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Winners for BEAT-PD DREAM Contest to Better Track Parkinson’s Named

Parkinson's challenge winners

The four winners of the Michael J. Fox Foundation (MJFF) and Sage Bionetworks Parkinson’s disease (PD) challenge to create new ways of using everyday technology to benchmark and predict disease progression remotely — including at home — have been announced.

Called the Biomarker and Endpoint Assessment to Track Parkinson’s Disease (BEAT-PD) Dream Challenge, the contest sought to determine whether Parkinson’s severity and progression can be assessed via sensor data collected as a person goes about daily life.

This year’s contest drew 43 teams, with winners sharing a $25,000 prize.

Teams had access to raw sensor (accelerometer and gyroscope) time-series data, hosted by BRAIN Commons, which they used to predict a patient’s treatment  status and symptom severity.

“We congratulate all the winners,” said Mark Frasier, PhD, senior vice president, Research Programs at MJFF, in a press release. “The Foundation has supported research into sensors and other digital tools for Parkinson’s for many years.”

BEAT-PD “projects are unlocking the potential of data collected by digital devices to help people with Parkinson’s, their physicians, and researchers. Now, more than ever, we understand the critical importance of remote monitoring for the safe and effective delivery of healthcare and the progress of clinical research.”

Winners of the BEAT-PD Challenge are:

The BEAT-PD Challenge built upon a previous data challenge, in which researchers showed that disease status and symptom severity could be predicted using data collected during the physician-monitored completion of certain tasks.

In the BEAT-PD Challenge, scientists sought to learn whether disease severity can be measured via passive sensor data gathered with consumer electronics and collected not during specific tasks, but day-to-day life. The ultimate goal is to be able to monitor disease progression at home.

In their efforts, teams ROC BEATPD, dbmi, and HaProzdor applied signal processing tactics to smartphone sensor data. Allowing for patient-specific characteristics, the results were subsequently used in machine learning models. Guan applied a deep-learning model using spatial and temporal sensor data augmentation.

The winners may now collaborate to optimize their models, and gauge them against clinician-validated symptom severity ratings. They also will co-author a publication on their findings.

Researchers can find more information and can apply to access these data here. Visit this site to learn more about the BEAT-PD Challenge and winners.

To host the challenge, MJFF and Sage partnered with Evidation Health, Northwestern University, Radboud University Medical Center, and BRAIN Commons.

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FDA Approves Medtronic’s Percept PC Deep Brain Stimulation System

Nuplazid NDA

The U.S. Food and Drug Administration (FDA) has approved the Percept PC Neurostimulator by Medtronic, designed to allow for a more individualized use of deep brain stimulation therapy in people with Parkinson’s disease and related disorders.

While this device is the fourth deep brain stimulation (DBS) system to be approved in the U.S., it is the first system able to sense and record brain signals while therapy is delivered. As such, it is expected to help doctors more precisely tailor treatment to a patient’s needs.

“Percept uses BrainSense technology, which captures brain signal data from implanted brain leads, combined with a patient diary system,” Joohi Jimenez-Shahed, MD, professor of neurology at Icahn School of Medicine at Mount Sinai, said in a news release by the Michael J. Fox Foundation.

“This device allows us to measure and record brain signals, which can be matched with a person’s symptoms as reported in the diary or what we see on exam. By looking at brain signals, we might be able to tell whether symptoms relate to medication wearing off or to dyskinesia, for example, and we can use this information to more precisely understand how a patient’s symptoms respond to DBS,” Jimenez-Shahed said.

“Eventually, we hope to be able to use this data to adjust DBS settings for more tailored and targeted treatment,” she added.

DBS is used to treat neurological disorders that include Parkinson’s, essential tremor, dystonia, epilepsy, and obsessive-compulsive disorder. Therapy is delivered via a small, implantable device that is somewhat similar to a pacemaker. Tiny wires inserted in the brain are used to send electrical signals from the device to specific brain regions, aiming to ease motor symptoms.

Percept is also the first approved DBS system that can be used in certain full-body MRI scans, allowing greater access to imaging for patients and clinicians, Medtronic reports in a press release.

The first U.S. center to implant the device will be the Mayo Clinic in Rochester, Minnesota, it added.

“Our goal is for patients to regain independence, and we know that DBS can significantly improve motor function in people with Parkinson’s disease compared to standard medication alone,” said Bryan Klassen, MD, a neurologist at the Mayo Clinic.

