Courage in the Face of Fear

my way, courage

We all fear something. Some of us fear death. Some of us fear being left alone. Others have a fear of failure. This journey we are on can be full of treks through deep, dark forests, roads full of potholes, and mountains we must climb.

When I hear the word fear, I almost always think of Psalm 23. It is one of the Bible verses kids learn early on in Sunday school. It talks about not fearing what might come: “Yea, though I walk through the valley of the shadow of death,” I will not fear.

The shadow of death

What is “walking through the valley of the shadow of death?” I think the shadow of death is anything that casts darkness over our lives. Surgeries, chronic diseases, and heart problems can fall under the shadow of death. The list could also include a dying marriage or a wayward child. Walking in a dark valley can bring a fear to fruition, leaving us to experience undue anxiety, an agitated spirit, and feelings of desperation.

Parkinson’s disease has a way of causing us to fear. But there is a way to deflect it.

When fear immobilizes us, faith can overcome that fear and give us much-needed courage. Faith speaks to our hearts, telling us a better day is coming. Faith walks with us through the valleys, shining a light ahead so our hope does not fail. It keeps us walking when we feel like collapsing and giving up.

Hope

Fear loses its power when we take a deep breath of courage and keep moving forward, refusing to give in. Courage can stand and fight when fear breathes down its neck. Courage faces diseases and refuses to stand down.

Courage refuses to give up. Courage is a state of mind that embraces the here and now and holds out for hope. I have seen people with Parkinson’s disease embrace it with both hands, determined to make the best of it. Do they have a secret that allows them immunity over the fear of Parkinson’s or any other illness? 

No. Instead, they have chosen to ax the fear and live courageously with unrelenting hope. A hope that speaks to their spirit and gives them courage as they choose to believe that change is coming. A hope that says change is possible.

Take heart

When the fear ogre comes to tamper with your courage, know that you have a band of comrades standing (or sitting) with you on the front lines. They are ready to do battle on your behalf.

You may feel as if the load you carry is unbearable. You may wonder whether you will make it another day with the pain and stiffness, the immobility, and more. Embrace the courage within you — no matter how small it may seem — and grab hold of the hope it offers. And don’t let go.

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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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High Exposure to Antibiotics May Increase Risk of Parkinson’s, Study Suggests

antibiotics, Parkinson's risk

High exposure to oral broad-spectrum antibiotics and those that kill anaerobic bacteria and fungi is associated with a high risk of Parkinson’s disease within the next decade or more, a study finds.

The findings were reported in the study “Antibiotic Exposure and Risk of Parkinson’s Disease in Finland: A Nationwide Case-Control Study,” which was published in Movement Disorders.

Excessive exposure to antibiotics may change gut bacteria composition, which in turn is associated with an increased risk of several psychiatric disorders, Crohn’s disease, and colorectal cancer. Now scientists are also starting to investigate the possible link between antibiotic use and Parkinson’s.

“The link between antibiotic exposure and Parkinson’s disease fits the current view that in a significant proportion of patients the pathology of Parkinson’s may originate in the gut, possibly related to microbial changes, years before the onset of typical Parkinson motor symptoms such as slowness, muscle stiffness and shaking of the extremities,” Filip Scheperjans, MD, PhD, principal investigator of the study and neurologist at Helsinki University Hospital, said in a press release.

“It was known that the bacterial composition of the intestine in Parkinson’s patients is abnormal, but the cause is unclear. Our results suggest that some commonly used antibiotics, which are known to strongly influence the gut microbiota, could be a predisposing factor,” he said.

To further explore the possible association between high exposure to antibiotics and the onset of Parkinson’s, investigators from Helsinki University Hospital in Finland carried out a nationwide case-control study to compare antibiotic exposure in a large group of people with and without Parkinson’s.

The study included data from 13,976 people who had been diagnosed with Parkinson’s in Finland between 1998 and 2014, and 40,697 people who were the same age and sex, and from the same place of residence, but who did not have the disorder (controls). Information from patients and controls was obtained from national registries.

Antibiotic exposure was estimated based on data about purchases of oral antibiotics and was analyzed in three different time-points: one to five years, five to 10 years, and 10 to 15 years before the onset of Parkinson’s. In their analyses, investigators also looked at antibiotic exposure after grouping medications in different categories (e.g. by chemical structure, antimicrobial spectrum, and mechanism of action).

