MJ Fox Foundation Gives Therapeutic Pipeline Award to Progenra, Supporting Work on New Therapies

Progenra, award, Michael J. Fox Foundation

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) has granted a 2018 Therapeutic Pipeline Award to Progenra to support the company’s development of small molecule treatment candidates for Parkinson’s disease.

“Progenra is pleased to have been selected by The Michael J. Fox Foundation to contribute to bringing Parkinson’s and other major neurodegenerative diseases under control by introducing new therapeutic agents,” Tauseef Butt, Progenra’s president and CEO, said in a press release.

The company’s goal is to find new medicines that target enzymes in the ubiquitin proteasome system (UPS). The UPS has been implicated in neurodegenerative diseases, based on the observation of protein deposits tagged with ubiquitin — a marker for degradation in cellular structures called proteasomes — in affected neurons.

Research has shown that impaired UPS function, due to the accumulation of aggregation-prone proteins, delays the degradation of substrates important in cellular processes such as signaling and apoptosis — which refers to “programmed” cell death, rather than death caused by injury — ultimately leading to neurodegeneration.

“We believe that augmenting the activity of a native enzyme known to be beneficial in combating neurodegeneration will provide both mechanistic information and the potential for breakthrough treatment,” Butt stated. “We look forward to working with the many excellent researchers in the foundation’s consortium.”

MJFF’s Therapeutic Pipeline Program grants awards to projects of clinical utility for patients and to proposals believed to have the potential to alter disease course and/or significantly improve treatment over the current standards of care.

Both industry and academic investigators may apply by proposing new strategies or clinically safe therapies used in other diseases. The program covers development from preclinical studies to clinical trials, which includes pharmacological and non-pharmacological approaches such as gene therapy, biological, surgical, and non-invasive methods.

In addition, MJFF’s Target Advancement Program aims to overcome the need for well-validated targets in the disease process. It seeks to foster critical target validation studies that may ultimately speed up subsequent therapy development. The program also supports continuing work on established targets — those already showing links to the disease in patients.

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The Pac-Man Cometh: Parkinson’s Disease Gobbles Up Time

pac-man

I used to be able to put long hours into just about anything I tackled: research, teaching, helping others, painting, writing, and gardening. But PD gobbles up time, just like the video game character Pac-Man gobbles up dots while chasing ghosts. Although I’m retired, I have less free time to accomplish personal goals, because every day, the PD Pac-Man cometh.

Following is a list of ways the PD Pac-Man gobbles up my time:

  • Bad days and “off periods” requiring a commitment of time to manage.
  • Medical appointments and traveling to them take time.
  • Pain and deep fatigue require more rest to help manage them.
  • Any illness (such as the flu) becomes more intense and takes more time to recover.
  • Heightened emotions along with stress of any kind (good or bad) require more time to manage.
  • The overall rehabilitation plan to address all the issues associated with PD (which I have mentioned in past columns) requires quite a bit of time.

Many evenings, as I get to the end of the day, it feels as if nothing was accomplished. It is a plaguing voice and annoying not just to me. My partner has heard it so many times that the response is now: “I’m going to have that on your tombstone: ‘Here lies Dr. C. He died wishing he got more done in his life.’”

Tons of magazine articles and books discuss time management. But PD has its own special problems that need to be considered when seeking to apply time management strategies. Think of time as money: You only have so much that you can spend each month. You can’t get back what the Pac Man gobbles up. You can decrease what the Pac-Man consumes by implementing a personally tailored rehabilitation plan. After that, it is important to cherish the time that is available and to allocate it in a meaningful and constructive way.

Misdirected attention is the Ms. Pac-Man of PD. It consumes time in two ways: First, by getting us to be off-task, and second, due to the set-shifting problems connected to scenario looping, we can end up staying off-task. It may even feel quite difficult to get back on-task (see my previous column on apathy reconsidered).

