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Role of Environmental Factors in Parkinson’s Development Investigated in Review Study

environmental causes

The hallmark presence of Lewy bodies in the pathway related to sense of smell and in the gut years before a Parkinson’s diagnosis, as well as the potential cumulative impact of different triggers, may help researchers understand the environmental factors that contribute to the development of the disease, according to a review study.

The study, “The Search for Environmental Causes of Parkinson’s Disease: Moving Forward,” appeared in the Journal of Parkinson’s Disease.

Environmental factors contribute at least partially to late-onset sporadic Parkinson’s disease. Because neurodegenerative changes are too advanced to be stopped or reversed by the time a diagnosis is reached, understanding modifiable risk factors that can help to identify the disease and allow for an early intervention may lead to more successful treatment of Parkinson’s, the neurological disease with the fastest-growing prevalence.

“The greatest risk factors for [Parkinson’s] are likely environmental and not genetic,” Honglei Chen, MD, PhD, from Michigan State University, and Beate Ritz, MD, PhD, from the University of California Los Angeles, said in a press release. “Yet we know relatively little about environmental causes or triggers. Identifying these and defining ways to reduce their impact will be great research challenges for the coming two decades.”

Environmental factors may trigger Parkinson’s or modify its progression during the prodromal (early) stage, in which early symptoms or signs are present, but clinical diagnosis is not yet possible. Among the reported factors, smoking, coffee, exercise, plasma urate, and use of ibuprofen have been linked to a lower risk of Parkinson’s, while pesticide exposure and traumatic brain injury have been associated with a greater risk.

Apart from two pesticides known as rotenone and paraquat, researchers have had difficulties in providing evidence that other risk factors can cause the disease. Reverse causation — meaning that Parkinson’s changes lifestyle and behavior before a clinical diagnosis rather than the other way around — has been proposed as an explanation for the link between these environmental triggers and Parkinson’s in its early stages.

“This prodromal stage is of major interest for prevention efforts,” the researchers said in the release, adding that the discovery of Lewy bodies — protein aggregates mainly composed of alpha-synuclein that are characteristic of Parkinson’s — in the olfactory pathway and the digestive tract made targeting factors that enter the body via the nose or gut “even more important.”

The Braak hypothesis presents a potential explanation for environmental contributions in Parkinson’s prodromal development. It suggests that Lewy pathology starts in the brain’s olfactory bulb — an area of the brain involved in the sense of smell — or in enteric (gut) nerves (nerve cells that control the function of the gastrointestinal tract) years, if not decades, before reaching the substantia nigra — an area of the brain key in the control of movement that shows progressive loss of dopamine-producing neurons in Parkinson’s disease.

Findings such as a reduced sense of smell and constipation years before a Parkinson’s diagnosis have supported the Braak hypothesis. Pesticides and other environmental toxins such as air pollutants, of which there is growing evidence of harmful effects on cognitive function, organic solvents, and meats cooked at high temperatures may lead to Parkinson’s through these pathways, although a proinflammatory gut microbiome — the community of bacteria, viruses and fungi that lives in the gut — has also been proposed as a potential starting point. Certain genetic factors may also interact with these environmental causes to boost the risk for the disease.

Besides the Braak hypothesis, the scientists also discussed reported epigenetic differences — alterations in gene function but not in the DNA sequence itself — in the blood and saliva of people with Parkinson’s as well as the importance of lifelong exposure to environmental triggers.

The exposome, which refers to all environmental exposures over a lifetime, suggests that multiple environmental stimuli combine to increase the risk of Parkinson’s. This has been shown with traumatic brain injury and paraquat exposure, and with smoking combined with factors such as caffeine intake and physical activity.

“We are at an exciting moment to unveil environmental contributions to [Parkinson’s] development and progression by taking a life-course approach, and utilizing novel tools to assess environmental exposures,” the researchers said.

While they caution that the long duration of the prodromal stage complicates understanding the extent to which environmental factors contribute to Parkinson’s, the investigators “nevertheless believe it will be possible to assess long-term exposures through large-scale environmental monitoring and by using novel biomarkers that reflect the exposome.”

Both the Braak hypothesis and the exposome concept provide “a theoretical framework for scientists to design future studies to decipher the environmental causes of [Parkinson’s] and develop early interventions to halt the progression to the characteristic motor dysfunction in [Parkinson’s],” they concluded.