“During the course of follow-up, 84.9% of [Parkinson’s disease] patients and 83.6% of controls had purchased at least 1 antibacterial course. Penicillins were purchased most frequently, constituting 22.8% of all purchases,” the researchers wrote.

On average, people with Parkinson’s purchased more antibiotic courses than controls (6.32 versus 6.25), but the controls were hospitalized more often due to bacterial infections (0.19 versus 0.16).

The strongest connection to Parkinson’s was found for exposure to oral macrolides and lincosamides, two different classes of antibiotics that target different types of bacteria and work by preventing bacteria from producing the proteins they need to survive.

Further analyses showed that exposure to broad-spectrum antibiotics such as tetracyclines, and those that specifically target anaerobic bacteria, were associated with an increased risk of Parkinson’s disease within 10 to 15 years.

In addition, other types of antibiotics, such as sulfonamides and trimethoprim, and antifungal medications, were found to be associated with an increased risk of the disease within one to five years.

“Although no conclusions regarding causality can be made, it is plausible that oral antibiotic exposure is one factor that makes the gastrointestinal tract more susceptible to [Parkinson’s] pathology,” increasing the risk of getting the disease, the researchers said.

“Our findings demand confirmation in different cohorts. However, if confirmed in future studies, a connection between commonly prescribed oral antibiotics and neurodegeneration could have major implications for prescribing practices and public health,” they added.

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New Large-Scale Data Portal Will Promote Parkinson’s Treatment Development

data portal

The Accelerating Medicines Partnership (AMP) for Parkinson’s (PD) has opened a data portal with de-identified information from 4,298 Parkinson’s patients and healthy control subjects for use by scientists seeking new treatments for the progressive neurodegenerative disease.

With unprecedented access to a data pool of this scale, investigators now can examine intricate data sets and conduct full-scale genomic analyses.

“AMP PD is a true example of the whole being greater than the sum of its parts,” said Walter Koroshetz, MD, director of the National Institute of Neurological Disorders and Stroke (NINDS), in a press release. “The combination of many data sets could allow researchers greater power to analyze potential biomarkers for Parkinson’s disease. This effort follows other AMP programs which have the shared goal of changing the way we go about the business of studying disease.”

Launched in 2014, the AMP is a public-private partnership between the National Institutes of Health (NIH), the U.S. Food and Drug Administration (FDA), multiple biopharmaceutical and life sciences companies, and non-profit organizations. Its goal is to transform the current model for developing new diagnostics and therapies by collaboratively identifying and validating promising biological treatment targets. The overarching mission is to develop new diagnostics and therapies relatively faster and at less cost.

Initial projects included Alzheimer’s disease, Type 2 diabetes, and rheumatoid arthritis, and lupus.

Last January, the AMP project on PD was launched. Managed by the Foundation of the National Institutes of Health (FNIH), the project includes the NIH, FDA, the Michael J. Fox Foundation (MJFF) for Parkinson’s Research, Celgene, Verily Life Sciences, Pfizer, Sanofi and GSK.

This project’s aim is to speed therapy development by providing the expertise and support necessary to learn which biomarkers demonstrate the most promise for predicting PD and disease progression. Biomarkers are molecular disease indicators.

“One important part of this platform is that, in addition to providing a place for storing complex data, we are also providing the tools to analyze that data within the platform itself,” said Debra Babcock, MD, PhD, NINDS program director and co-chair of the AMP PD steering committee. “In this way, we are bringing scientists to the data, which will increase opportunities for collaboration.”

Data in the officially named AMP PD Knowledge Portal was collected through the MJFF, NINDS and several other programs, studies and institutions. It includes information from samples of DNA, RNA, plasma, and cerebrospinal fluid, which is the liquid that surrounds the brain and spinal cord. The portal also offers a platform that can assimilate additional types and sources of data. For example, there is an upcoming study involving proteomics, the large-scale study of proteins.

With the longitudinal data in the portal, scientists can study patients’ information throughout the disease course. And, the data have been harmonized, allowing for comparison of information from different programs, and providing best practices for how to incorporate into the platform data from the PD community.

“The AMP model has provided a unique platform for bringing together diverse patient cohorts, advances in technology and scientific expertise to study Parkinson’s disease on a scale that has not been attempted before,” said David Wholley, senior vice president, research partnerships, FNIH. “With the AMP PD Knowledge Portal, we are helping the scientific community worldwide to fast-track discoveries that we hope will ultimately help Parkinson’s disease patients and their families.”