After physical exercise and good medical care, mental attentiveness is the third most important treatment focal point for early PD folks. Like physical exercise, mental attentiveness needs to be practiced daily. This is one of the reasons I recommend virtual reality game-playing.

Capitalize on using the good days, and the good hours in a day, when they occur. Without being fierce about it, jump into those good days and focus on accomplishing tasks that have rich meaning and purpose. At times during the illness, the mind is more lucid. Use those times wisely with directed attention. Be patient and allow those times to arrive.

Be flexible on the mild days. Get done what you can and then be willing to rest. On the bad days (and especially the ugly days), be willing to let it go. As boring as it seems, rest is needed to limit the extent of the bad days.

With these suggestions in place, make a schedule. Make broad goals and then weekly goals. Use those good times during the week to apply yourself with mental attentiveness to those goals. This is a little bit different than saying, “On Monday, I will do this and on Tuesday, that.” Instead, make a flexible schedule that says, “I would like to get this done by the end of the week.” Then, when the good and lucid times arrive, you can apply yourself to getting that weekly goal done. I write these columns that way.

Finally, keeping track of appointments on a calendar (paper, computer, and cellphone) is important. It helps to know when you will be able to apply those good days to your weekly goal.

How does the PD Pac-Man affect your life? What do you do to keep the PD Pac-Man from gobbling up too much of your free time? Share in the comments below.

***

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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Neurofeedback System Lets Patients Control Brainwaves Linked to Movement, Researchers Say

Neurofeedback system

Parkinson’s disease patients voluntarily controlled brainwaves associated with motor symptoms using a neurofeedback system, according to new research.

These findings have implications for how to best harness brain activity and deep brain stimulation to treat Parkinson’s disease symptoms.

The study, “Real-time neurofeedback to modulate β-band power in the subthalamic nucleus in Parkinson’s disease patients,” was published in eNeuro.

Many studies have reported a relationship between the beta-band power — a brainwave with a frequency between 12 and 30Hz — in the subthalamic nucleus and motor symptoms in Parkinson’s disease. The subthalamic nucleus is a brain region thought to implement the so-called “hyperdirect pathway” of motor control critical to suppressing erroneous movement.

Parkinson’s disease is characterized by abnormal neuronal oscillations in the subthalamic nucleus. Consequently, abnormal oscillations of beta-band power are commonly observed and correlate with disease symptoms.

The use of dopaminergic (L-dopa) medications has been shown to decrease beta-band oscillations while relieving Parkinson’s disease symptoms, such as bradykinesia — impaired ability to move one’s body.

Similarly, researchers have been able to suppress beta-band oscillation in the subthalamic nucleus using deep brain stimulation (DBS) — a neurosurgical procedure involving the implantation of a device that electrically activates specific clusters of neurons in the brain to treat movement disorders.

However, the best way to use deep brain stimulation to treat Parkinson’s disease symptoms remains unclear.

There are two main types of deep brain stimulation currently being examined for therapeutic use: continuous DBS and adaptive DBS. Continuous deep brain stimulation applies the same electrical stimulation continuously without any external control, the way a pacemaker controls a constant heartbeat; adaptive deep brain stimulation changes the amount of electrical stimulation with the fluctuating beta-band oscillations.

Recent studies have demonstrated that adaptive deep brain stimulation using beta-band oscillation reduced Parkinson’s disease symptoms more effectively than continuous DBS. These improvements correlated with attenuation of beta-band oscillations. As such, “beta-band oscillation in the [subthalamic nucleus] may be a therapeutic target for clinical interventions such as rehabilitation,” researchers stated.

However, it was unclear whether Parkinson’s patients could voluntarily moderate beta-band oscillations in the subthalamic nucleus, which could change the way deep brain stimulation is implemented to improve Parkinson’s rehabilitation.