“As with any therapy, considering DBS and choosing between specific devices is about weighing pros and cons,” Jimenez-Shahed said. “Because Percept is a new approach, doctors and patients will learn together in the months ahead who are the best candidates for the new technology and the best ways to take advantage of what it has to offer.”

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Cell Protein Recycling Linked to Toxic Buildup in Brain in Early Study

Lewy bodies and proteins

Lower than usual activity in a complex that recycles proteins in cells — called the proteosome — leads to an age-related buildup of protein aggregates in the brains of fish, similar to that seen in neurodegenerative diseases such as Parkinson’s, a study reported.

Low proteasome activity early in life also shortened a fish’s lifespan.

The study, “Reduced proteasome activity in the aging brain results in ribosome stoichiometry loss and aggregation,” was published in the journal Molecular Systems Biology

Neurodegenerative diseases such as Parkinson’s are characterized by the deterioration of nerve cells (neurons). In most people with Parkinson’s, proteins accumulate in neurons and form toxic aggregates called Lewy bodies.

Protein buildup in neurons also is known to occur as a result of aging.  The underlying mechanisms that trigger aggregate formation, however, remain unknown. 

It is thought that a contributing factor is a breakdown in the process known as protein homeostasis — the steady production, location, and degradation of proteins in a cell, which is essential for all living organisms.

To understand how and why proteins accumulate during aging, researchers at the Leibniz Institute on Aging – Fritz Lipmann Institute in Germany, along with investigators in the U.K., Greece, Italy, and the U.S., designed a study to understand the chain of molecular events that leads to the age-associated loss of protein homeostasis in the brain.

As a model they chose the killifish (Nothobranchius furzeri), which is the shortest-lived vertebrate (3 to 12 months) bred in captivity. Given its brief lifespan, age-related processes are accelerated in this fish species, and rapid aging induces changes in the brain that mimic those typically seen in aging human brains. 

A recent study using killifish also found an age-dependent formation of protein deposits containing alpha-synuclein, the protein that is the primary component of Lewy bodies associated with Parkinson’s disease.

Researchers analyzed the brains of killifish at three different ages: young sexually mature fish, adult fish without aging characteristics, and older fish that showed signs of neurodegeneration. 

They used a technique called mass spectrometry to conduct a large-scale analysis of proteins, and they sequenced RNA, the molecule that carries information from DNA to make proteins. 

Of the almost 9,000 protein groups that were quantified, nearly half were significantly affected by aging. Additionally, RNA levels in aging brains, which typically correspond to protein levels, no longer matched the levels of half of the proteins identified. 

Decoupling of RNA and protein levels was found to occur in a critical structure within the cell known as the ribosome. Ribosomes convert the DNA message to a protein message, and are composed of several proteins along with other RNA molecules assembled in specific ratios (known as stoichiometry). 

In aging brains, the ratios of these proteins were altered, and analysis of protein aggregates found an abundance of these ribosomal proteins. Rations of proteins in other complexes involved in energy production were also affected by aging.

“[T]here is a progressive loss of stoichiometry of protein complexes during aging, mainly affecting the ribosomes, which is one of the most important protein complexes in the cell, responsible for producing all other proteins,” Alessandro Ori, PhD, the study’s lead author, said in a press release

To understand the trigger for the aggregation of ribosomal proteins, researchers focused on the proteosome — a complex within the cell that digests and recycles old and defective proteins, and is an essential component of protein homeostasis.

Similar to the altered ratios of ribosomal proteins, the ratios of proteins that form the proteosome were also affected, resulting in decreased activity. This reduction occurred early in life, and progressed during adulthood. To confirm this result, when adult fish were treated with a chemical that blocked proteasome activity in the brain, their brains showed a premature aging signature. 

“Decrease of proteasome activity is an early sign of brain aging, but is it relevant for aging of the entire organism?” said Alessandro Cellerino, PhD, a study co-author. “To answer this question, we correlated individual variations in proteasome activity with individual variations in lifespan.”

By comparing gene expression in more than 150 killifish to their lifespan, researchers found that fish with a significant early decrease in proteasome production lived a considerably lesser time than did fish that maintained or increased production. 

“Reduced proteasome levels are a major risk factor for early death in killifish,” the researchers wrote. 