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Parkinson Voice Project Going Global with Speech Therapy Grant Program

speech therapy grants

This year, Parkinson Voice Project (PVP) is broadening its SPEAK OUT! & LOUD Crowd Grant Program to include support for international speech therapy clinics.

The expanded grant program is intended to help Parkinson’s disease patients around the world gain access to quality speech treatment to maintain their speaking abilities and minimize the threat of swallowing problems.

In addition to facilities in the U.S., grant recipients this year will include five clinics based outside the country. Applications are now being accepted and are due March 1. Recipients will be announced in April during Parkinson’s Awareness Month. Go here for full eligibility requirements, and visit this site to apply.

Nonprofit organizations, universities/graduate students, and hospitals who would like to bring PVP’s speech therapy program to their communities are encouraged to apply. Applicants must have the physical space and clinical staff necessary to provide both individual and group speech therapy. Last year’s winners may reapply for continued support of their programs.

For international applicants, awards are open to any clinic that can use English or Spanish-based therapy materials.

To achieve its mission of making speech treatment widely accessible, PVP recognized a need to support speech language pathologists. These professionals, according to the organization, get low insurance reimbursement for services, and also often have trouble securing funding from employers for specialized training and supplies. The grants are designed to provide pathologists with the knowledge and tools needed to help the Parkinson’s community.

The grant program, which honors the late Parkinson’s speech expert Daniel R. Boone, PhD, was launched last year with 92 grants awarded to speech therapy clinics nationwide. Of them, 34 were university-based clinics.

More than 900 speech language pathologists and graduate students received training in SPEAK OUT! and LOUD Crowd therapy protocols, plus speech therapy supplies, funding support for their organizations, and a trip to PVP’s clinic in Dallas-Fort Worth for hands-on training.

“Our grant program was a huge success in 2018,” said PVP CEO Samantha Elandary, in a press release. “Our goal is to make quality speech treatment available to those living with Parkinson’s around the globe.”

According to Elandary, Parkinson’s affects more than 1 million U.S. residents, and up to 10 million people worldwide. Some 89 percent of patients are likely to develop speech disorders that can lead to swallowing difficulties.

Combining speech, voice, and cognitive exercises, SPEAK OUT! addresses the motor speech issues related to Parkinson’s. LOUD Crowd is a voice maintenance program consisting of speech therapy groups and a singing segment to foster voice strength retention.

Using the two-part trademarked speech therapy program, the patient and a speech language pathologist tackle a series of speech, voice, and cognitive exercises outlined in a specialized workbook. Stressing “speaking with intent,” the program switches speech from an automatic function to a deliberate act. Because speech muscles are also used for swallowing, the benefits of the therapy are twofold.

Grant funding will come from the more than $2 million PVP raised over the past holiday season.

Through intensive speech therapy, follow-up support, research, education and community awareness, the nonprofit aims to preserve the voices of those with Parkinson’s and related disorders. To date, it has trained more than 1,300 speech language pathologists nationwide. Internationally, it has trained therapists in eight countries.

Among other offerings, the organization also hosts an educational lecture series. Earlier this month, Susan Imke, a certified gerontological nurse practitioner who focuses on families living with Parkinson’s disease and other neurodegenerative disorders, discussed “Optimal Nutrition for Living Well with Parkinson’s.” The next presentation, “Packing Some ‘Punch’ Into Your Parkinson’s Exercise Routine,” will be Feb. 9.

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My PD Frustration Consists of More Than Only Symptoms and Treatments

 

 

by Jean Mellano

You don’t have to be positive all the time. It’s perfectly okay to feel sad, angry, annoyed, frustrated, scared and anxious. Having feelings doesn’t make you a ‘negative person.’ It makes you human.” –Lori Deschene

As many people with Parkinson’s will attest, both Parkinson’s disease (PD) symptoms and finding the right treatment to alleviate them can be extremely frustrating.

The perception

Just as frustrating for me is that everyone thinks I am fine. Since I have no tremors, there are no obvious symptoms. Most well-meaning, healthy people either tell me I look great or that they have the same issues as me — cognitive decline, balance, poor fine motor skills, slowness of movement, and fatigue.

The truth

I struggle to maintain balance and must consciously avoid walking into furniture. My body, especially on the left side, does not always listen to me when I tell it to do something. Trying to maintain focus to do this is draining in itself. I also feel weak inside and I am always extremely fatigued. It is an exhaustion that no amount of sleep or rest can diminish.