For these reasons, researchers at Osaka University in Japan wanted to test the relationship between brain activity and disease symptoms in Parkinson’s patients. They examined whether Parkinson’s patients could voluntarily or involuntarily influence control over adaptive deep brain stimulation- generated impulses using a neurofeedback system — sensors that monitor how fast or slow one’s brainwaves are firing and subconsciously teaches the brain to fire at optimal speeds.

To do so, the researchers studied brain activity from deep brain stimulation electrodes implanted in the subthalamic nucleus in eight patients who were connected to a neurofeedback system.

The researchers examined subthalamic nucleus activity before and after a 10-minute test. Patients were shown a circle whose diameter was controlled by their own beta-band power through the neurofeedback system. The patients were instructed to make the radius of a black circle on a computer screen smaller by using their thoughts and without moving their bodies. If the size of the circle changed throughout the test, it would mean that the patients were voluntarily influencing their beta-band power.

Four patients were induced to decrease the beta-band power during the feedback training (down-training condition); the others were induced to increase (up-training condition).

For the four patients in the down-training group, beta-band power was significantly decreased after the training, whereas only two out of four patients in the up-training group showed a significant increase in the beta-band power. “The powers in other frequency bands … did not, however, change significantly before and after the neurofeedback training,” researchers noted.

Overall, the patients could control the beta-band power in the subthalamic nucleus through neurofeedback. However, the researchers did not observe reductions in patients’ motor symptoms.

These results show that feedback training successfully demonstrated that the beta-band power of the subthalamic nucleus could be modulated to increase or decrease based on patients’ voluntary control.

The neurofeedback training may be an effective method for revealing the functional changes that accompany atypical beta-oscillations. Although this method did not relieve Parkinson’s disease symptoms, the study paves the way for a new approach toward managing Parkinson’s-related brain activity that could inform the development of new treatments.

“Here, we have developed a novel neurofeedback technique using intracranial electrodes implanted in deep brain structures to modulate subthalamic nucleus activity,” researchers said. “This is the first report to demonstrate that human patients with Parkinson’s disease were able to voluntarily control their [beta]-band power in subthalamic nucleus to induce changes in the power.”

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Encephalitis Symptoms Masked as Worsening Parkinson’s Disease, Case Report Shows

encephalitis case report

Parkinson’s disease can sometimes mask the symptoms of other neurological disorders, according to a case report.

The report, titled “NMDAR encephalitis presenting as akinesia in a patient with Parkinson disease,” documents the case of a 71-year-old woman who was eventually diagnosed with encephalitis, the symptoms of which were first thought to be caused by a worsening of her Parkinson’s.

It was published in the Journal of Neuroimmunology.

The patient, who had a two-year history of Parkinson’s, had initially experienced some difficulty moving her left arm, a condition called bradykinesia, but was generally responding well to levodopa, a mainstay of Parkinson’s treatment.

Then, at the end of 2017, her symptoms started to worsen. Her bradykinesia increased to the point that she was unable to move her arm at all, defined as akinesia. In April 2018, she was admitted to a hospital due to difficulty moving and swallowing.

She stopped responding to levodopa treatment, and her condition continued to decline. She eventually became unresponsive; the authors described her state as being nearly catatonic.

Because the disease was continuing to progress and wasn’t responding to treatment, the doctors decided to examine her cerebrospinal fluid, the liquid that surrounds the brain and spinal cord.

After taking a sample of the patient’s cerebrospinal fluid and running a series of tests, they found antibodies against N-methyl-D-aspartate receptor (NMDAR). These antibodies are a hallmark of encephalitis, which occurs when there is inflammation in the brain — essentially, the body’s immune system attacks cells in or near the nervous system, which is not conducive to proper neurological function.

Typically, encephalitis presents as a severe disease with rapidly worsening symptoms. In this particular case, this was still true — but because the patient had Parkinson’s, which shares some similar symptoms, she was believed to be experiencing worsening Parkinson’s, and not an altogether separate disease.