Scientists may visit this site to apply for access to the knowledge portal and interact with the data set.

Globally, roughly 7 to 10 million individuals have Parkinson’s, the second most common neurodegenerative disorder after Alzheimer’s disease.

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Sunovion Re-Submits Approval Request for APL-130277 to FDA for Treating Parkinson’s Off Periods

APL-130277 fda resubmission

Sunovion Pharmaceuticals has re-submitted a new drug application (NDA) to the U.S. Food and Drug Administration (FDA), once again seeking the approval of its below-the-tongue formulation of apomorphine — called APL-130277 — for Parkinson’s off periods.

The re-submission is a follow-up to the FDA’s “complete response letter” from earlier this year, in which the agency requested additional information — but no new clinical trials — before deciding whether to approve APL-130277.

The new submission includes additional analysis of clinical data, and information about the intended packaging of APL-130277, according to Sunovion.

Off periods in Parkinson’s are characterized by the reappearance or worsening of symptoms such as tremors and dyskinesia, or involuntary movements. These effects are due to a gradual decline in the effectiveness of levodopa, which is the first-line therapy for the neurodegenerative disease. About half of all patients on levodopa experience off episodes, which, although frequent in the morning after awakening, may occur multiple times throughout the day. These episodes become more frequent and severe as the disease progresses.

In the U.S., people with Parkinson’s currently have only Apokyn (apomorphine hydrochloride), developed by US WorldMeds, as an approved medicine for off periods. A form of apomorphine, the medicine is able to quickly penetrate the brain, where it stimulates dopamine receptors to provide short-term relief. However, Apokyn’s subcutaneous, or under-the-skin delivery may cause pain and injection-site reactions.

APL-130277 is a sublingual or under-the-tongue formulation of apomorphine, which may be easier for patients to take. It is intended to provide on-demand and fast-acting lessening of all types of off episodes — meaning those that are unpredictable, those that occur at the end-of-dose, or those occurring after awakening in the morning.

The therapy was designed to be administered up to five times a day, with a minimum of two hours from the prior dose.

This new formulation of the medication contains a two-layer film — one with apomorphine and the other with an acid neutralizer to improve absorption and reduce oral irritation. Compared with Apokyn, APL-130277 is less likely to induce nausea due to a more gradual absorption.

The new drug application for APL-130277, first filed in April 2018, was supported by a 12-week, double-blind Phase 3 trial (NCT02469090). The results showed that, within 30 minutes of dosing, APL-130277 induced a clinically meaningful reduction in the Movement Disorder Society Unified Parkinson’s Disease Rating Scale Part 3 score, a measure of Parkinson’s motor symptoms, in comparison with placebo.

The benefits were seen as early as 15 minutes after dosing and were maintained for 90 minutes. Improvements were still detected at weeks four, eight and 12. A higher percentage of patients achieved a full-on response — or control of motor symptoms — within 30 minutes with APL-130277.

“OFF episodes in people with Parkinson’s disease can occur at any point throughout the day, often occurring in the morning after awakening and periodically throughout the day and can disrupt the ability to perform everyday activities,” Antony Loebel, MD, president and CEO at Sunovion, said in a press release.

“We look forward to continuing our dialogue with the FDA during the review period with the intention of bringing a much needed on-demand treatment option for OFF episodes to those living with Parkinson’s disease.”

An ongoing open-label extension study (NCT02542696) is testing the safety and tolerability of APL-130277 when used in the long-term. The trial is still recruiting at Los Angeles and at some European sites. More information can be found here.

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Researchers Identify Gene Networks Underlying Parkinson’s Development

STMN2, Parkinson's

Researchers have found new gene networks associated with the development of Parkinson’s disease, which may help them understand the underlying mechanisms of this neurodegenerative disorder and identify potential new therapeutic targets.

The study, “The landscape of multiscale transcriptomic networks and key regulators in Parkinson’s disease,” was published in the journal Nature Communications.

Parkinson’s disease is a neurodegenerative disorder characterized by the impairment or loss of nerve cells (neurons) responsible for producing dopamine — a chemical messenger that transmits nerve signals from one neuron to another and plays a role in many basic functions of the brain, such as movement control, reward, and memory.