“[O]ur work identifies the maintenance of proteasome activity upon aging as being critical to ensure the correct stoichiometry of protein complexes involved in key biological functions such as protein synthesis, degradation, and energy production,” they added. 

“Further detailed mechanistic studies will show whether the changes that we have described during aging contribute to a functional impairment of these protein complexes, or whether they are themselves a response to the aging process,” Ori said.

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Melatonin Levels in Parkinson’s Patients May Be Linked to Non-motor Symptoms

melatonin

Alterations in the levels of melatonin — the hormone that controls sleep-wake cycles — circulating in the blood are associated with certain non-motor symptoms of Parkinson’s disease, namely sleep disturbances, gastrointestinal issues, and heart problems.

The study with that finding, “Elevated Plasma Melatonin Levels Are Correlated With the Non-motor Symptoms in Parkinson’s Disease: A Cross-Sectional Study,” was published in the journal Frontiers in Neuroscience.

Melatonin is a hormone produced by the pineal gland, a small pea-shaped gland in the brain that regulates sleep. Higher levels of this hormone are usually present at night.

In addition to its main role in regulating the body’s internal clock (circadian rhythm), melatonin also controls the production of other hormones, helps regulate the body’s internal temperature, and influences cognitive performance and mood.

Although some studies have reported that patients with Parkinson’s have altered levels of melatonin that possibly are associated with their motor symptoms and other disease features, the findings have been inconclusive.

To explore the possible relationship between melatonin levels and non-motor symptoms of Parkinson’s, researchers now measured the levels of melatonin circulating in the blood of 61 patients with Parkinson’s (average age 62.4 years) and 58 age and sex-matched healthy individuals (controls).

Within the Parkinson’s group, 14 patients had cardiovascular symptoms (23%), 42 had gastrointestinal dysfunction (68.9%), and 51 had sleep disorders (83.6%).

Blood samples were collected in the dark, or under a dim light, following a 12-hour overnight fasting period in all study participants. Melatonin levels were determined by enzyme-linked immunosorbent assay (ELISA), a commonly used test that allows researchers to measure the levels of specific molecules using an enzymatic reaction.

Non-motor symptoms of Parkinson’s were assessed in all patients using the Hamilton Anxiety Rating Scale, the Hamilton Depression Rating Scale, the Parkinson Disease Sleep Scale, the Epworth Sleepiness Scale, and the Non-Motor Symptoms Scale for PD.

Disease severity also was evaluated in all patients using the Unified Parkinson’s Disease Rating Scale and the Hoehn and Yahr Staging scale.

Statistical analyses were used to identify possible relationships between melatonin levels and Parkinson’s non-motor symptoms and disease severity.

Researchers found that, compared to healthy individuals, patients with Parkinson’s had higher levels of melatonin circulating in their blood (19.40 versus 12.82 picograms per milliliter (pg/mL)).

Within the overall Parkinson’s population, there was a significant negative correlation with melatonin levels and levodopa equivalent doses, meaning lower levels of melatonin were associated with higher levodopa dosages.

This suggested that “the increased plasma melatonin level in PD patients may be related to the degeneration of dopaminergic neurons and the use of dopaminergic drugs,” the researchers wrote.

Likewise, among Parkinson’s patients, lower melatonin levels were associated with heart problems, sleep disturbances, and gastrointestinal issues.

”This finding suggests a potential underlying link between plasma melatonin levels and the non-motor symptoms in PD [Parkinson’s disease] patients,” the researchers wrote.

No relationships between hormone levels and other non-motor symptoms of the disease, including sexual and urinary dysfunction, memory impairments, hallucinations, and mood changes, were found.

Also, no link was found between melatonin levels and disease severity.

“Current research indicates that circadian rhythm dysfunction is associated with the clinical manifestations of PD, and changes in melatonin levels are associated with the non-motor symptoms in patients with PD,” they wrote.

“The relationship between melatonin and PD still needs further research, which is also valuable for exploring biomarkers for early diagnosis of PD,” they added.

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Seelos Begins Animal Study Investigating SLS-007 as Parkinson’s Treatment

SLS-007 animal study

Seelos Therapeutics has begun a preclinical study in rodents to test a gene therapy approach to deliver its investigational candidate SLS-007, a potential treatment for Parkinson’s disease. Results are expected by late this year or early 2021.

One hallmark of Parkinson’s disease progression is the formation of Lewy bodies, abnormal protein clusters that form in brain cells and disrupt their regular function. These clusters are toxic to nerve cells and are thought to underly the development of Parkinson’s. A major component of Lewy bodies is the protein alpha-synuclein.