“Our case should alert neurologists that NMDAR-E [encephalitis associated with antibodies against NMDAR] onset in PD [Parkinson’s] patients could manifest mainly as worsening of PD,” the researchers wrote.

After the correct diagnosis was made, appropriate treatment was swiftly given, and the patient responded well. She gradually regained her function and had completely recovered within three months, her symptoms returning to just bradykinesia of her left arm.

As is often the case in acute encephalitis, the patient has no memory of what occurred during the worst parts of the disease.

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Targeting Enzyme Has Potential as Parkinson’s Therapy, Yumanity Announces

targeting enzyme

Blocking a key enzyme responsible for the production of a type of fat can become a potential therapeutic approach to treat Parkinson’s disease, Yumanity Therapeutics recently announced.

The company revealed that inhibiting an enzyme called stearoyl-CoA desaturase can protect human neurons from alpha-synuclein-derived toxicity and improve their survival.

Based on these promising results, the company plans to initiate the first-in-human clinical trial of its most advanced experimental therapy, YTX-7739, in the fourth quarter of 2019.

The findings were reported in the study, “Inhibiting Stearoyl-CoA Desaturase Ameliorates α-Synuclein Cytotoxicity” published in the journal Cell Reports.

Previous research had found that certain fat molecules, called unsaturated fatty acids, are important mediators of the neurotoxicity caused by the protein alpha-synuclein — a key constituent of Lewy bodies, protein clumps that are a hallmark of Parkinson’s disease.

Importantly, in cell and animal models of the disease, inhibiting the enzyme stearoyl-CoA-desaturase (SCD), key for the production of unsaturated fatty acids (specifically palmitoleic and oleic), could protect against the formation of alpha-synuclein aggregates and its related toxicity.

Using Yumanity’s drug discovery platform, researchers screened for compounds that could protect against alpha-synuclein-induced toxicity. They found a series of small molecules — including YTX-7739 — that was able to rescue yeast cells from the cellular defects and growth impairments caused by alpha-synuclein. YTX-7739 worked by blocking SCD, further supporting the enzyme as a potential therapeutic target for Parkinson’s.

SCD is the first potential target identified by Yumanity’s discovery engine, a group of screening platforms based on yeast and human neurons aimed at finding new and druggable targets for difficult-to-treat, protein misfolding-related neurodegenerative diseases including Parkinson’s, Alzheimer’s and amyotrophic lateral sclerosis (ALS).

The team confirmed its hypothesis in a laboratory model of human neurons derived from pluripotent stem cell (iPCS). iPSCs are derived from either skin or blood cells that have been reprogrammed back into a stem cell-like state, which allows for the development of an unlimited source of any type of human cell needed for therapeutic purposes.

When these model neurons were treated with a commercially available inhibitor of SCD, the neurodegenerative effects of alpha-synuclein were reduced and the cells lived longer. As expected, this protective effect was linked to a decrease in the levels of unsaturated fats inside neurons.

Even though it seems like a promising therapeutic approach to explore, its “precise mechanism of protection is not entirely defined” researchers wrote.

Fatty acids, and oleic acid in specific, are crucial components of cell membranes — both the plasma membrane, which separates the interior of cells from the outside environment, and membranes that enclose crucial structures within the cell.

Based on this knowledge and the study’s results, researchers propose three possible mechanisms for the protective effects of blocking SCD: a toxic increase in fatty acid desaturation is directly reversed by SCD inhibition; reduced fatty acid desaturation (a consequence of blocking SCD) reverses the toxic effects of alpha-synuclein on membrane properties or transport processes within the cell (cellular trafficking); or the reduced fatty acid desaturation enhances a direct toxic interaction of alpha-synuclein with cell membranes.

“The lack of effective new disease-modifying treatments for these disorders stems largely from a scarcity of novel drug targets, and a poor understanding of disease biology,” Ken Rhodes, PhD, chief scientific officer of Yumanity Therapeutics and senior author of the study, said in a press release.