The substantia nigra, a brain region that controls balance and movement, is the most affected brain area during Parkinson’s progression, with the greatest extent of nerve cell death.

Some cases of Parkinson’s are directly caused by genetic mutations (more than 20 mutations have been reported), but these cases are rare. In most cases, about 80%, the origin of the disease is unknown. However, Parkinson’s is suspected to result from a complex interplay between multiple genes and environmental factors.

In the study, researchers at the Icahn School of Medicine at Mount Sinai sought to investigate the complex network of genes involved in Parkinson’s and how they interact with each other to drive the disease.

“This study offers a novel approach to understanding the majority of cases of Parkinson’s,” Bin Zhang, PhD, a professor and director at the Icahn School of Medicine, and one of the senior authors of the study, said in a press release.

“The strategy not only reveals new drivers, but it also elucidates the functional context of the known Parkinson’s disease risk factor genes,” Zhang added.

The development of high-throughput molecular profiling techniques has advanced the research of complex diseases. It has helped scientists uncover patterns of gene activity and regulation, and find links between them that point to novel pathways and genetic targets for certain diseases.

Supported by the National Institutes of Health and the Accelerating Medicines Partnership – Alzheimer’s Disease program, Zhang and his team developed a method to analyze large datasets collected from patient samples, called multiscale gene network analysis (MGNA), which they had applied to understand complex diseases, ranging from Alzheimer’s to cancer.

The team used MGNA to analyze a combined data set of eight studies that included postmortem samples of the substantia nigra of 83 Parkinson’s patients.

By comparing this data with that of 70 controls who did not have Parkinson’s, the scientists identified a number of key genetic regulators that had not been associated with the disease before.

One of the genes — called STMN2 — stood out as a key regulator of the Parkinson’s molecular network. The gene is normally active in neurons that produce dopamine, providing instructions for making a protein called stathmin 2. The analysis revealed that STMN2 was down-regulated in the brains of people with Parkinson’s.

To directly test the effects of STMN2 on Parkinson’s disease, the team genetically engineered mice to dampen the activity of STMN2 in the substantia nigra as a way to mimic what happens in the brain of human patients.

This manipulation “turned on” nine genes known to increase the risk of Parkinson’s disease, and mice developed Parkinson’s-like symptoms such as a loss of dopaminergic neurons in the substantia nigra and an increase in toxic clumps of alpha-synuclein protein, two hallmarks of the disease.

The animals also had trouble in motor tasks such as maintaining balance — suggesting that they were impaired in their ability to control movements, which resembled Parkinson’s motor symptoms.

Although the findings need to be validated in larger studies, “The work opens up a new avenue for studying the disease,” said Zhenyu Yue, PhD, a professor and director at the Icahn School of Medicine and one of the senior leaders of the research.

“The new genes we identified suggest that new pathways should be considered as potential targets for drug development, particularly for idiopathic [of unknown cause] Parkinson’s cases,” he added.

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Staying Strong Despite Our Parkinson’s Challenges

courage

This column is about strength and how we endure despite our challenges with Parkinson’s.

As politician and actor Arnold Schwarzenegger once said, “Strength does not come from winning. Your struggles develop your strengths. When you go through hardships and decide not to surrender, that is strength.”

We often feel weak and tired. Our bodies can’t move in the ways they once could. We can’t exert ourselves the way we used to. Though physically we may feel that we are losing ground with Parkinson’s disease, we persevere, putting one foot in front of the other as we keep moving forward.  

Our abilities are stronger than our disabilities

When we have Parkinson’s disease, we are considered disabled. Our movements, our senses, and our abilities to engage in the activities we once enjoyed may be limited or impaired. We can feel that we are powerless against a force that seeks to destroy us.

However, we are strong despite this disease. Though our physical strength might wane, we summon our mental and emotional resources to push onward. We are resilient and unrelenting in our determination to win our battle with this disease.

I believe that people with a chronic disease such as Parkinson’s often have a greater tendency than others to exhibit a positive attitude. We have been forced to face our mortality, and as a consequence, we can be more open and see clearly the daily blessings bestowed upon us.

A positive attitude brings life into a room

Negativity is replaced with optimism and laughter. Having a positive attitude is a sign of strength of character. When things are on the downturn, we are looking for a way up and out. A positive attitude is a frame of mind that says “I can” instead of “I can’t.” We believe that “it’s possible” rather than “impossible.”

