Sometimes Grace Hurts

faith

Sherri Journeying Through

Steven Curtis Chapman said it best:


”I don’t even wanna breathe right now
…I don’t even wanna be right now
I don’t wanna think another thought
…I don’t wanna feel this pain I feel 
[but] right now, pain is all I’ve got.”

It was a hard day.

I waved goodbye to my son, his wife, and my two grandchildren as they drove down the street. They were heading north to a new home, new jobs, a new life. Twelve hours away instead of 12 minutes. My two grandchildren — one 5, the other 1 — I had watched almost every day. All day.

I helped those little ones learn to walk. Eat with a spoon. Drink from a cup. I sat in that rocking chair over there and rocked them to sleep. Sang them songs. I read to them the story about the pants with nobody inside of them, by Dr. Seuss. I held them when they were sick or well or when they just wanted to be held. We jumped in puddles, planted flowers, played games, went for walks.

I sat at that table over there and played games with “Boo.” We colored, we painted, we had tea parties. Then my son announced a new job opportunity and you can guess the rest. That’s why I stood outside on that summer morning, waving goodbye to a car filled with oh-so-precious ones.

I went to the rose garden later, and everywhere I walked, I heard Boo. I saw her chasing blackbirds. I heard her excitement upon finally seeing the elusive jackrabbit we’ve been tracking for months.

The next day, I worked in the garden and watered her row: larkspur, bachelor buttons, poppies. She was so proud of her little garden. I worked out there all day. I worked until I couldn’t move. I worked so I didn’t have to think. I watered the ground with tears.

The following day, I still couldn’t move because I moved too much the day before. I had lost mobility and gained pain. I sat on the couch and worked on pictures and cried. My grandchildrens’ smiles fill my digital albums; I could almost hear the giggles behind those smiles.

The next day, I felt like I was locked in a blackened room — hopeless, lost, empty — weeping for lost things. And it felt like my heart was breaking in two. The crack in my heart a week before was now a massive crevice. The strength that held me together became jello.

God, how am I going to do this? I whispered through tears I hadn’t spilled out so hard in so long.

My head told me those two little ones were not mine to hold onto. I was not even their parent. Can a grammy love her little grandchildren so much? Yes. She most definitely can.

I sat on the bathroom floor. I cried more and through the tears, whispered, God, I lived for those kids.

They were my daily dose of laughter, love, smiles, hugs, and joy. God used those little ones to bless me over and above in so many ways never deserved. I viewed them as little disciples, and we talked about God everywhere we went. In everything we did.

How I found the energy to do it every day, only God knows. I napped when they napped and again when they went home. I fought through the pain within my body and never refused to hold them or change diapers, even when I didn’t think I could stand the pain another minute. I was determined not to let Parkinson’s dictate my life, but my body was screaming to let go. My heart was screaming to hold on. My head was saying it was time. Time to listen to the body. The disease that strives to claim more ground with each passing day was doing its job. It was time to let go.

The grace of God intervened. Sometimes grace hurts. That still, small voice that you can hear because you’re not busy making incessant chatter. The comforting, life-giving voice of God.

God, I lived for those kids, I had whispered through tears. And before I could go on to the next thought of despair, He whispered back, “Live for me.

Uncontrollable sobbing became controlled. The tears dried up as a tiny ray of sunshine, a tiny grain of hope took hold deep inside my heart — the crevice began to close. A few more tears fell, not from grief but because of grace. The grace of God. The trustworthy grace of a merciful God.

I don’t know what living for Him looks like in the days ahead as I live this life with Parkinson’s disease, but as I live for Him, I will trust Him completely. I’ve been through too much in my lifetime to do anything less.

As I said, Steven Curtis Chapman says it best: “Even when I don’t understand, even then I will say …
 You are my God, and I will trust You.”

Through losses, heartaches, pain, diseases, we can trust Him.

***

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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Working Memory Problems Tied to Binge Eating in Patients on Dopamine Replacement Therapy

binge eating and Parkinson's

Deficits in short-term memory, known as working memory, may underlie the compulsive “binge eating” observed in some Parkinson’s patients undergoing dopamine replacement therapy, a new study suggests.