“These new findings are important because they pinpoint a novel mechanism underlying alpha-synuclein toxicity and offer a potential new therapeutic approach to treating Parkinson’s disease through the inhibition of SCD activity,” he said.

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Nicotine May Protect the Brain from Toxic Trace Metals Linked to Parkinson’s, Cell Study Finds

nicotine study

Nicotine may protect the brain from manganese and iron metal trace elements thought to be involved in the onset of Parkinson’s disease, a study based on a disease cell model reported.

The study, “Nicotine protects against manganese and iron-induced toxicity in SH-SY5Y cells: Implication for Parkinson’s disease,” was published in Neurochemistry International.

Parkinson’s is characterized by the gradual loss of dopaminergic neurons in the substantia nigra — a region of the brain responsible for movement control — leading to motor and cognitive impairments.

Although the exact causes of Parkinson’s are not yet fully understood, scientists believe the accumulation of metal trace elements, such as manganese and iron, could play a role in its onset. At low concentrations, these elements are crucial for cell growth and physiological functions; indeed, they are important for all growth and healthy workings of the body. But at high levels, they become toxic, and have been associated with several neurodegenerative disorders, including Parkinson’s.

Nicotine, a potent stimulant originally found in plants that activates the nicotinic acetylcholine receptor (nAChR) in the brain, has been shown to protect dopaminergic neurons from damage caused by different types of toxins. However, no study had addressed possible neuroprotective effects of nicotine against specific metal trace elements.

The new study from Howard University College of Medicine examined the effects of nicotine on toxic manganese and iron elements in a neuroblastoma cell line (SH-SY5Y), a standard in vitro model to study Parkinson’s disease cells, due to their dopaminergic activity.

When researchers exposed SH-SY5Y cells to high concentrations of manganese or iron for a day, toxicity levels increased by 30% and 35%, respectively. Pretreatment with nicotine was seen to completely prevent these toxic effects.

As expected, nicotine’s neuroprotective properties against toxic trace elements were lost when researchers used different types of nicotinic receptor antagonists (molecules that block the activity of nAChRs). This was true for “dihydro-beta erythroidine (DHBE), a selective alpha4-beta2 subtype antagonist and methyllycaconitine (MLA), a selective alpha7 antagonist,” the study noted.  

“In summary, the results of this study provide evidence for neuroprotective effects of nicotine against toxicity induced by Mn [manganese] or Fe [iron] in a cellular model of PD [Parkinson’s disease],” the researchers wrote.

“Moreover, both high and low affinity nicotinic receptors (i.e., alpha4-beta2 and alpha7 subtypes) appear to mediate the effects of nicotine. Thus, utility of nicotine or nicotinic agonists in trace element-induced Parkinson-like syndrome may be suggested,” they concluded.

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Dietary Supplements May Help Control Metabolism, Brain Inflammation in Parkinson’s, Study Finds

dietary supplements

Supplements of omega-3 fatty acids and vitamin E may help control genes involved in brain inflammation and body metabolism in patients with Parkinson’s disease, a study has found.

The study, “The effects of omega-3 fatty acids and vitamin E co-supplementation on gene expression related to inflammation, insulin and lipid in patients with Parkinson’s disease: A randomized, double-blind, placebo-controlled trial,” was published in Clinical Neurology and Neurosurgery.

Parkinson’s disease is characterized by the gradual loss of dopaminergic neurons in the substantia nigraa region of the brain responsible for movement control, leading to a lack of body balance, coordination, depression, and cognitive impairment.

It is well-known that inflammatory cytokines — molecules that mediate immune responses — such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1), are also involved in disease progression.

A team of Iranian researchers had previously shown that Parkinson’s patients taking supplements of omega-3 fatty acids together with vitamin E for a period of 12 weeks “had benefit effects on Unified Parkinson’s disease rating stage [which assesses both motor and non-motor symptoms], insulin metabolism … and total antioxidant capacity.”