A glimpse into my frustration

To help my fine motor skills, I have taken up ukulele lessons. I never played any instrument in my life, so I have no muscle memory to call on. The left hand and fingers play a huge role in learning how to use this instrument.

Recently, I had a meltdown in one of my lessons. My left fingers were not listening to me while trying to play some chords. The instructor was very patient, but I don’t think he understood the extent of my struggles. I was trying to play a G chord, which requires positioning three fingers from my left hand on various frets. These fingers would not cooperate and they just froze. With all the energy I expended trying to get my fingers positioned, I worked up a sweat.

Finally, so full of despair and frustration over what I have lost, I just broke down in tears. I can no longer control my body.

Empathy

The frustration continues on many fronts for me: the symptoms themselves, trying to find something to help treat my symptoms, and well-intentioned people not comprehending what I struggle with daily. Many years before I was affected by this disease, a friend of mine was diagnosed with PD. I could never understand why it was so hard for her to put on a seat belt.

Now I know.

I have a form of Parkinson’s disease, which I don’t like. My legs don’t move when my brain tells them to. It’s very frustrating.” –George H. W. Bush

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Meditation and Parkinson’s Disease: Looking for Lightness of Being

meditation

Living with Parkinson’s disease is a struggle against the loss of both motor and cognitive functions. One must invest effort into an action plan that reduces the impact of the disease — a rehab plan. This effort is daily (sometimes hourly) and can be exhausting.

Living with PD is like carrying a large backpack of rocks. It is at times a crushing burden that can overwhelm. Balance needs to be established in my life so that the work I do in fighting the disease does not consume me. I must spend time looking for lightness of being to balance out the heavy PD burden. I do this through a regular practice of meditation.

There are many ways to practice meditation: sitting and listening to calming music, sitting and gazing at a fireplace, practicing tai chi, or exercising with rhythmic breathing. These practices seek to help one enter the quiet mind. It is within the quiet mind that one experiences lightness of being. Meditation helps relieve stress and focus attention — both of which are of benefit to those with PD. There are books providing instructions on how to do this, but none deal directly with PD.

Practicing meditation with PD presents some unique challenges. The meditation practice starts with calming the body, and this is the first obstacle PD complicates. Repetitive motor activities like cycling, tai chi, or gardening are helpful when combined with focused breathwork.

Focused breathwork is diaphragm breathing in which you focus your full attention on the breath. Guided meditation, either from a teacher, in person, or from a recording, can help with this process of shifting attention. This shifting of attention is the second obstacle PD complicates.

Once past the first two obstacles, you should feel a little more relaxed. This relaxed state is the path leading to the door into the quiet mind, but I am prevented from going down that path by a third obstacle.

This third obstacle is heightened emotions and difficulty in regulating them. I have written about how PD heightens the impulse signals to the brain. During the meditation process, the signal-to-noise ratio changes, meaning that as one practices quieting the mind, the noise goes down and the signals connected to emotion appear louder.

The quiet mind is a mental state that silences the noise of the world, the body, and the self while at the same time maintaining a sense of peace and safety. It is something I practiced for decades and then lost touch with over the last seven years while battling PD. As my life has become stable, I am now returning to the practice and finding it much more difficult. I feel like a novice struggling with all the obstacles I used to walk around with ease. This third obstacle does impede my looking for lightness of being.

As I have helped patients to find a place of peace and safety, together we would often experience loud emotions. These are emotions connected to things we feel (consciously or subconsciously) that need attention. They are like boulders in the path, looking like obstacles blocking the way forward to the quiet mind. But one can learn to walk around them.

Most of the folks I worked with would have several boulders to walk around and needed multiple sessions to learn how to walk around them. As I write this, I remember the tender patience I should offer to myself.

Once past the boulders of emotion, you then arrive at the doorstep of the quiet mind. PD has made looking for lightness of being much more difficult for me, but not impossible. I have memories, and recently have felt glimpses of peace and deep calmness.

Seeking lightness of being ties into my New Year’s resolution. For me to quiet down the old tapes (emotional boulders in the path), I need to have a new mental state to go to. I can’t just remove the tapes and leave a void, because that void will be quickly filled back in with the old mental habits. Looking for lightness of being will be a lifetime adventure.