The research “Reward sensitivity in Parkinson’s patients with binge eating” was published in the journal Parkinsonism and Related Disorders.

Parkinson’s patients using dopamine replacement therapy are at risk of developing impulse control disorders such as binge eating — consuming large portions of food, often quickly, without being able to stop and to the point of feeling uncomfortably full.

These disorders are reported to occur in 3.5% to 42.8% of patients, and likely reflect the interaction of dopaminergic treatments (dopamine agonists and/or dopamine replacement therapy) with the patient’s susceptibility and the underlying neurobiology of Parkinson’s.

Researchers at Scuola Internazionale Superiore di Studi Avanzati, in Trieste, Italy, investigated possible causes for this compulsive behavior in these patients.

They found that difficulties with “working memory,” a brain function that allows people to keep past information about an action — like eating until satisfied — in mind while carrying out that action, and in alterations to so-called reward sensitivity mechanisms are the causes underlying this behavior.

“Binge eating may affect different Parkinson’s patients as a side effect of dopaminergic drugs which they need to take,” Damiano Terenzi, the study’s first author, and Marilena Aiello, a research coordinator, said in a press release.

“In literature, impulse control disorders, such as hypersexuality or gambling, have often been described in Parkinson’s disease and associated to an alteration of working memory and of reward sensitivity. On binge eating, it has never been investigated,” they said.

Reward sensitivity is mediated by two factors: “liking,” a factor that measures the pleasure associated with a specific action, in this case eating; and “wanting,” the drive or desire to repeat the action linked to a pleasure sensation.

Researchers recruited Parkinson’s patients with and without binge eating disorders, and healthy people to serve as controls. All were assigned a number of tasks related to food liking and wanting.

Participants began the study by responding to prompts that distinguished their degree of liking and wanting different foods.

The visual stimuli used were high-quality colored photographs depicting items related to foods and those depicting unrelated items. The team selected sweet and salty foods, among those more frequently consumed by an independent sample of Parkinson’s patients. Sweet and salty foods were matched according to their frequency of consumption and tastiness.

Researchers then measured patients’ affective reactions towards foods (liking), and their motivation for food rewards (wanting).

Results showed that Parkinson’s patients who were binge eaters displayed an altered liking for sweet foods but not an increased wanting.

When measuring liking through patients’ attitudes and reactions — but not conscious reflection — binge eaters showed a negative attitude toward sweet food compared to controls, which the researchers said was “is in line with studies reporting a less positive attitude for palatable foods in individuals with eating alterations.” Importantly, this difference seemed to emerge only when implicit measures were used, while no differences emerged in self-report ratings of liking and wanting.

As with unsuccessful dieters, sweet foods are seen to pose a particular challenge for binge-eating Parkinson’s patients. As researchers noted, patients with impulse control disorders “frequently report preoccupations, the inability to control the urges or impulses … that arise to act on these urges.”

Patients with binge eating did not exhibit an increased “wanting” of food, a result that seems to contradict previous studies. This result was possible because the tasks used to measure “liking” and “wanting” failed to capture changes in food incentive salience, and that binge eating in Parkinson’s patients “is preferably associated with altered liking for rewards or … with affective abnormalities.” The team found an association between binge eating and depression in this patient population.

Most importantly, researchers also found that a potential deficit in working memory — a cognitive function — may underlie binge eating in Parkinson’s patients, making them unable to stop eating uncontrollably.

According to researchers, “this study gives precise indications about the mechanisms that are altered in binge eating in Parkinson patients. It is a first and important step to understanding its origins.”

“Other surveys must be conducted to confirm and explore this evidence regarding a behaviour which not only heavily affects the quality of life of patients but also exposes them to serious long-term consequences for their health, such as weight gain and related diseases,” the researchers concluded.

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Eating More Fish Could Help Prevent Toxic Protein Aggregates in Neurological Disorders, Study Shows

fish Parvalbumin alpha-synuclein

A protein abundant in fish, called β-parvalbumin, can prevent alpha-synuclein aggregation, which is a hallmark of Parkinson’s disease and other neurological disorders, according to a recent study.