Omega-3 fatty acids are fatty substances the body is incapable of producing that are crucial for many functions, including muscle activity and cell growth. For this reason, they must be obtained from certain foods, such as fatty fish and seeds.

Vitamin E is an antioxidant — a substance that protects cells from damage caused by high levels of oxidant molecules — that is essential for blood, brain and skin health.

The same team has now investigated the effects of omega-3 fatty acids and vitamin E supplements on the expression of genes involved in inflammation and body metabolism in patients with Parkinson’s disease. Gene expression is the process by which information in a gene is synthesized to create a working product, like a protein.

The randomized, double-blind, placebo-controlled clinical trial (IRCT2017061234497N1) assessed the effect of dietary supplements in 40 patients for a period of 12 weeks.

Study participants were randomly divided into two groups: one taking 1,000 mg of omega-3 fatty acids from flaxseed oil together with 400 IU of vitamin E supplements daily; and another taking a placebo. The expression of genes involved in inflammation and body metabolism was measured in peripheral blood mononuclear cells (PBMCs) collected from patients.

After 12 weeks, PBMCs from patients taking daily dietary supplements had lower activity of TNF-alpha, but not of other genes involved in inflammation, such as IL-1 and interleukin-8 (IL-8), compared with those on a placebo.

“Therefore, omega-3 fatty acids and vitamin E co-supplementation due to their beneficial effects on inflammatory markers may be useful to control neurological symptoms in a population with PD [Parkinson’s disease],” the researchers wrote.

In addition, omega-3 fatty acids and vitamin E supplements enhanced the activity of peroxisome proliferator-activated receptor gamma (PPAR-gamma), a gene involved in lipid (fatty molecules) and insulin (a hormone that helps control blood sugar levels) metabolism.

Conversely, treatment reduced the activity of low-density lipoprotein receptor (LDLR), a gene involved in controlling the amount of cholesterol in the blood, compared with the placebo group.

“Increased gene expression of PPAR-γ[gamma] improves insulin sensitivity [and] can have additional effects upon cellular physiology, including anti-proliferative and anti-inflammatory,” the investigators wrote.

“To our knowledge, this study is the first [to] report [beneficial] effects of omega-3 and vitamin E co-supplementation on gene expression related to inflammation, insulin and lipid in populations with PD,” they concluded.

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My DaTscan Results Made My PD Diagnosis ‘Real’

DaTscan

When I was first diagnosed with Parkinson’s disease (PD) in 2015, I asked the neurologist if there was a definitive test to confirm a PD diagnosis. I mentioned a DaTscan, but he said the test is not entirely conclusive. He also indicated that DaTscan results likely would not change his prescribed course of treatment for me.

His view was that the best way to confirm a PD diagnosis is to give a patient the medication levodopa to see if PD symptoms disappeared. Other neurologists I consulted for second opinions concurred with his assessment.

What is a DaTscan?

DaTscan is a medication that is injected into the bloodstream to assess dopamine-containing neurons that are involved in controlling movement. The contrast agent ioflupane (123I) is distributed around the body in the bloodstream and accumulates in the area of the brain called the striatum, where it attaches to the structures that transport dopamine. The patient then has a single-photon emission computed tomography (SPECT) scan.

The DaTscan test was designed to differentiate parkinsonian syndromes from essential tremor. PD is the most common form of parkinsonian syndromes, but there are other forms, including multiple system atrophy and progressive supranuclear palsy.

My DaTscan

A comparison between a normal and an abnormal DaTscan can be viewed here. A normal DaTscan will show two distinct comma-like or crescent shapes. An abnormal DaTscan will have two period-like or oval shapes, or a combination of period and comma shapes, indicating a reduced uptake of DaTscan in certain areas of the brain. Parts of the image that are “lit up,” indicate more surviving brain cells. Dark areas could mean either PD or parkinsonism.