What ways do you practice meditation, and how have you found it to be helpful?

***

Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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MJFF and Blackfynn Collaborate on Parkinson’s Study to Discover Biomarkers

MJFF and PPMI

The Michael J. Fox Foundation (MJFF) and Blackfynn are joining forces to make optimal use of an initiative that could uncover Parkinson’s disease biomarkers and bring about new therapies.

Called the Parkinson’s Progression Markers Initiative (PPMI), the MJFF-backed effort is an ongoing observational study of more than 1,300 volunteer participants both with and without Parkinson’s to validate biomarkers and, over time, identify disease risk factors. Participants undergo a battery of tests and assessments.

Biomarker discovery is critical in the quest for therapies that can slow or halt Parkinson’s progression. Specifically, it would allow for earlier diagnosis, better disease tracking, and more efficient therapy tests. Current treatments only temporarily ease symptoms.

To glean as much as possible from patient data, Blackfynn will lead the PPMI Advanced Analytics Core, established to analyze biomarker discovery. The firm has a data integration and analysis platform it uses to drive development of therapies, and advance translational research for neurological diseases.

“The goal of the Advanced Analytics Core is to accelerate our analysis of the comprehensive within-subject data collected through PPMI,” Kenneth Marek, PPMI principal investigator, said in a news release.

“By combining this rich, multimodal data with Blackfynn’s platform and data science expertise, we hope to uncover insights into the determinants of [Parkinson’s disease] progression that will lead to new therapies and improved quality of life for patients.”

The Blackfynn infrastructure incorporates a full complement of medical and scientific data to enable swift assessment of data correlations and complex data visualizations. PPMI scientists plan to use the platform to interpret data, develop verifiable hypotheses, and better collaborate with the goal of more targeted translational research.

“Our work with MJFF and the PPMI investigators will maximize the value of this important patient dataset and help drive novel discovery with the potential to lead to the development of effective therapies for patients with PD,” said Amanda Christini, president of Blackfynn.

“Blackfynn will enable a new lens through which discoveries can be made, by looking at all raw and metadata together, in context, to find new patterns that are otherwise obscured when data are in isolation.”

Citing an unwieldiness caused by an abundance of Parkinson’s-related biomarker information, an editorial in the journal The Lancet Neurology heralded the efficiencies of collaborative research. Particularly, it applauded the Accelerating Medicines Partnership for its efforts to find a Parkinson’s cure.

As for the PPMI, five-year results have already shown that clinical trials in patients with early-stage Parkinson’s may benefit from assessing markers of disease progression — namely, changes in the Movement Disorder Society (MDS)-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) and dopamine transporter imaging.

Launched in 2010, PPMI is underway in the United States, Europe, Israel and Australia.

The MJFF is dedicated to finding a cure for Parkinson’s by funding research and ensuring the development of improved therapies for those living with the disease. It has funded more than $800 million in research to date.

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Parkinson’s Institute and Clinical Center, Retrotope Collaboration to Test RT001 in Progressive Supranuclear Palsy

Parkinson’s Institute and Clinical Center and Retrotope have paired up to explore the therapeutic potential of the investigational agent RT001 in patients with progressive supranuclear palsy (PSP), a type of treatment-resistant Parkinson’s disease.

Under Retrotope’s expanded access program for RT001, the institute’s physicians started dosing two PSP patients with the investigational therapy. This pilot study is expected to provide information to help guide future randomized placebo-controlled trials in PSP.

“The Parkinson’s Institute and Clinical Center brings novel therapies for [Parkinson’s disease] to patients in need,” Carrolee Barlow, MD, PhD and CEO of the institute, said in a press release. “We look forward to working with Retrotope in evaluating the responses to this therapeutic candidate in these patients.”
RT001 belongs to a new therapy class called deuterated polyunsaturated fatty acids, or D-PUFAs, that protect mitochondria and cells from damage caused by oxidation of fat molecules, which often results in cell death that is a hallmark of numerous neurodegenerative diseases including Parkinson’s. Mitochondria provide energy and are known as the “powerhouses” of the cells. The investigational agent is an engineered, more stable form of linoleic acid that mimics the protective effects of the fatty molecule Omega-6.

RT001 is integrated in cell and mitochondria membranes and, as it is a stabilized fatty molecule, does not react with damaging free reactive oxygen elements — toxic compounds produced as a consequence of cellular oxidative stress — restoring membrane function and cellular health.

