution because of the possibility of the placebo effect – when a patient feels better despite taking a medicine with no active ingredient.

Researchers hope that further trials could look at increasing the doses of GDNF or the duration of treatment.

Experts said it was “disappointing” that the difference in symptoms was not significant. But they said the study was still of “great interest” and warranted follow up research.

The findings from the trials are published in the medical journals Brain and the Journal of Parkinson’s Disease.

The study also features in a two-part BBC Two documentary series, The Parkinson’s Drug Trial: A Miracle Cure? on 28 February and 7 March, at 21:00. (Viewable only from the UK.)

Article from BBC.

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How gut bacteria affect PD treatment

Patients with Parkinson’s disease are treated with levodopa, which is converted into dopamine, a neurotransmitter in the brain. In a study published on 18 January in the journal Nature Communications, scientists from the University of Groningen show that gut bacteria can metabolize levodopa into dopamine. As dopamine cannot cross the blood-brain barrier, this makes the medication less effective – even in the presence of inhibitors that should prevent the conversion of levodopa.

‘It is well established that gut bacteria can affect the brain’, explains Assistant Professor in Microbiology Sahar El Aidy, lead investigator of the study. ‘There is a continuous chemical dialogue between gut bacteria and the brain, the so called gut-brain axis.’ El Aidy and her team investigated the ability of gut microbiota to influence the bioavailability of levodopa, a drug used in the treatment of Parkinson’s disease.

The drug is usually taken orally, and the levodopa is absorbed in the small intestine and then transported through the blood stream to the brain. However, decarboxylase enzymes can convert levodopa into dopamine. In contrast to levodopa, dopamine cannot cross the blood-brain barrier, so patients are also given a decarboxylase inhibitor. ‘But the levels of levodopa that will reach the brain vary strongly among Parkinson’s disease patients, and we questioned whether gut microbiota were playing a role in this difference’, says El Aidy.

In bacterial samples from the small intestines of rats, Aidy’s PhD student Sebastiaan van Kessel found activity of the bacterial tyrosine decarboxylase enzyme, which normally converts tyrosine into tyramine, but was found to also convert levodopa into dopamine. ‘We then determined that the source of this decarboxylase was Enterococcus bacteria.’ The researchers also showed that the conversion of levodopa was not inhibited by a high concentration of the amino acid tyrosine, the main substrate of the bacterial tyrosine decarboxylase enzyme.

As Parkinson’s patients are given a decarboxylase inhibitor, the next step was to test the effect of several human decarboxylase inhibitors on the bacterial enzyme. ‘It turned out that, for example, the inhibitor Carbidopa is over 10,000 times more potent in inhibiting the human decarboxylase’, says El Aidy.

These findings led the team to the hypothesis that the presence of bacterial tyrosine decarboxylase would reduce the bioavailability of levodopa in Parkinson’s patients. To confirm this, they tested stool samples from patients who were on a normal or high dose of levodopa. The relative abundance of the bacterial gene encoding for tyrosine decarboxylase correlated with the need for a higher dose of the drug. ‘As these were stool samples, and the levodopa is absorbed in the small intestine, this was not yet solid proof. However, we confirmed our observation by showing that the higher abundance of bacterial enzyme in the small intestines of rats reduced levels of levodopa in the blood stream’, explains El Aidy.

Another important finding in the study is the positive correlation between disease duration and levels of bacterial tyrosine decarboxylase. Some Parkinson’s disease patients develop an overgrowth of small intestinal bacteria including Enterococci due to frequent uptake of proton pump inhibitors, which they use to treat gastrointestinal symptoms associated with the disease. Altogether, these factors result in a vicious circle leading to an increased levodopa/decarboxylase inhibitor dosage requirement in a subset of patients.

El Aidy concludes that the presence of the bacterial tyrosine decarboxylase enzyme can explain why some patients need more frequent dosages of levodopa to treat their motor fluctuations. ‘This is considered to be a problem for Parkinson’s disease patients, because a higher dose will result in dyskinesia, one of the major side effects of levodopa treatment.’

Article from University of Groningen.

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Experimental cancer drug repurposed for Parkinson’s

As promising as a drug candidate may be, the unfortunate truth is that not all of them end up performing as hoped – but that doesn’t mean they’re completely useless. Researchers at Oxford University have managed to give second life to an experimental cancer drug known as tasquinimod, which has now shown promise for Parkinson’s.

Tasquinimod emerged as a promising drug in fighting solid tumors, with most research focusing on using it to treat prostate cancer. The drug made it through to phase three clinical trials, but unfortunately it didn’t seem to extend overall survival rates in patients, and after those disappointing results development was discontinued for prostate cancer treatment.

But the work wasn’t for nothing – the clinical trials so far have shown that tasquinimod is well tolerated by the body, and it could still potentially help treat other illnesses, such as Parkinson’s disease.

To investigate the drug, the Oxford team first took skin cells from patients with a rare genetic form of Parkinson’s, and turned them into a type of stem cell known as induced pluripotent stem cells (iPS). From these the researchers grew brain cells in vitro, allowing them to observe progression of the disease in the lab.