SLS-007, which was developed originally by a team of researchers at the University of California, Los Angeles, is a family of molecules, known as peptide blockers, that are designed to lessen alpha-synuclein aggregation.

Specifically, SLS-007 targets the non-amyloid core region of the alpha-synuclein protein, which is more prone to aggregation.

Previous, in vitro studies — experiments conducted outside of a live animal — showed that SLS-007 had the potential to block Lewy body formation by preventing the clustering of alpha-synuclein.

This was accomplished by preventing the propagation and seeding of alpha-synuclein, a process in which a small amount of the protein provides the template for the aggregation of normal protein into larger clusters, or clumps.

“In in vitro models, halting or slowing the aggregation of alpha synuclein dramatically slowed the formation of Lewy Bodies which are the hallmarks of the pathogenesis of Parkinson’s,” Raj Mehra, PhD, chairman and CEO of Seelos, said in a press release.

Having established the potential benefit of SLS-007 as a disruptor of Lewy body formation, the researchers now have begun to investigate the treatment in mice.

The team will use a transgenic mouse model that previously was designed to study the propagation of alpha synuclein. Researchers will test a modified, harmless form of a virus, called an adeno-associated virus (AAV1/AAV2), as a vehicle (or vector) to deliver SLS-007.

Two specific peptides that comprise SLS-007, called S62 and S71, have been tagged with a unique marker that will allow researchers to track their activity. Production of the AAV vectors already has been completed by Seelos.

Researchers will assess the ability of SLS-007 to protect dopaminergic neurons in these mice. The study also will determine the pharmacokinetics, pharmacodynamics, and target engagement of SLS-007 in mice.

(Pharmacokinetics refers to the movement of a medication within the body while pharmacodynamics refers to the interactions between the body and a compound.)

Research on SLS-007 will augment Seelos’ ongoing studies of SLS-004, an investigational gene therapy that uses another harmless virus, called a lentivirus, to deliver an enzyme called DNA methyltransferase 3A that is thought to limit the production of alpha-synuclein.

“This program [SLS-007] should complement SLS-004 in which we also recently began studies,” said Mehra.

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3 Nurse Educators Win Parkinson’s Foundation Grants for Local Projects

Parkinson's Foundation award

The Parkinson’s Foundation announced the three winners of this year’s Nurse Faculty Award, giving about $10,000 to each of these nurses to support projects that might better the lives of Parkinson’s patients in their communities.

Each winner is a graduate of the organization’s 50-hour accredited Edmond J. Safra Visiting Nurse Faculty Program, which works to improve Parkinson’s disease (PD) care across the U.S. by providing additional training and support to nurse educators.

“Nurses are vital in caring for people with Parkinson’s in all settings, from a clinic to an emergency room,” Elizabeth Pollard, the Parkinson’s Foundation vice president, chief education and training officer, said in a press release. “The Parkinson’s Foundation …  is excited to continue providing our Edmund J. Safra Visiting Nurse Scholars with an opportunity to develop their independent projects and provide unique tools to further educate nurses to improve PD care.”

Donna G. Hood, PhD, RN, is an awardee. A chronic illness researcher and director of the Division of Nursing at Louisiana Tech University, she will use her award to expand the school’s Parkinson Resource Center program, established through a Foundation grant to support underserved communities in rural Louisiana and southern Arkansas.

The award will double to four the number of participating undergraduate students, provide Parkinson’s patients across the region with resources, mentor future nursing leaders, and help support the program’s replication.

“We have excellent students who have expressed their desire to join us as future nursing student scholars, and we are excited to see this program grow and see how this impacts the Parkinson community in our region and beyond as these student scholars become our future PD champions,” Hood said.

An associate professor of nursing at Seattle University, Mo-Kyung Sin, PhD, RN, will use her award to gauge the impact of the school’s nursing student ambassador program on students’ knowledge of, and competence in, Parkinson’s care. The program includes educating juniors about Parkinson’s care and related case studies, a one-day intensive Parkinson’s education segment, and a group project for six selected seniors who plan to become neurologists.

The project will help develop nurses trained in Parkinson’s care.