This suggests that eating more fish may help prevent toxic events associated with alpha-synuclein aggregation and progression of several neurological diseases.

This finding was reported in the study, “Abundant fish protein inhibits α-synuclein amyloid formation,” published in the journal Scientific Reports.

Fish has long been regarded as a healthy food, linked to improved long-term cognitive health. These benefits are often assumed to come from the high content of omega-3 and omega-6 fatty molecules in the fish. However, scientific evidence to support this hypothesis is controversial, and other molecules could be involved.

To study this, researchers at Chalmers University of Technology in Sweden evaluated the potential role of β-parvalbumins in human health. This protein is present at high levels in most fish species and has been recognized as the main trigger of allergic reactions in patients sensitive to fish.

Researchers found that when β-parvalbumin and alpha-synuclein are in contact, they can interact and form new aggregates, preventing alpha-synuclein from reacting with itself and forming the toxic amyloid plaques that are the basis of several neurodegenerative diseases.

“Parvalbumin collects up the ‘Parkinson’s protein’ [alpha-synuclein] and actually prevents it from aggregating, simply by aggregating itself first,” Pernilla Wittung-Stafshede, PhD, professor and head of the chemical biology division at Chalmers and lead author of the study, said in a press release.

Herring, cod, carp, and redfish, including sockeye salmon and red snapper, have particularly high levels of parvalbumin. Notably, the levels of parvalbumin can also vary widely throughout the year.

“Fish is normally a lot more nutritious at the end of the summer, because of increased metabolic activity. Levels of parvalbumin are much higher in fish after they have had a lot of sun, so it could be worthwhile increasing consumption during autumn,” said Nathalie Scheers, PhD, assistant professor in the department of biology and biological engineering.

This finding sheds new light on the health benefits of fish consumption, not only adding new knowledge on ways to prevent neurological damage caused by amyloid aggregation, but also possible new therapeutic options for several diseases, including Parkinson’s, amyotrophic lateral sclerosis (ALS) and Huntington’s disease.

“These diseases come with age, and people are living longer and longer. There’s going to be an explosion of these diseases in the future — and the scary part is that we currently have no cures. So we need to follow up on anything that looks promising,” Wittung-Stafshede said.

The team is planning additional studies to further evaluate the potential benefit of β-parvalbumin to treat human diseases. Scheers, together with Ingrid Undeland, a food science professor at Chalmers, is planning a new study to analyze β-parvalbumin from herring and its transport mechanisms in human tissues.

“It will be very interesting to study how parvalbumin distributes within human tissues in more depth. There could be some really exciting results,” Scheers said.

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Intense Exercise Helps Early Parkinson’s Patients Retain Motor Skills, Phase 2 Trial Shows

exercise

High-intensity exercise is not only safe and feasible, but it can also delay disease progression in early stage Parkinson’s patients, results of a Phase 2 trial report.

The study, “Effect of High-Intensity Treadmill Exercise on Motor Symptoms in Patients With De Novo Parkinson Disease,” was published in the journal JAMA Neurology.

SPARX, or a Study in Parkinson Disease of Exercise (NCT01506479), was a Phase 2 multicenter trial led by researchers at the University of Colorado’s UC Health. It addressed if high-intensity exercise was safe for people in very early stages of the disease, and what physical intensity might be of most benefit to them.

It enrolled 128 people with early Parkinson’s disease, between 40 and 80 years old and diagnosed within five years. None were   taking any Parkinson’s medications.

Participants were randomly assigned to one of three groups — moderate exercise, vigorous exercise, or usual care — for six months.

Disease progression was assessed at the study’s start and again after six months using the Unified Parkinson’s Disease Rating Scale (UPDRS) Motor Score: the higher the score, the greater a patient’s motor disability.

Exercise intensity was measured using heart rate monitors at all workout sessions.

People in the moderate group engaged in treadmill exercises four times a week, bringing their heart rate up to 60 to 65 percent of maximum capacity. Those in the vigorous group also exercised on a treadmill with the same frequently, but brought their heart rates to 80 to 85 percent of maximum.