The team found that the key may be an error with a protein known as HDAC4. When that happens, this protein begins to repress certain genes, which in turn messes with the brain cells’ ability to regulate the natural cycle of proteins. That means those proteins build up in the cells, which has long been known to contribute to Parkinson’s and related neurodegenerative diseases like Alzheimer’s.

Tasquinimod comes to the rescue by blocking HDAC4, meaning those key genes aren’t “switched off,” and effectively halting progression of the disease.

“We think that switching off these genes in brain cells may play a vital role in the cell damage and death that occurs in Parkinson’s,” says Richard Wade-Martins, co-lead author of the study. “Finding a way to ‘turn them back on’ with a drug could be a promising, unexplored way to develop new treatments.”

The researchers then repeated the study using iPS cells gathered from people with the more common non-genetic form of Parkinson’s, and found that the same pattern of inactive genes seems to be at play. That indicates that these people might also benefit from the treatment, although the team also acknowledges that some people don’t seem to respond to it.

“The study also highlights the growing number of drugs which can be repurposed from their original medical use to treat Parkinson’s,” says David Dexter, Deputy Director of Research at Parkinson’s UK, which funded the study. “Developing a drug from scratch is a long, slow and expensive process. By finding existing drugs and moving them rapidly into clinical trials, we can make them available for people with Parkinson’s much more quickly, easily and cheaply.”

Although that process may be streamlined, it is still early days for tasquinimod. The study has only been conducted on a total of 10 patients so far, so more testing will need to be done before it could become a viable treatment option.

The research was published in the journal Cell Stem Cell.

Article from New Atlas.

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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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Deep Brain Stimulation for Parkinson Disease

This article appeared in the Spring 2018 issue of The Network magazine.

Deep brain stimulation (DBS) is an advanced therapy for patients with Parkinson disease (PD) suffering from complications of carbidopa/levodopa treatment. It has been FDA approved for use in PD since 2002 and for tremor prior to that. DBS involves the surgical implantation of a device with electrodes that deliver electrical signals to specific areas within the brain. Once the electrodes are placed, they are then connected to an implanted pulse generator (battery) which is placed under the skin, typically in the chest. When the device is activated, it delivers regular electrical pulses to that area of the brain and results in improvement of PD symptoms. The exact mechanisms of how DBS improves symptoms are not known. However, we do know that it disrupts pathological signals that occur within the brain of PD patients.

Currently, DBS is approved for those patients with a diagnosis of idiopathic PD, who have had symptoms for four or more years and suffer from motor complications that are not controlled with medications. Motor complications refer to the medications not lasting as long (wearing off), levodopa induced dyskinesias (extra, abnormal and involuntary movements) and dose failures.

Individuals who would not benefit from DBS are those with atypical forms of PD, those with signs of dementia and those whose symptoms do not improve with levodopa. Depression and anxiety do not preclude someone from receiving DBS, but these should be addressed, treated and well controlled prior to proceeding.

The process of implanting DBS for patients is a lengthy process. It involves careful pre-surgical screening, two or three surgeries and many follow up programming appointments. The first step is what is called an “Off/On Test.” For this test, the patient comes to an appointment with the neurologist after not taking PD medications from the night before. The patient is then examined in this “Off” medication state. Then, the patient receives a higher than usual dose of carbidopa/levodopa and then re-examined once those take effect.

The next step is to have a formal neuropsychological evaluation performed. This evaluation typically takes about a half of a day and includes extensive testing of memory, language and other cognitive abilities. Once these two preliminary evaluations are complete, most DBS centers hold a multi-disciplinary case conference to discuss these results and the patient’s candidacy for DBS surgery. If there are no contraindications to surgery, the patient will meet with the neurosurgeon who reviews the procedure and the potential risk of surgery. Often times, an additional pre-operative medical evaluation is also required to screen for other medical conditions that could pose additional surgical risks or potential complications. The patient also receives a pre-surgical MRI of the brain to assist with placement of the DBS electrodes.

Most centers perform DBS implantation in two or three individual surgeries. After the DBS device is implanted, the patient then returns to the clinic to turn the device on, typically after three or four weeks. The number of programming appointments needed varies from one patient to the next but can take 6-12 months to reach optimal settings. The battery is checked at routine follow-up appointments and depending on which device is implanted, the battery will need to be replaced from time to time.

Not all symptoms of PD will improve from DBS therapy. The general rule of thumb is if particular symptoms improve after taking carbidopa/levodopa then those symptoms can be expected to improve with DBS. The caveat to this rule are refractory tremors. Tremor in PD can often be resistant to carbidopa/levodopa, but responds well to DBS. In addition, DBS can significantly reduce problems with medication wearing off and dyskinesias. Walking difficulties in PD can be varied and complex. Some of these may respond to DBS but many do not, including balance. Therefore, patients should consult with their DBS physician prior to surgery in regard to their specific walking issues.

Symptoms that are unlikely to improve with DBS are those symptoms that worsen with levodopa, balance, memory problems, speech and swallowing difficulties. DBS can also allow the reduction of some of the PD medications, although it is not realistic to expect to stop all PD related medications after surgery.

It is important to understand that DBS is not a cure however, it is very effective at treating many motor symptoms of PD and improving quality of life.

Ryan T. Brennan, D.O. is an assistant professor in the Department of Neurology at Medical College of Wisconsin.

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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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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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