Going from Zero to 60 in 4 Months



A cannon shot shakes the windows of the house. No, it’s not terrorists showing up in rural New England. It’s just winter. We have a steel roof. When the temperature is just right, the snow slides off the roof with the force of a cannonball and hits the ground with just as much noise.

Every winter, I’ve been out helping to clear the snow. But not this year. The ruin of stagnation has forced me to practically abandon any physical activity while I healed. Slow progress was made as I increased exercise each day from zero to 60 minutes. It is very slow healing. I am not used to the slow pace, and that nags at me, like a child wanting to get to the next carnival ride.

Neo interrupts my thinking: “Well, it’s been four months. What have you accomplished over all that time?” I can always count on Neo to hit me with a direct shot, without a warning over the bow. (Neo is my brain’s neocortex, which I’ve mentioned in previous columns.)

“I have tried to push harder and go faster to make this healing happen,” I reply. “It’s not helping. The old way of using the fierce ‘push harder’ is not working. I have used anger to motivate myself, to push myself harder, so that I can accomplish more. But no longer. The anger now adds stress experienced in a raw and unfiltered manner. I can no longer afford to do things the old way if I’m looking for genuine wellness.”

“Sounds like you want to get rid of anger. That’s a tall order,” Neo points out, puffing his chest. “There are many good reasons for keeping anger in your back pocket and pulling it out when needed.”

I take a deep breath, and with unusual calmness, say: “I don’t think I can get rid of it. I think it’s a part of who I am. But I do think I have misused and abused the energy of the calling behind anger. For me, the injustice connected to suffering and the objectification of others inflame me. I have used this fire to fuel my motivation, to continue the good fight.”

Neo retorts, “Yeah, man. Help the good guys and kill the bad guys — anger is good for that.”

I shake my head. “There is an attacking edge to anger, but it is not an absolute quality of anger. Rather, it is a self-imposed one. I willingly choose to attack with anger. It is unnecessary for wellness, and I see this attacking edge as harmful to my search for healing. I need to remove this self-imposed attack quality and embrace a transformed anger,” I say.

Turning his head slightly in a gesture of acknowledgment, Neo says, “Peace on earth and goodwill to all. I get it. But anger is also good for helping to get a point across. Get attention.”

“Not always, Neo. Powerful ideas have enough of a spark in them to kindle awakening in the hearts of all who can listen. All the fire of anger does is obscure the discovery of that spark. While healing, I need that spark, I need what’s behind that spark, and using anger to incite just gets in the way.”

As I walk over to the kitchen to cut up zucchini (there’s always too much zucchini in New England), I can see Neo crinkling as he wrestles with his thoughts about anger. As if a lightbulb had been illuminated over him, Neo blurts, “Sometimes I just want to blow off some steam. Anger is a good way of doing that.”

I respond, “Whenever I’m in one of those venting moods, I also have this internal dialogue that is filled with negative statements about people, life, and past events. It’s inner dialogue that points fingers at ‘he said this,’ ‘she did that,’ ‘not fair that this happened to me,’ and ‘I want this to go away.’ The venting is filled with a lot of energy, and somewhat of a rush can go with it. In the past, it may have helped. But now the emotional intensity of this venting is no longer healthy for me. And it can hurt people around me.”

I take a sip of holiday cider and continue. “There is a different way to look at how to use the energy behind anger, the energy of perceived injustice. It is a way of taking that energy and focusing it solely on solutions — not on people, not on personal injury, not on personal feelings. Every problem is a solution waiting to happen. It is shifting the focus of the energy toward constructive change, and in doing so, it changes the nature and quality of anger.”

Neo has been tapping lightly on the table for the last 30 seconds, and now he jumps in. “You will need that anger if your life is threatened or the lives of your children or grandchildren are threatened. You’ll need that anger energy then for sure.”

Taking a deep breath after a lengthy pause, I say, “Most of us are not faced with actual life-threatening situations. There are places in the world where such threats are real, and in those situations people need to act in a way that preserves both life and humanity. But for most of us, it is the perceived threat or illusions of threat that enter our lives. Remove the illusions and you remove the need for anger to function in this manner. Anger is reframed, transformed.”

Neo nods. “So the gift of forgiveness, tolerance, and patience is in keeping with the holiday season. It’s a good gift for yourself and for others. And a good New Year’s resolution!”

This is an example of reframing, a powerful tool to help facilitate positive change. Anger will no longer motivate me to push harder and faster. Let it go! It’s OK if it took four months to go from zero to 60.