“The patients we treat with these fatal, degenerative diseases are willing to try therapies which appear safe and for which there is a mechanistic rationale that they may benefit from the treatment,” Barlow said. “Retrotope is a willing partner with a highly unique and well-studied approach to addressing neurodegenerative diseases.”
“The institute’s goal is to find a cure for Parkinson’s and Expanded Access programs like Retrotope’s are really at the forefront of generating hope for patients from novel therapies, and data for pharmaceutical companies to plan their drug trials,” she added.

The therapeutic potential of this investigational agent is being tested in patients with inherited Friedreich’s ataxia (FA) and infantile neuroaxonal dystrophy (INAD).
In addition, this new agent has been shown in preclinical studies to hold therapeutic potential in other illnesses where mitochondria function and induced cell death play a role, including Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis (ALS).

Preclinical data has shown that RT001 orally administered to mice with induced Parkinson’s disease could effectively improve the levels of dopamine by 2.5 times in the brain area most affected by the disease. In addition, the treatment effectively prevented brain cells’ degeneration in these animals.“Early results in clinical trials of RT001 and Expanded Access programs for a variety of neurodegenerative diseases have generated encouraging results along with a favorable safety profile,” said Peter G. Milner, MD and chief medical officer of Retrotope. “We look forward to providing updates on this and other studies in the coming months as we support patients and investigators exploring the utility of RT001 to block lipid peroxidation in a range of primary neurodegenerative diseases.”

Source: Parkinson’s News Today

Linked Clinical Trials Initiative Boosts Number of Parkinson’s Clinical Studies

The Linked Clinical Trials (LCT) Initiative, a repurposing program that aims to identify existing medicines which can slow the progression of Parkinson’s disease, has resulted in a growing number of clinical trials. The partnership’s history, purpose and activities are the focus of an article, “The Linked Clinical Trials Initiative (LCT) for Parkinson’s disease,” that recently appeared in the European Journal of Neuroscience.

The International Parkinson’s LCT Initiative was conceived in 2010 by Tom Isaacs, late president and co-founder of the London-based Cure Parkinson’s Trust (CPT), and Richard Wyse, the organization’s current director of research and development.
CPT decided to support preclinical and clinical studies of potential disease-modifying therapies (DMTs) and of medications approved for other illnesses in therapy repurposing trials. Symptomatic treatments were not explored, as they were already being extensively investigated in industry-sponsored studies.

The Committee to Identify Neuroprotective Agents for Parkinson’s program greatly influenced the launch of LCT. Initiated in 2003, the program assessed more than 20 potential Parkinson’s therapies. Several were selected to enter clinical trials, but none met their primary clinical goals.

Yet given the ensuing discovery of new disease mechanisms and therapeutic targets, as well as the growing notion that some of the first events in Parkinson’s development occur outside the brain, it seemed “very reasonable to revisit the concept of drug repurposing in [Parkinson’s],” researchers wrote.
LCT’s initial focus was to gain insight from key opinion leaders on appropriate medications to test for potential therapies in Phase 2 trials of Parkinson’s. If successful, these trials would lead to Phase 3 studies and market possible new therapies.
The goal was to have multiple parallel trials comparing different therapies with a similar protocol. Yet the need to for different placebos and durations of treatment, among other factors, made this impossible.

Patrik Brundin, MD, then working at Sweden’s Lund University, agreed to chair the LCT scientific committee. Isaacs and Wyse approached Brundin because of his contributions to the Parkinson’s field and deep understanding of clinical and basic science. Overall, the scientists involved in LCT felt that studies should look at impaired processes — such as neuroinflammation or energy metabolism — and favor compounds able to affect more than one such process. Also, as there was no DMT for Parkinson’s, the disease was an attractive target for therapy repurposing, an approach that can be significantly time- and cost effective to find new medications.

The effort included eight scientists, including Brundin. Another scientist, Jeffrey Conn, PhD, of Tennessee’s Vanderbilt University Medical Center, was a global expert in blood-brain barrier penetration and pharmacology. The blood-brain barrier is a semipermeable membrane that protects the brain from the outside environment. Penetrating this barrier and reaching the brain is critical in treating neurological diseases.