At six months, the UPDRS score for the high-intensity exercise group had barely changed, indicating these patients’ motor skills did not worsen.

But these scores rose on average by 8 percent among patients in the moderate exercise group, and by 15 percent in those given usual care, indicating a worsening in movement and motor skills in these people. 

No serious side effects were reported in any group, and adverse events were considered “anticipated,” the researchers wrote, including falls, pain, muscle and joint disorders.

These results show that high-intensity exercise can preserve movement abilities in early stage Parkinson’s patients and can do so safely if exercise programs are guided by specialists.

They also warrant further investigation in a Phase 3 trial evaluating more fully the benefits of regular high-intensity exercise in Parkinson’s patients, the team said.

“The study shows that neurologists can rest assured that it’s safe and feasible for their patients to exercise at a high intensity. That’s huge. We can get people started right away on exercise habits, when that is easier to do,” Margaret Schenkman, director of the Physical Therapy Program at the UC School of Medicine, and principal investigator for the SPARX study, said in a UC Health news release.

Previous studies have shown that exercise can help Parkinson’s patients maintain balance, mobility, and the ability to perform daily routines while preserving a better quality of life.

But studies to date have only tested moderate exercise programs, and most have not addressed whether exercise intensity might affect disease severity or its progression.

 

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Peptron, NIH Establish Agreement to Develop SR-Exenatide for Neurodegenerative Diseases

Peptron SR-exenatide

Peptron recently obtained an exclusive worldwide license of intellectual property from the National Institute on Aging (NIA), a National Institutes of Health (NIH) center, covering the delivery and use of sustained-release (SR) exenatide in the treatment of Parkinson’s disease and other neurodegenerative disorders.

The intellectual property was developed as part of a cooperative research and development agreement between Korea-based Peptron and the NIH to create a form of exenatide that effectively crosses the blood-brain barrier and provides sustained release of the neuroprotective peptide to treat Parkinson’s and other degenerative diseases of the central nervous system.

“As experienced leaders in developing sustained-released therapeutics, the scientists at Peptron have enhanced the ability of SR-exenatide to cross the blood-brain barrier and deliver long-acting therapeutic effects of the neuroprotective peptide,” Ho-Il Choi, PhD, CEO and director of Peptron, said in a press release. “Neurodegenerative disorders, such as Parkinson’s and Alzheimer’s diseases, remain a great unmet medical need for millions of people around the world, and we are dedicated to innovating and advancing therapeutics for these life-altering diseases.”

The blood–brain barrier is a highly selective semipermeable membrane that separates circulating blood from the brain and extracellular fluid in the central nervous system, and allows the passage of water, some gases, and molecules.

However, large-molecule and most small-molecule drugs are not able to cross this barrier, making it challenging to deliver therapeutic agents to specific regions of the brain and treat most brain disorders.

SR exenatide is a glucagon-like peptide 1 (GLP-1) receptor agonist, which means it binds to the GLP-1 receptor, involved in controlling blood sugar levels, and promotes its action by enhancing insulin secretion.  GLP-1 receptors are found in the pancreas but also in the brain, and are used to treat Type 2 diabetes by stimulating insulin release.

According to the Cure Parkinson’s Trust, GLP-1 agonists are safe and well-tolerated medications that can mimic the action of human gut hormones, with a more stable profile than the actual hormones.

The systemic insulin resistance typically associated with Type 2 diabetes is also thought to somehow be associated with the onset of Parkinson’s disease, as patients often display impaired glucose tolerance — which then leads to brain insulin resistance.

Because of this link, there has been a growing interest in GLP-1 receptors and exenatide treatment for neurodegenerative diseases, and preclinical studies have shown evidence that exenatide may have beneficial disease-modifying effects.

However, delivering exenatide across the blood-brain barrier to the central nervous system is a major challenge.

Peptron is using part of the proceeds from a convertible bond that raised $24 million to establish a new manufacturing facility in Osang, Korea, equipped to produce SR-exenatide. Funds will also be used to support preparations for a Phase 2 clinical trial of SR-exenatide in Parkinson’s disease and evaluate the peptide in the treatment of Alzheimer’s disease.