My DaTscan image showed that the right side of my brain is less “lit up” than the left side. The right hemisphere of the brain coordinates the left side of the body. The left side of my body is the one most affected by PD, so it makes sense that my right side brain is less “lit up.”

Am I convinced that I have PD?

Three years after my diagnosis, I am still struggling to find relief from my symptoms and slow the progression of this disease. I exercise, eating a mostly vegan and gluten-free diet, take Sinemet (carbidopa-levodopa), and use the Neupro transdermal patch. I am working with my current neurologist to fine-tune my medication “cocktail.”

I had wondered whether I did have PD since I’ve never had an “aha” moment in which I feel somewhat normal after taking medications. People tell me I look fine and they don’t observe any external signs of the disease. However, my tremors are internal and I feel horrible and constantly fatigued.

Why now?

I am subjecting my body to what I believe are toxic medications to treat a disease that I feel has been subjectively diagnosed. My symptoms have not been completely alleviated with my current exercise, diet, and prescription medication regimen. I wanted more concrete evidence that I have PD, so my neurologist prescribed a DaTscan. Much to my dismay, the results were abnormal and compatible with Parkinson’s syndrome.

Seeing my brain image with areas not “lit up” where they should be, when contrasted with a normal DaTScan, made my diagnosis very real for me. I have a form of parkinsonian syndrome — most likely PD.

Would I still have gotten a DaTscan?

It was important for me to have confirmation other than my symptoms of abnormalities in my brain. I think this scan can be used as a baseline to follow my disease progression.

So, yes, I would have still gotten this test, although the $2,000 out-of-pocket cost upfront may have given me pause.

***

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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New Art Initiative Aims to Improve Understanding and Discussion of Parkinson’s Off Periods

art initiative, off periods

A new initiative by Acorda Therapeutics uses art to help people with Parkinson’s disease recognize and communicate about their off-period experiences.

The initiative, called Framing OFF Through Art, builds on Acorda’s Live Well. Do Tell program, launched earlier this year.

Framing OFF Through Art includes artwork inspired by the experiences of patients with Parkinson’s and their caregivers. The artists who created the pieces also have personal connections to the disease. Each artist partnered with two patients and their caregivers. The art aims to educate and encourage others with Parkinson’s and their care partners to identify off-period symptoms and discuss them with their healthcare professionals.

“Art is a powerful way to engage a community, and in Framing OFF Through Art, our goal is to create an emotional connection that results in better dialogues about Parkinson’s symptoms,” Ron Cohen, MD, Acorda’s president and CEO, said in a press release.

The artwork debuted on Oct. 23 at an event in New York, where the artists, patients, and their caregivers were guests. The first piece was created by Julie B., whose mom is living with the disease, and is available on the Live Well. Do Tell website. More art and personal stories will be revealed each month.

“I know that some of these symptoms are really difficult to put into words. A visual representation can really communicate what you are going through,” Julie B. said in a video interview. “One of the big takeaways from this initiative is the idea of an open and honest conversation.”

Off periods are a common complication in Parkinson’s patients, characterized by the return of motor and non-motor symptoms — such as anxiety and sadness — when levodopa’s effects wear off. The need to better understand off periods, as well as how to talk with others about them, had been originally highlighted in the Live Well. Do Tell statement of need.

This report was the first output of the campaign, and includes six actions for the Parkinson’s community: tailor resources at diagnosis; broaden the Parkinson’s community’s ability to identify off periods; educate about motor fluctuations and how they do not necessarily mean disease progression; identify opportunities for caregivers to discuss their experiences with healthcare professionals; enhance the patient-clinician dialogue; and improve clinical practice via insights from movement disorder specialists and a new tool to measure off periods.

The report was based on insights from the campaign’s steering committee meeting that included Parkinson’s community leaders. Others may join the conversation by signing up for initiative updates and news.