Strong people are grateful despite their circumstances and know how to encourage others because of what they have been through. They continue on their journey, bringing hope to others and light to the dark places.

Do you shine light into the lives of others? I hope that I do. 

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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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Compound That Protects Mitochondria May Be Possible Therapy Candidate for Parkinson’s, Study Suggests

Miro1, Parkinson's

A small molecule that can protect the function of mitochondria — known as the powerhouses of cells — and prevent cell death can also prevent brain damage in a rodent stroke model, highlighting its potential as a possible therapeutic candidate for neurodegenerative disorders such as Parkinson’s disease, a study has found.

The results were published in an article, “A small molecule protects mitochondrial integrity by inhibiting mTOR activity,” in the Proceedings of the National Academy of Sciences.

Although the exact trigger for Parkinson’s disease remains to be identified, research indicates that its causative mechanism involves genetics, problems in the mitochondria, and oxidative stress — an imbalance between the production of harmful free radicals and the ability of cells to detoxify, which results in cellular damage.

Taken together, these molecular and cellular changes eventually lead to the death of dopamine-producing neurons, the type of nerve cell that is gradually lost in Parkinson’s disease.

Mitochondrial dysfunction can lead to many diseases including neurodegenerative ones. Damage in the cell’s powerhouse triggers a natural process inside the cell, known as apoptosis (or programmed cell death), with the ultimate goal of killing that same cell.

Using a lab model that mimicked the activation of damaged mitochondria-induced apoptosis, researchers at Tsinghua University, in China, were able to screen and identify compounds that could block cellular death by protecting mitochondrial integrity and function.

One small molecule, which scientists called compound R6, was found to block apoptosis by inhibiting the release of cytochrome c and protect both mitochondrial integrity and function.

Cytochrome c is a protein that is released by the mitochondria and initiates apoptosis following the reception of an apoptotic stimulus, functioning like a “go” signal for the cell to initiate its own destruction.

In addition to inhibiting the release of cytochrome c, Compound R6 also prevented apoptosis by inhibiting another major cellular signalling pathway, called mTOR. This induced the activation of autophagy, a process by which the cell removes unnecessary or dysfunctional components and, in contrast to apoptosis, does not result in cell death.

Scientists then tested Compound R6’s therapeutic potential in a rat model of stroke. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is blocked by a clot or it bursts. As a result, the part of the brain that is irrigated by that vessel cannot get the blood (and oxygen) it needs, resulting in the death of nerve cells.

Compound R6 was able to cross the blood-brain barrier after being administered via an intraperitoneal (through the abdominal wall) injection. The blood-brain barrier is a semipermeable membrane that protects the brain against the external environment, and is a major barrier for the efficient delivery of certain therapeutics that need to reach the brain and central nervous system.

Animals that were given Compound R6 showed significantly less neuronal injury than rats without such pre-treatment after a stroke was induced in them. These neuroprotective effects were dose-dependent, with higher (25 mg/kg ) doses having a bigger protective effect than smaller ones (12.5 mg/kg).

“Given increasing appreciation that mitochondrial damage affects the etiology [cause] of several common and devastating neurodegenerative diseases, Compound R6’s ability to pass the blood-brain barrier and confer strong anti-apoptotic effects should encourage preclinical and medicinal chemistry research efforts, perhaps even extending (…) into evaluation of possible anti-aging effects,” the researchers wrote.

Compound R6’s molecular and cellular benefits make it a promising potential therapeutic candidate for age-related diseases, such as stroke and Parkinson’s, where mitochondrial damage plays a key role, the researchers said.

This is not the first time that they have found a molecule able to block cell death. Three years ago, they found a molecule, named Compound A, that could halt the death of dopamine-producing neurons by a different mechanism than that of R6, in a rat model of Parkinson’s disease.

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Parkinson’s Limits Ability to Read Emotional Changes in Faces, Small Study Finds

emotions and expressions

Changes in facial expression are limited by Parkinson’s disease, and people with PD also are less able than others to read emotions expressed through facial changes or shifts in eye gaze, a study suggests.

Its researchers say this “impaired emotion recognition” may be related to problems patients have with social communication and empathy.

The study, “Measuring emotion recognition by people with Parkinson’s disease using eye-tracking with dynamic facial expressions,” was published in the Journal of Neuroscience Methods.