“The support we have received from our NIH collaborators as well as our investors has allowed us to make significant progress in advancing a novel proprietary formulation of SR-exenatide to GMP manufacturing and Phase 2 clinical studies in Parkinson’s disease,” Choi said. “Moreover, our new facility enables us to manufacture additional sustained-release formulations of peptide and biologic drugs under GMP conditions to deliver further value in our collaborations with leading pharmaceutical and biotechnology companies.”

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Most Parkinson’s Patients Show Non-movement Symptoms Like Depression, Sleep Problems, Survey Finds

non-movement symptoms

Nearly all Parkinson’s disease patients experience non-movement symptoms, such as sleep disturbances or depression, which affect their quality of life as much as movement-related symptoms, according to an online survey of 700 participants, nearly 600 of whom completed it in full.

Patients’ caregivers are those most likely to detect non-movement manifestations of the disease.

These are the two main conclusion of the online survey, conducted by the Parkinson & Movement Disorder Alliance (PMDAlliance) with the support of Acadia Pharmaceuticals, as part of Parkinson’s Disease Awareness Month.

Of the survey’s respondents, 286 were Parkinson’s patients; 377 were care partners; 10 were noncare partners or family members of Parkinson’s patients; and 27 were categorized as “others.”

The survey, conducted online with members of the PMDAlliance from March 19-31, 2018, revealed that 90% of Parkinson’s patients show non-movement symptoms, manifested as sleep problems (84%), cognitive challenges (75%), anxiety (65%), depression (55%), hallucinations (41%), and delusions (24%).

The negative impact of non-movement symptoms on quality of life was recognized by 84% of the respondents, with nearly half of the patients (49%) finding coping with these symptoms even more challenging that Parkinson’s-related movement symptoms.

The non-movement side of the disease has a generally negative impact on the lives of patients, affecting their social activities with friends and family (70%), intimacy with their partner (68%), and with daily activities, such as household chores (68%) and running errands (67%).

“This survey clearly shows that non-movement symptoms of Parkinson’s disease make it difficult for people with Parkinson’s and their care partners to participate in activities most of us take for granted — running errands, going to the movies, eating out, or simply cooking and cleaning,” Sarah Jones, the CEO of PMDAlliance, said in a press release.

“We urge the entire Parkinson’s community — from the people with Parkinson’s and care partners, to healthcare professionals and support groups — to continue initiating conversations about Parkinson’s symptoms, especially the non-movement ones that greatly impact day-to-day living,” Jones said.

Despite its negative impact on quality of life, care partners detected the non-movement side of Parkinson’s two to four times more than patients themselves.

Hallucinations were observed by 51% of care partners and 23% of patients, and delusions were spotted by 32% of caregivers compared to 8% of patients.

These results both highlight and correlate with literature reporting that non-movement symptoms, like hallucinations and delusions, are often not reported to clinicians — only 10-20% of the cases are actually reported. This may be due to embarrassment or a misunderstanding that the symptoms are associated with the disease, since most of the time devoted to a patient’s visit with a doctor is generally focused on motor symptoms.

Other non-motor symptoms, such as cognitive challenges, anxiety, and depression were more easily detected by caregivers than patients.

“Parkinson’s disease changes how both people with PD [Parkinson’s disease] and care partners think about their future and cope with day-to-day living,” Jones said.

“Care partners are particularly attuned to how the disease is progressing in their loved one, which is why PMDAlliance added new educational resources to our website about the onset and impact of non-movement symptoms of PD,” she said.

“We want to encourage people to report symptoms to their healthcare providers, seek support, and participate in the community. This spring, we’re also hosting several Learn, Live, Connect educational conferences across the country where people can learn more about Parkinson’s disease and its many symptoms,” Jones added.

Doral Fredericks, PharmD (doctor of pharmacy), vice president of medical affairs at Acadia Pharmaceuticals, said Acadia is “honored to partner with PMDAlliance to highlight the impact of non-movement symptoms on both people with Parkinson’s and their care partners.

“We encourage people with Parkinson’s and caregivers to join the effort to raise awareness about this important aspect of Parkinson’s disease,” Fredericks added.