Awardee Stephanie Stewart, MSN and a board-certified registered nurse, will launch Navigating the Parkinson’s Journey, aimed at improving life quality by helping patients feel more connected to each other. The program will open in St. Joseph, Missouri, and findings will be accessible to anyone interested. Stewart is an assistant professor of nursing at Missouri Western State University.

Open exclusively to those who complete the Edmond J. Safra Visiting Nurse Faculty Program, the award supports projects that enhance the scholars’ ability to teach about Parkinson’s, or that increase Parkinson’s knowledge among nurses, students, or patients. The award is for a maximum of $10,000 annually. More information is available here.

Parkinson’s disease affects nearly 1 million people in the U.S. and 10 million individuals globally.

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Equfina, Known as Xadago in US, Approved in S. Korea as Levodopa Add-on

therapy approval

Equfina (safinamide) has been approved in South Korea as an add-on therapy to levodopa for Parkinson’s disease patients who experience “off” episodes, Eisai, which is marketing this medication in parts of Asia, announced.

The approval makes South Korea the first country in Asia outside of Japan to sell Equfina.

Under the brand name Xadago, the add-on therapy was approved for the same indication in Europe in 2015 and in the U.S. in 2017. In Canada it is marketed under the name Onstryv.

“Off” periods in Parkinson’s are characterized by the reappearance or worsening of motor symptoms — such as tremors and dyskinesia (involuntary movements) — due to a gradual decline in levodopa’s effectiveness throughout the day.

Safinamide, developed by Newron Pharmaceuticals, increases the level and function of dopamine — the neurotransmitter, or signaling molecule, missing in those with Parkinson’s — in the brain. It does so by inhibiting the enzyme monoamine oxidase B that normally breaks down dopamine, and also by inhibiting (blocking) transporters that are responsible for its uptake, meaning its absorption and retention.

Safinamide also inhibits an excessive release of the neurotransmitter glutamate.

Equfina’s approval in South Korea was based on clinical results from the SETTLE Phase 3 study (NCT00627640). The global trial enrolled 549 patients experiencing off episodes while on a stable regimen of levodopa plus benserazide or Lodosyn (carbidopa).

Participants were randomized to either oral safinamide (50 mg per day, increased to 100 mg per day if tolerated) or a placebo as an add-on therapy for 24 weeks.

The study’s main goal was changes in mean daily “on” time (the period in which motor symptoms are efficiently controlled) about six months of treatment or placebo use.

Results showed that adding safinamide to levodopa significantly increased the length of “on” periods without dyskinesia by almost one hour (57.6 minutes) compared with placebo.

Adverse treatment reactions were seen in 28.5% of patients in the safinamide group and in 27.6% of those given a placebo, with the most frequent including dyskinesia, nausea, and somnolence (sleepiness).

Newron entered a licensing agreement with Meiji in 2011, granting the company exclusive rights to manufacture and commercialize safinamide in Asia. Based on a licensing agreement between Eisai and Meiji, Eisai now has exclusive rights for developing and marketing safinamide in much of Asia.

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MJFF Offering Comprehensive Guide for Newly Diagnosed Patients

MJFF guide

The Michael J. Fox Foundation (MJFF) is offering a guide to help people newly diagnosed with Parkinson’s navigate the early days of their disease, and better prepare for the future.

Called “If I Knew Then What I Know Now: The Michael J. Fox Foundation Patient Council’s Guide for People Newly Diagnosed with Parkinson’s,” the resource is meant to provide encouragement, insights, and practical strategies to those living with this disease.

This year alone, about 60,000 people in the U.S. are expected to be diagnosed with Parkinson’s. Compounding matters, many of those diagnoses will come during a global pandemic.

The free 32-page guide was written by five members of MJFF’s Patient Council, which represents the patient perspective and works to educate the community.

Rachel Dolhun, MD, MJFF’s vice president of medical communications and a movement disorder specialist, also contributes tips for managing life with Parkinson’s. Among topics covered are disease information and specialists, building a support system, diet and exercise, and research participation.

“A Parkinson’s diagnosis brings many questions and concerns and a series of inevitable hurdles,” Soania Mathur, MD, guide contributor and Patient Council co-chair, said in a press release. “We may not have a choice in our diagnosis, but how we face those challenges is ours to determine.”

The guide comprises short, mostly first-person articles categorized into sections. A section called “I’ve Got What?” covers the diagnostic process, second opinions, the Parkinson’s journey, inheritance, and causes of Parkinson’s disease.