“Off periods can be frustrating and challenging, as symptoms are varied and often difficult for patients to communicate effectively to their care providers,” said Matthew Stern, MD, director emeritus of the Parkinson’s Disease and Movement Disorders Center at Penn Medicine.

“By helping people with Parkinson’s understand how to verbalize what they are experiencing, we, as their healthcare providers, can better understand their needs and help them achieve a better sense of well-being,” added Stern, who is the chair of the Live Well. Do Tell steering committee.

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Parkinson’s Patients Show Reduced Workforce Participation Even Before Diagnosis, Study Finds

workforce participation

Parkinson’s patients show less ability to participate in work life even in the early stages before they are diagnosed with the disease, a study shows.

In combination with biochemical and genetic biomarkers, this finding may help identify patients at risk of developing this progressive neurodegenerative disease before motor symptoms occur, the researchers suggest.

The study, “Reduced workforce participation 5 years prior to first Parkinson’s disease sick-leave,” was published in the journal NPJ Parkinson’s Disease.

Non-motor symptoms, such as depression and anxiety, are recognized as part of the prodromal (early) phase of Parkinson’s disease. These manifestations often arise approximately 10 to 20 years prior to the onset of motor symptoms.

At least 30 percent of people who have Parkinson’s are of working age, according to the study.

“At the group level, persons who later will get diagnosed with PD [Parkinson’s disease] have been reported to exhibit higher medical expenses and a lower employment rate up to 8 years prior to the diagnosis in comparison with controls,” the researchers wrote.

However, it is not fully understood how early non-specific motor and non-motor symptoms can affect workforce participation during prodromal and early Parkinson’s disease.

Researchers in this study aimed to investigate whether individuals eventually diagnosed with Parkinson’s exhibit increased sickness absences one, two, and five years prior to a first sick-leave episode attributed to the disease.

They reviewed clinical records of all sick-leave absences that exceeded 14 days in Sweden between 2008 and 2014. They identified a total of 537 incident Parkinson’s disease sick-leave cases and 537 sick-leave cases of other diagnoses, which were used as controls. Most Parkinson’s sick-leave cases were men (63.7%), and the median age was 59 years.

A larger portion of the Parkinson’s sick-leave cases, compared with sick-leave controls, were found to have had more than one sick-leave episode one, two, and five years prior to the first Parkinson’s sick-leave.

“Persons who later were allowed sick-leave due to PD were more absent from work due to illness than matched sick-leave controls already 5 years prior to the incident PD sick-leave episode,” the researchers wrote.

Those later diagnosed with Parkinson’s had more sick-leave absences due to musculoskeletal problems up to five years prior to the first Parkinson’s sick-leave episode. Total sickness absences were also increased among Parkinson’s sick-leave cases five years prior to the first sick-leave episode due to the disease.

“It is possible that an increased occurrence of pain is a partial explanation of the increased sickness absence due to musculoskeletal diagnoses in the present study,” the researchers noted. Increased pain, tremor, fatigue, dizziness, shoulder pain or stiffness, balance impairments, rigidity, and reduced blood pressure were factors that “either on their own or indirectly could result in sickness absence due to musculoskeletal diagnoses,” they added.

The incidence of sick-leave absences due to mental and behavioral problems was similar between the two groups.

In general, Parkinson’s sick-leave cases were less likely to be of patients working in occupations with lower education requirements compared with the control group. In addition, Parkinson’s patients were 2.16 times more likely to be self-employed or unemployed than sick-leave cases with other diagnoses.

This pattern could be caused by the gradual increase of symptoms that prodromal and early Parkinson’s patients may experience.

Based on these findings, the team believes that “the capacity to participate in working life is reduced already at the early prediagnostic stages of Parkinson’s disease.”

“This finding can be used as a basis for further research into the process of identifying individuals at risk for developing Parkinson’s, particularly in combination with further investigation into biochemical, genetic, and imaging biomarkers,” they concluded.

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