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Molecule from Fat Burning Linked to Protein Clumps That Typify Parkinson’s in Study

acrolein and protein clumps

A molecule created by the brain burning fat for fuel can accumulate in some people and turn toxic, playing a key role in their possibly developing Parkinson’s disease,  researchers at Purdue University report.

These findings, in the study “Acrolein-mediated neuronal cell death and alpha-synuclein aggregation: implications for Parkinson’s Disease” published in Molecular and Cellular Neurosciencecould also aid in earlier disease diagnosis and new treatment discoveries.

The researchers found that acrolein, a byproduct of burning fat — which brain uses as fuel — that  is normally eliminated from the body can promote the accumulation of alpha-synuclein. This buildup, in turn, leads to nerve cell death in the substantia nigra, a brain area crucial for movement control. Damage to nerve cells in this region linked to clumping of the alpha-synuclein protein is a hallmark of Parkinson’s disease.

Using a rat model of Parkinson’s, the team observed that acrolein levels were unusually high in these rats and toxic, leading to  alpha-synuclein clumps in their brains.

Importantly, they also found a molecule that in these animals addressed both the toxic protein accumulation and the disease symptoms linked to it.

“Acrolein is a novel therapeutic target, so this is the first time it’s been shown in an animal model that if you lower the acrolein level you can actually slow the progression of the disease,” Riyi Shi, PhD, the study’s senior author, said in a Purdue news article written by Steve Tally. “This is very exciting. We’ve been working on this for more than 10 years.”

Early promise an animal model, however, may or may not lead to discoveries that help patients. “In decades of research, we’ve found many ways to cure Parkinson’s disease in pre-clinical animal studies, and yet we still don’t have a disease therapy that stops the underlying neurodegeneration in human patients,” said Jean-Christophe Rochet, PhD, a study co-author.

Still, “it’s possible that a drug therapy could be developed based on this information,” Rochet added. “We’ve shown that acrolein isn’t just serving as a bystander in Parkinson’s disease. It’s playing a direct role in the death of neurons.”

The investigators found that hydralazine, a molecule that widens blood vessels and lowers blood pressure  — and is an approved blood pressure treatment, eased behavioral problems in these rats, as well as in healthy rats injected with the compound.

Hydralazine, which scavenges acrolein, was also able to lessen neuronal death and lower levels of rotenone, another Parkinson’s-related toxin. “Luckily, this is a compound that can bind to the acrolein and remove it from the body,” Shi said. “It’s a drug already approved for use in humans, so we know there is no toxicity issue.”

Hydralazine may not be the best choice for Parkinson’s patients, however, due to its effects on blood pressure. But “we may find there is a therapeutic window, a lower dose, that could work without leading to unwanted side-effects,” Rochet said. “Regardless, this drug serves as a proof of principle for us to find other drugs that work as a scavenger for acrolein.”

In fact, the team has already “identified multiple candidates” that might “lower acrolein with similar or greater effectiveness, but without lowering blood pressure,” Rochet added.

This discovery might also allow earlier disease detection, Shi said, as acrolein levels “can be detected easily, such as using urine or blood,” meaning its levels could serve as a biomarker.

“The goal is that in the near future we can detect this toxin years before the onset of symptoms and initiate therapy to push back the disease … [maybe] indefinitely. That’s our theory and goal,” Shi added.

Rochet previously worked with a research team in Norway that showed that salbutamol, a common asthma medicine, could lower Parkinson’s risk by half, according to a University of Bergen 2017 report.

“Evidence suggests that salbutamol acts by a different mechanism than hydralazine — that is, by reducing alpha-synuclein accumulation — and thus perhaps salbutamol and an acrolein-scavenging drug could be used together to achieve an even greater therapeutic effect,” Rochet hypothesized.

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Look for the Pockets of Hope

hope

Sherri Journeying Through

If you’ve flown on an airplane from here to there and the weather was bad and visibility nil, you likely didn’t see much more than a layer of dark, gray clouds. However, every once in a while there is a little hole — a pocket — in which to view the earth below. Under that dark canopy are homes with people and cars driven by other people who are bustling down deserted roads. People who are hurting. People who are rejoicing. People who live with — and without — hope.