Another section, “Managing Emotions in the First Days,” has essays about disease acceptance, the relationship between symptoms and stress, and reasons for hope.

“Coming to terms with my Parkinson’s was not something that happened overnight,” one contributor  wrote. “I had to tell myself many times that my diagnosis was here, it was happening now, and it was unavoidable. And that I needed to start planning for what would come next.”

Added Michael J. Fox, the actor who founded MJFF after being diagnosed with Parkinson’s in 1991 at age 29: “My first thought was, ‘What the hell happened to me? What am I going to do?’ That took time to work through, but I found out that if I could accept what my situation was, and be honest about it, I could move forward.

“And my happiness grows in direct proportion to my acceptance,” Fox said.

In “Taking Control of Parkinson’s Disease,” authors discuss the best sources for advice, symptom management, early medication and treatment, caregiving, and making the most of doctor appointments. There is also an article about clinical trial participation, and a column by Bill Rasmussen, a Patient Council member and founder of the U.S. sports channel ESPN, who was diagnosed in 2014.

The guide also includes a question-and-answer section, titled “How and When Will I Know I’m Ready to Share My Diagnosis?” Another section addresses early onset PD, generally defined as a Parkinson’s diagnosis before age 50.

The publication also provides a listing of MJFF resources, covering many aspects of life with the neurodegenerative disorder.

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Stopping Trimetazidine May Ease Parkinson’s Symptoms, Improve Quality of Life, Study Says

trimetazidine and Parkinson's symptoms

Discontinuing trimetazidine treatment in people with Parkinson’s disease may lessen their motor and non-motor symptoms and improve their quality of life, a study has found.

The study, “The Impact of Trimetazidine on Disease Severity and Quality of Life in Parkinson’s Disease,” was published in the journal Scientific Reports.

Trimetazidine, which is sold under the brand name Vastarel and also available as a generic, is an antianginal medication used as add-on therapy for treating stable coronary heart disease — conditions that cause a reduction of blood flow to the heart. It is approved for this indication in Europe and other countries but not in the U.S. 

Previous studies have shown trimetazidine to have adverse effects on motor function, including causing reversible parkinsonism, tremor, and orofacial dyskinesia (involuntary repetitive movements of the mouth and face). It can also worsen symptoms of existing movement disorders like Parkinson’s disease.

These effects may be caused by the medication’s piperazine core, a chemical compound also found in antipsychotic medications that have been reported to induce parkinsonism and worsen Parkinson’s symptoms. 

Piperazine is thought to block the action of dopamine receptors, which play an important role in movement regulation. 

Based on previous studies, in 2012, the European Medicines Agency recommended against the administration of trimetazidine to patients with Parkinson’s disease.

However, recent data show that this recommendation is not followed strictly enough, and trimetazidine is still being prescribed to people with movement disorders.

Researchers at University of Pécs in Hungary have now evaluated the impact of trimetazidine treatment on the severity of clinical symptoms and its effects on health-related quality of life in people with Parkinson’s disease. 

The study included 42 patients with Parkinson’s disease, at a mean age of 71.1 years, who had been prescribed trimetazidine. All patients were also taking oral anti-parkinsonian medications.

At the start of the study, patients had been taking trimetazidine for a mean of 6.5 years, at a mean dose of 72.1 mg. Participants underwent detailed neurological and neuropsychological assessments.

Trimetazidine was stopped and patients were again reevaluated three months later. Their oral antiparkinsonian treatment was kept stable until the follow-up.

Results showed significant lessening of Parkinson’s clinical symptoms at follow-up, measured by the Movement Disorder Society-sponsored Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), a four-part assessment of motor and non-motor Parkinson’s symptoms.

Clinically relevant improvements were observed upon discontinuation of trimetazidine according to changes in scores of different parts of the MDS-UPDRS, compared with the beginning of the study: a 25.7% change in part 1, which relates to non-motor experiences of daily living; a 23.8% change in part 2, which assesses motor experiences of daily living; a 28.5% change in part 3, a motor examination that included notable lessening in disturbances of posture, gait (walking) problems, and postural instability; and a 30.1% change in part 4, which also measured motor complications.

Trimetazidine discontinuation also lessened Parkinson’s disease severity in 16 patients (38.1%), including two whose motor symptoms completely disappeared. However, in these two cases, “discontinuation of antiparkinsonian medications resulted in the reemergence of Parkinsonian symptoms,” the researchers wrote.