People with Parkinson’s often lack strong facial expressiveness, a condition sometimes referred to as facial masking or hypomimia. This can affect both their ability to express themselves and to recognize emotions in someone else, based on the idea that we recognize the emotions of others, in part, by mimicking them ourselves.

“The loss of facial movement in PD may therefore contribute to difficulties in recognising facial expressions of emotion,” the researchers, all with the University of Manchester, wrote.

Some studies have suggested that people with PD have difficulty recognizing emotions in others, but many of those studies tended to use static (unmoving) images of people’s faces.

Movement is a critical component of facial expressions —  studies in young healthy adults suggest that it is generally easier to recognize emotion in a face that’s changing than a still one.

The researchers set out to investigate how motion impacts the ability to recognize facial expressions in people with PD.

They assembled two groups of people — one with mild to moderate idiopathic PD (17 people, mean age 63.2), the other without (9 people, mean age 71) — to view either static images or moving video of people making facial expressions of basic emotions (happiness, sadness, disgust, anger, surprise, or fear). The participants then had 10 seconds to select the appropriate emotional label.

Overall, there was a higher rate of correct emotional recognition for moving or dynamic than static faces (91.92% vs. 89.88%).

The type of emotion being displayed also significantly impacted recognition accuracy: except for anger, there was a lower overall accuracy for fear compared to all other expressions.

Researchers also calculated the effect of motion based on mean deviation (MD), which is essentially a measure of how different one set is from the overall average — in this case, moving faces compared to all faces, moving or not — with values further from zero indicating a greater difference.

In the non-PD group, dynamic faces had a significant impact on participants’ ability to recognize emotion, as evidenced by a mean deviation of 5.71. But among Parkinson’s patients, MD was zero — suggesting that movement did not at all aid their ability to recognize emotions via changing facial expressions.

The researchers also used eye tracking to measure where participants were looking as they completed their tasks, but no significant differences were found between the groups. This suggested that the participants tended to look at the same facial regions to detect emotional cues, regardless of whether they had PD or not.

Significant differences in viewing patterns were noted when participants looked at dynamic and static faces. When viewing dynamic faces, they tended to focus on certain areas — particularly the mouth — for longer stretches of time. Again, this pattern was generally similar in both groups.

“Consistent with findings from healthy young adults, we found higher accuracy rates for recognition of dynamic compared to static facial expressions in a control group of healthy older adults,” the researchers wrote. “In contrast, the PD group showed no significant advantage for dynamic expressions.

“This suggests that the loss of facial expressiveness in PD may impact upon the ability to utilise motion as a cue to facial emotion recognition.”

These researchers noted their study was very small and its results cannot be reliably generalized; its size may mean it’s not  statistically powerful enough to detect subtle differences. In particular, they highlighted that there were many person-to-person differences, particularly in the PD group, that likely limited their ability to find significant differences between the groups as wholes. Further research is recommended.

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Understanding the Relationship as Sanctuary

relationship

The healing relationship holds a sacred place for people as they search for a path to well-being moments. This relationship offers every possibility for allowing those moments to occur. It is a safe place and a sanctuary that aims to facilitate and bear witness to the experience of well-being.

The healing relationship starts with an agreement to enter the compassion space for the purpose of exploring well-being. Some people enter the compassion space almost effortlessly and without a great deal of resistance. Some move to experience well-being in the compassion space quickly, while others take longer. Understanding how to sit with resistance and eventually let go is part of the relationship as sanctuary.

Resistance can be more intense with relationship sanctuary than with sanctuary formed in connection to a place. So many deep emotions — good and bad — are tied to the memories of our relationships. We enter the healing relationship with a “relationship stance” built upon our history. Within that stance is resistance to sanctuary.

Working with a healer or a guide as a form of relationship sanctuary can be helpful. An experienced guide can show you your resistance obstacles, teach you to move around them, and help you to experience a well-being moment.

Finding healing relationships while battling a chronic illness is tough, but necessary. We are by nature social creatures and our health benefits from nurturing relationships. I long for conversations that explore the sacredness of life rather than the sickness of strife. Chronic illness consumes much of my time, but it does not define me. I’ll always have time for stimulating discourse.

Everything seems so rushed these days. Henry David Thoreau said there was no need for people to travel so fast on those locomotives going 25 mph. I giggled, and then thought that we are still going fast. Relationships are affected by a technological train that steamrolls into our lives without conscious consent. Texts, tweets, and obligatory holiday visits give us brief glimpses of those we love as they go dashing about their lives.