I think about being on the other side of that cloud cover where I have often stood under dark, gray clouds and looked up to see a little pocket of sunshine coming through the sky. Sometimes the rays have been so amazing that I often have felt a multitude of angels could come right there and then through that ray of brilliant sunshine. I have stood there, looking upward on those gray days and felt the warmth stream down through those little pockets of sunshine and upon my face. Something happens inside of me. My hope is restored.

I have focused on my surroundings so often that it can be hard to lift my head. However, I have a mighty God who sits enthroned up there where the sun still shines. He looks down below and sees and knows our state of mind and the condition of our spirits. That is why He gives us little pockets of hope, rays of sunshine that shine down upon us with their brilliance in our darkest moments. They encourage us to take a deep breath and focus above and know that God is still God and He is still in control. The little pockets of sunshine encourage us to keep going.

It’s not hard to look around and see chaos. We search within and can often find despair because of the trials in our life: our diseases, broken relationships, financial worries, and more. God looks around and sees a plan set into motion for our good. He sees wounded and weary spirits in need of hope and healing. We look up and see clouds that hide a clear view of who God is. We look up and fear the storms that are pressing in on us. He looks past and sees the rainbow He’s about to stretch across the sky. We see the now — He sees the tomorrows.

It can be difficult to find hope in the hard times. It can be hard to find sunshine in the storms. But, as the winds of broken dreams and the rains of helplessness beat against us and wear us down, that’s when He does it.

He reaches down and gently parts the gray skies, sending a brilliant ray of light that spreads over the chaos around us. A ray of light that is captivating — luring even — as we stand there and soak up the warmth He is pouring down upon us. Amazing hope that builds up our faltering faith. Hope that gives us the strength to press on through the storms of this life.

That is why I write. To hopefully show you that there is indeed hope for those who are weary, for those who are hurting. To offer a little something that might make you smile — laugh even — as you journey through this hard life.

God has given me countless little pockets of hope on the darkest of days, and I have learned to look for them in the hard times. They are there. I have seen them. The trick is to look for the light and not focus on the dark clouds hanging overhead.

Lift your face from despair, from fear and hopelessness, and look up — up to Him — and He will give you those little pockets of hope. Hope that will break through on even the darkest of days. That’s a promise.

***

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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Potential Treatment for Daytime Sleepiness in Parkinson’s Patients Moving to Phase 2 Trial

THN102 for daytime sleepiness

Theranexus announced it is starting a Phase 2 clinical trial investigating  THN102  as a potential therapy for Parkinson’s patients who struggle with inappropriate and excessive sleepiness during daytime hours.

The trial (2017-004475-31), which is planned to enroll 60 patients at 20 sites across Europe and in the U.S., was approved to start in Hungary, the French company announced in a press release. Requests to allow this trial have been submitted to regulatory agencies elsewhere.

Affecting almost half of all Parkinson’s patients, excessive daytime sleepiness is a common non-motor symptom of this disease.

The safety and tolerability of THN102 (modafinil/flecainide combination) capsules, given at two doses of each active agent — either 200 mg/18 mg or 200 mg/2 mg of modafinil/flecainide — will be compared to placebo.

Additional or secondary study goals include measuring the treatment’s effectiveness in easing sleepiness, improving patients’ attention spans, vigilance, and cognition, again relative to those given placebo.

Patients enrolled have disease-related excessive daytime sleepiness, denoted by a score of 14 or higher in the Epworth Sleepiness Scale, a self-administered questionnaire for which the highest score is 24. Eligible patients also are those who “complain of daytime sleepiness impacting their quality of life and/or daytime functioning (e.g., falling asleep while reading or watching TV, while eating or talking with other people),” according to the trial’s official page.

THN102 is a combination therapy of modafinil, a first-line treatment for narcolepsy (a sleep disorder characterized by excessive sleepiness) and flecainide, a compound that acts on glial cells of the central nervous system. The therapy showed a safe profile in healthy volunteers deprived of sleep in a Phase 1 trial (NCT03182413), and is being tested in people with narcolepsy in a Phase 2 trial (NCT02821715) in France.