Three patients, including Isaacs, attended the first LCT meeting in 2012 at the Van Andel Research Institute in Grand Rapids, Michigan. Also present were representatives from the Michael J. Fox Foundation for Parkinson’s Research, the Parkinson’s Foundation, and Parkinson’s UK. Since then, patient participation has increased, providing immediate access to their perspectives and discussions on trial design and continuation, as well as compliance with specific therapies.
The first LCT meeting led

Source: Parkinson’s News Today

Participation of Early Parkinson’s Patients in Clinical Trials Crucial to Finding Cure, Expert Says

The time between diagnosis and implementation of symptomatic treatment is critical in the effort to find a cure for Parkinson’s disease. However, many early Parkinson’s patients wait too long before seeking medical attention, leaving researchers with a small group of candidates for clinical trials, says Robert A. Hauser, MD, the director of the Parkinson’s & Movement Disorder Center at the University of South Florida.

In his commentary, “Help cure Parkinson’s disease: please don’t waste the Golden Year,” published in the journal npj Parkinson’s disease, Hauser stresses the importance of early Parkinson’s patients participating in clinical trials before they start taking symptomatic medications.

The discovery that Parkinson’s is associated with aggregation of misfolded alpha-synuclein proteins in the central nervous system suggests there are many potential targets for therapeutic intervention.
Researchers are enthusiastic about the idea that the disruption of this process, or removing toxic aggregates, can slow or stop disease progression. Unfortunately, there are still no validated biomarkers, such as a simple blood test, that can help monitor disease progression or test promising therapies in Parkinson’s patients.

So far, the most common way to test a therapeutic candidate is to assess its capacity to slow the progression of clinical signs and symptoms compared with placebo over time in patients with early Parkinson’s who are not yet receiving symptomatic Parkinson’s medications — such as levodopa, dopamine agonists, and MAO-B inhibitors.

However, this can prove to be a challenge, since patients with early Parkinson’s disease can only be followed, without the use of symptomatic medication, for about six to 12 months, what Hauser calls the “Golden Year.” After this, many patients will need medication to relieve symptoms.

“The critical time of about one year from when the patient can be diagnosed with early PD [Parkinson’s disease] based on mild classic motor features until they truly require symptomatic therapy can be considered the Golden Year,” Hauser said in a press release. “It is during this early, untreated phase, that progression of clinical symptoms reflects the progression of the underlying disease.”

Interference from symptomatic medications makes it difficult for researchers to tell if the potential treatment being tested is slowing disease progression or if they are just seeing effects from those other therapies.
However, patients with early Parkinson’s who are available to enroll in a clinical trial and whose symptoms are mild enough are in short supply.

Therefore, to test promising potential disease-modifying therapies, patients with early Parkinson’s have to be identified and referred to clinical trials before they go on symptomatic medications. Unfortunately, this is often not the case.
“If the time period over which we test the intervention is short, we reduce our ability to identify a difference between the intervention and placebo. If the time period over which we attempt to test the medication is too long, a substantial proportion of patients may require institution of symptomatic therapy and we lose our ability to monitor clinical disease progression during the observation period,” Hauser wrote.

Source: Parkinson’s News Today

Inflammatory Bowel Disease Linked to Risk of Parkinson’s in Large Review Study

People with inflammatory bowel disease (IBD), an umbrella name for disorders marked by prolonged inflammation of the digestive tract, are at a higher-than-usual risk for Parkinson’s disease, a review study involving 8.9 million IBD patients suggests.
The study, “The risk of Parkinson’s disease in inflammatory bowel disease: A systematic review and meta-analysis,” was published in the journal Digestive and Liver Disease.

Inflammatory bowel disease (IBD) is a term that includes two main disorders — ulcerative colitis and Crohn’s disease — and is characterized by an imbalanced immune response that triggers prolonged inflammation of the digestive tract.
Inflammation in ulcerative colitis is confined to the colon (large intestine), while in Crohn’s disease it can involve any part of the digestive system. But inflammation in Crohn’s is most common at the end of the ileum (the last section of the small intestine) or the colon.

Several studies have reported that some of the inflammatory pathways impaired in Parkinson’s are also found in IBD. Certain population-based studies have also reported an increased prevalence of Parkinson’s among IBD patients, but the link between both disorders remains controversial. Another follow-up study failed to confirm those initial findings.
Researchers in China conducted a meta-analysis of published literature focusing on Parkinson’s risk in IBD using two databases, PubMed and Embase, and including in their search the keywords “ulcerative colitis” and “Crohn’s disease.” For the meta-analysis, they included cohort or case-control studies with patients diagnosed with IBD, either ulcerative colitis and Crohn’s disease, and whose main outcome was Parkinson’s.