They also noted an overall lessening of non-motor symptoms, especially sleep problems and depression. 

“The use of [trimetazidine] in patients with [Parkinson’s disease] and the negative impact of the drug on the severity of Parkinsonian symptoms seem to be clinically meaningful problems,” the researchers wrote.

Additionally, patients experienced better health-related quality of life, as measured using the 39-item Parkinson’s Disease Questionnaire, which assesses patient-reported health status and quality of life.

Stopping trimetazidine and using alternative antianginal treatment did not cause any cardiovascular events in these patients up to 12 months of follow-up.

“Our results provide clinical rationale for avoiding the use of [trimetazidine] in [Parkinson’s]. [Trimetazidine] seems to worsen the severity of Parkinsonian symptoms in a clinically meaningful manner and have a negative impact on the [health-related quality of life],” the team wrote. 

“Therefore, discontinuation of the drug in patients with [Parkinson’s] seems to be a clinically adequate therapeutic intervention,” they concluded.

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Subtle Alterations in Postural Behavior May Help Diagnose Parkinson’s Earlier

Postural behavior

People with Parkinson’s have postural adjustments even at early stages of the disease when clinical symptoms of postural instability are not evident and despite the use of antiparkinsonian medications, a recent study shows.

Researchers believe these findings suggest that postural behavior may be used as an early indicator to diagnose the disease.

The study, “Postural Behavior in Medicated Parkinson Disease Patients: A Preliminary Study Searching for Indicators to Track Progress,” was published in the Journal of Central Nervous System Disease.

Parkinson’s disease usually is diagnosed based on the presence of classic  motor symptoms. But other signs of the disease are present sometimes years before motor symptoms are evident, though still insufficient to make a definite diagnosis.

Identifying patients in this earlier phase would ensure they receive treatment early, before their disease progresses to more advanced stages and significantly affects daily activities.

Generally, Parkinson’s patients with early disease are classified as not having postural instability. But modern technologies are more sensitive to subtle impairments in balance, and potentially may identify changes in postural behavior that take place even in earlier stages of disease.

To clarify the presence of postural changes in early Parkinson’s disease, and whether these changes can be used to diagnose the disease before motor symptoms are evident, researchers at the Western Michigan University and collaborators at the Federal University of Piauí, Brazil, investigated two groups of Parkinson’s patients, and compared them to a group of healthy controls.

Participants included nine patients with early disease — defined as a Hoehn and Yahr Stage rating scale up to 2, which means their balance was not yet affected — and nine patients with mid- to advanced disease (a Hoehn and Yahr Stage of 2.5 or higher, whose balance was already compromised).

These patients were all taking antiparkisonian medication, allowing researchers to account for the effects of medication on balance, which the team believes is a clear limitation of prior studies that lacked a standardization on this parameter. Controls included nine healthy subjects matched by age, who had no history of sensory, muscular, or neurological disorder.

Participants were asked to perform two simple postural tasks: stand quietly on a force platform with arms crossed, with eyes open or closed. Each task took 120 seconds. During that time, the platform collected information regarding participants’ center of pressure, including body sway trajectory (how the center of pressure moved), sway amplitude (how far in each direction it went), sway velocity (how fast it moved), and sway jerkiness (how shakier body sway was).

The team found that most measures were similar across patients and controls when they did the test with their eyes open. But Parkinson’s patients already showed greater sway velocity and jerkiness compared to controls in this task. Late-stage patients also had more overall sway movement and greater sway amplitude.

When the task was done with eyes closed, patients also had higher sway jerkiness — though sway was only laterally shakier — compared to controls, but not higher sway velocity. Those with advanced disease also had greater sway amplitude.

No significant differences were seen between groups of Parkinson’s patients in either task. Also, while controls and early-stage patients swayed more, faster, and shakier when they stood still with their eyes closed, no differences were seen in advanced patients with eyes open and closed.

The findings show that Parkinson’s patients have alterations in postural behavior starting in early stages of disease, and despite the use of dopaminergic medication. “This finding indicates that balance control is affected even before clinical signs surface,” the researchers wrote.

“Therefore, postural markers used in this study are [of] great importance to improve early diagnosis of postural instability in PD [Parkinson’s disease], record progress of balance control, and assess fall risk. They should also be implemented in clinical trials of pharmacotherapy and balance training protocols specific to populations diagnosed with PD,” they concluded.

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