No treatments are approved to help Parkinson’s patients manage excessive daytime sleepiness.

“We would like to thank the regulatory agencies with whom we are in contact and we are delighted with this first authorisation for the phase 2 study for our drug candidate THN102 in Parkinson’s disease,” Franck Mouthon, CEO of Theranexus, said in the release.

The post Potential Treatment for Daytime Sleepiness in Parkinson’s Patients Moving to Phase 2 Trial appeared first on Parkinson’s News Today.

Source: Parkinson's News Today

#AAN2018 — Vercise Deep Brain Stimulation Improves Motor Control in Parkinson’s Patients, Trial Shows

Parkinson's DBS

People with Parkinson’s disease show better motor control, longer “on” periods, and an improved quality of life when treated with a recently approved deep brain stimulation system, one-year results from a clinical trial show.

The research, “INTREPID: A Prospective, Double Blinded, Multicenter Randomized Controlled Trial Evaluating Deep Brain Stimulation with a New Multiple Source, Constant Current Rechargable System in Parkinson’s Disease,” was presented Tuesday at the 2018 American Academy of Neurology (AAN) Annual Meeting, taking place through April 27 in Los Angeles.

Deep brain stimulation, or DBS, is a surgical procedure to treat disabling neurological symptoms in Parkinson’s, such as tremors, rigidity, stiffness, slowed movement, and walking problems. It uses a small, pacemaker-like device called a neurostimulator to deliver electrical stimulation to electrodes surgically placed in specific areas of the brain.

Although diverse clinical trials have shown DBS to be an effective adjunct Parkinson’s therapy, the degree of improvement is variable.

The INTREPID study (NCT01839396), for this reason, is specifically evaluating the safety and effectiveness of Boston Scientific‘s Vercise DBS system in people with advanced but levodopa-responsive Parkinson’s, whose symptoms are not adequately controlled by the medication. Full study results are expected after it concludes in 2021.

The Vercise DBS system, which targets the subthalamic nucleus (STN) part of the brain that is hyperactive in patients,  was approved to treat motor symptoms by the U.S. Food and Drug Administration in late 2017. It works using implanted leads with eight electrodes, and allows a doctor to vary the amount of current delivered by each electrode.

Reported results from this multicenter, double-blinded study involved 292 patients at 23 U.S. medical centers. All used the STN-implanted Vercise system for 12 weeks, and were randomly assigned to either an active (medium and continuous dose) or control (low and intermittent dose) treatment group.

INTREPID’s primarily goal was changes in the duration of “on” periods, characterized by improved motor control following levodopa treatment.

Improvements in motor function and quality of life were evaluated using a Parkinson’s diary, the Unified Parkinson’s Disease Rating Scale (UPDRS), the 39-item Parkinson’s Disease Questionnaire (PDQ-39), and neuropsychological assessments. Safety was measured through reported adverse events.

Results showed that 12 weeks of treatment increased the duration of “on” periods by a mean 3.03 hours in active patients compared with those in the control group. Secondary outcomes included a 49.2% improvement in motor symptoms in UPDRS scores, and a sustained and better life quality through the patient questionnaire, Boston Scientific also reported in a company press release.

Safety data showed low rates of infection and brain hemorrhage during the implant surgery.

Overall, these findings show the “DBS system is safe and effective in the treatment of Parkinson’s disease symptoms,” the researchers wrote.

“This study meets a new level of rigor in evaluating the effectiveness of a DBS system,” Jerrold Vitek, MD, PhD, chair of neurology at the University of Minnesota Medical School and the coordinating principal investigator for  INTREPID, said in the release. “The double-blind design gives us confidence that the improvements in patients on time with good symptom control, as evaluated by the diary data, are an objective measure of the outcomes and suggests patients will benefit from the Vercise System.”

The Vercise DBS system is also approved to treat Parkinson’s patients in Europe and Australia.

The post #AAN2018 — Vercise Deep Brain Stimulation Improves Motor Control in Parkinson’s Patients, Trial Shows appeared first on Parkinson’s News Today.

Source: Parkinson's News Today