I don’t dash any more. Well, maybe to that emergency bathroom call, but not much else. I remember when I used to dash, both mentally and physically. I can’t push hard like that anymore. Stress hit me hard with the progression I experienced following the ruin of stagnation.

My disease took a turn for the worse this summer. It wasn’t a big crash into a tree, but a noticeable bump in the road. The ruin of stagnation was part of the progression. Everything is more difficult than it was three months ago. It’s hard to share all of this in a way that doesn’t come across as a pity party.

The relationship as sanctuary is a compassion space for me to be heard, understood, welcomed, and embraced. My partner does this day in and day out without complaint. I get tired of being with myself more often than that.

Relationship as sanctuary has been my life’s work. I find that the more I learn, the less I seem to know. It’s an old saying, but it is deeply poignant when applied to the sacred quality within the healing relationship. It is the best thing that I do as a human being in my service to humanity.

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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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Glassy Carbon Electrodes Safer Than Metal in MRIs, Study Suggests

glassy carbon electrodes

Implantable electrodes made of glassy carbon may be safer for use in MRI scans than traditional electrodes made of metal for people who undergo deep brain stimulation, a new study shows.

The study, “Glassy carbon microelectrodes minimize induced voltages, mechanical vibrations, and artifacts in magnetic resonance imaging,” was published in Microsystems & Nanoengineering.

In cases where Parkinson’s patients are not responding well to medication, deep brain stimulation (DBS) can be used to treat motor symptoms associated with this neurodegenerative disease. The treatment involves surgically implanting an electrode directly in the brain, then using that electrode to electrically stimulate specific brain regions.

Traditionally, electrodes used for DBS have been made of metal, most typically platinum. But metal electrodes pose a problem when a person needs to undergo an MRI scan. Such scans can be used to image the brain using powerful magnets, but those magnets can interact badly with metal electrodes.

Specifically, the electrodes can lead to large “white spots” on the MRI images themselves, which can limit the utility of the images. Plus, the magnetic fields generated in MRI can cause electrodes to vibrate, or they can generate electrical currents that make the electrode heat up. These circumstances run the risk of causing damage or irritation in the brain.

In the new study, researchers wondered if electrodes made of glassy carbon, instead of metal, would be resistant to these issues. Glassy carbon (GC) is basically a bunch of very thin layers of carbon pressed together.

The researchers previously had created GC-based electrodes designed for DBS, and in a previous study, they showed that these electrodes were more durable than traditional platinum ones.

“Inherently, the carbon thin-film material is homogenous—or one continuous material—so it has very few defective surfaces. Platinum has grains of metal which become the weak spots vulnerable to corrosion,” Sam Kassegne, PhD, a professor at San Diego State University (SDSU) and co-author of both studies, said in a press release.

The researchers tested their GC electrodes in an MRI; but, rather than using actual human brains, they implanted the electrodes in a substance sort of like Jell-O. The researchers demonstrated that, while the metal electrode created a bright white patch on the MRI images themselves, the CG was nearly invisible — suggesting that, in an actual brain, this type of electrode would interfere with imaging far less.

They measured the currents generated in these electrodes during an MRI scan, as well as how much they vibrated, and compared these measurements to similar measurements obtained using traditional metal probes.

They found that the current generated in the GC electrodes was about 10 times lower than that in the metal probes. Similarly, vibrations in the GC electrode were about 40 times weaker than those in the metal ones, Researchers noted, however, that “for both types of microelectrodes, the measurable forces were below the detection limit” — that is, the vibrations were very small for both, even if they were smaller for the GC electrode.

“Our lab testing shows that unlike the metal electrode, the glassy carbon electrode does not get magnetized by the MRI, so it won’t irritate the patient’s brain,” said Surabhi Nimbalkar, study co-author and doctoral candidate at SDSU.

Although the researchers noted that they did not directly assess heating of the electrodes, which may be an avenue for further study, they nonetheless concluded that “GC microelectrodes demonstrate superior behavior with respect to MR safety compared to [platinum]-based electrodes.”

“Since GC has recently been demonstrated to have a compelling advantage over other materials for neural stimulation (…), this MRI compatibility validated in this study offers an additional advantage for long-term in vivo use in clinical settings,” they wrote.

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