Out of an initial pool of 172 studies, four studies accounting for a total of more than 8.9 million patients were included in the meta-analysis. (A meta-analysis is a statistical technique used to summarize in a quantitative manner the findings of multiple studies.)
Performed in the United States, Denmark, Sweden and Taiwan, these four studies assessed the incidence rate of Parkinson’s in IBD patients, specifically those with Crohn’s and ulcerative colitis. Three had been conducted in 2018, and one in 2016.
“To our knowledge, this is the first MA [meta-analysis] to focus on the risk of PD [Parkinson’s] in IBD patients,” the research team wrote. “Despite the small number of studies included, the patient numbers were large due to the population-based nature of the included studies.”

Pooled results of all studies suggested that an IBD diagnosis was associated with a 41% increased risk of developing Parkinson’s.
Assessing the risk of ulcerative colitis and Crohn’s disease separately, researchers found that both disease subtypes were linked to a higher Parkinson’s risk compared with age- and sex-matched controls — Crohn’s patients had a 28% higher risk of Parkinson’s, and those with ulcerative colitis a 30% increased risk, the study reported.
Among the IBD patients, the risk for Parkinson’s was not affected by gender, with similar rates seen in male and female patients, or by age.

Overall, this meta-analysis “identified an increased risk of PD in IBD patients,” the reseachers wrote, which “remained significant when separately analysing CD [Crohn’s disease] and UC [ulcerative colitis] subgroups.”

Source: Parkinson’s News Today

Parkinson’s Patients with Tendency to Fall Control Balance Differently than Non-Fallers, Study Suggests

Parkinson's fall risk

Parkinson’s disease patients who have a tendency to fall use different strategies to control their balance than those who do not fall, according to a recent study.

The study, “Fallers with Parkinson’s disease exhibit restrictive trunk control during walking,” was published in Gait and Posture.

Due to Parkinson’s-related motor imbalance, falls are a common consequence of the disease, and the risk of falling increases as patients get older and as the disease progresses.

Parkinson’s patients are twice as likely to fall than older adults living independently, and are also nine times more likely to have recurrent falls.

Observational studies suggest these patients underestimate the amount of work necessary for their muscles to produce a certain movement. They compensate for this lack of motor and perceptual ability by adopting distinct postural strategies to keep their balance during both static and dynamic movements.

Static measures of posture control can distinguish Parkinson’s patients from healthy older adults, but not Parkinson’s fallers from non-fallers.

“A better understanding of the relationship between falls and static and dynamic movements may provide further insight into falls-risk assessment in this clinical population,” the researchers said.

To study this, researchers at the University of Ottawa in Canada conducted a study that recruited 25 Parkinson’s patients and 17 healthy older adults used as controls.

They analyzed postural differences between Parkinson’s fallers and non-fallers, based on the self-reported occurrence of falls in the previous three months, and between healthy controls.

Motor disability was measured using the Unified Parkinson’s Disease Rating Scale III, cognitive impairment by the Montreal Cognitive Assessment, and freezing of gait by the Freezing of Gait questionnaire.

Participants were given static and dynamic motor tasks, consisting of one quiet standing condition and one walking condition (walking 15 meters while looking straight ahead).

Both tasks were presented twice and lasted for 30 seconds. Testing was performed while patients were optimally medicated with dopaminergic therapies.

The standing test was sensitive enough to distinguish between Parkinson’s patients and healthy controls, but not between fallers and non-fallers with Parkinson’s disease. However, static tasks were less sensitive in differentiating between fallers and non-fallers with Parkinson’s disease and healthy older adults than dynamic tasks.

Fallers had difficulty controlling their upper body (torso) when walking, compared with non-fallers and the control group. This was also true for individuals with Parkinson’s disease versus older healthy adults.

Importantly, falling was associated with static and dynamic postural control in Parkinson’s patients, with fallers and non-fallers adopting different postural strategies to regulate balance.

“Overall, this study provides useful information for falls-risk assessments as well as for developing fall prevention program specific to fallers and non-fallers with PD,” the researchers concluded.

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Source: Parkinson’s News Today

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