How can the holidays be a time for practicing reframing and letting go for you? Please 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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Phase 1 Trial Opens into Potential Parkinson’s Therapy, Anle138b

Phase 1 trial opens

A Phase 1 clinical trial of MODAG Neuroscience Solutions’ lead candidate anle138b is now underway and recruiting healthy participants at its one site in Nottingham, England, to study the compound’s safety.

The small molecule is being developed to treat multiple system atrophy (MSA), but holds the potential to be used in other diseases caused by clumping of the protein alpha-synuclein, such as Parkinson’s disease.

“With the start of this trial, we are on track to run the tests necessary to bring anle138b one step closer to patients,” Torsten Matthias, PhD, chief executive officer of MODAG, said in a press release.

Many neurodegenerative disorders involve the aggregation of misfolded (harmful) proteins in the brain. Anle138b works by binding to harmful forms of alpha-synuclein — a key protein involved in Parkinson’s disease — to clear the brain of existing clumps and to prevent new clumps, also known as Lewy bodies, from forming.

The compound has been shown to reduce the buildup of these toxic clumps and delay disease progression in models of MSA, Parkinson’s, and Alzheimer’s disease. Moreover, anle138b was found to reverse Parkinson’s-related motor symptoms in mice models of the neurodegenerative disorder.

This Phase 1 study’s primary goal is to evaluate the safety and tolerability of oral anle138b in healthy volunteers. Secondary objectives include dose-finding evaluations and assessments of its pharmacokinetics  — essentially how a compound is absorbed, distributed, metabolized, and excreted by the body.

Recruitment is ongoing and being overseen by Quotient Sciences in Nottingham.

“Anle138b has the potential to become a tangible treatment option to stop MSA, a highly underserved indication, in its tracks. MSA patients are severely impacted by progressing movement, balance and autonomic function impairments and as with many neurodegenerative diseases, there are no disease-halting treatment options available,” said Johannes Levin, MD, chief medical officer of MODAG.

“If successful, the Phase 1 trial also opens the opportunity for MODAG to investigate anle138b in other Parkinsonian disorders and Parkinson’s itself,” Levin added.

The biotech company has already secured a worldwide patent for anle138b.

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Cancer Medication Tasigna Safely Boosts Dopamine Levels in Brain of Parkinson’s Patients, Phase 2 Trial Shows

Tasigna, Parkinson's

Tasigna (nilotinib), an approved leukemia medication being tested as a repurposed treatment for Parkinson’s disease, was found to be safe and increased the levels of dopamine in the brain of patients with Parkinson’s disease, a Phase 2 trial shows.

The findings were reported in a study, “Nilotinib Effects on Safety, Tolerability, and Potential Biomarkers in Parkinson Disease: A Phase 2 Randomized Clinical Trial,” and published in JAMA Neurology.

Tasigna, developed by Novartis, is approved by the U.S. Food and Drug Administration and the European Medicines Agency to treat adults with chronic myeloid leukemia, a type of blood cancer that typically affects older adults.

The medicine blocks the activity of a protein called BCR-ABL, which is known to support cancer development. But this protein is also intimately linked to several mechanisms in the brain, such as oxidative stress (cellular damage as a consequence of high levels of oxidant molecules) and alpha-synuclein-induced neurodegeneration, which play critical roles in Parkinson’s and other brain disorders.

For that reason, researchers wondered if Tasigna could be repurposed to treat Parkinson’s disease. Drug repurposing refers to the process of testing a medication with established safety in conditions other than those for which it was originally intended.

pilot study in 12 individuals with Parkinson’s disease dementia and dementia with Lewy bodies suggested that this therapy could effectively treat Parkinson’s motor and non-motor symptoms, while also increasing dopamine metabolism (its use in the brain) and lowering alpha‐synuclein levels.

Subsequently, researchers in the new study sought to investigate the safety, tolerability, and pharmacokinetic properties of Tasigna in a placebo-controlled, Phase 2 trial (NCT02954978) carried out at Georgetown University Medical Center (GUMC). Pharmacokinetics refers to how a drug is absorbed, distributed, metabolized, and eliminated from the body.

The study enrolled 75 patients with moderate-to-severe Parkinson’s disease who were randomly assigned to receive one of two oral doses of Tasigna (150 or 300 mg daily), or a placebo, for a period of one year, followed by a washout period of three months, in which they stopped taking the medication or the placebo.

The mean dose of levodopa at enrollment was similar between groups.

Earlier findings from the study showed that treatment with a single low dose of Tasigna improved the brain’s ability to use dopamine stored in small vesicles in specific brain regions of Parkinson’s patients by reducing inflammation and the levels of toxic alpha-synuclein.

Most of the patients enrolled (88%) completed the study. A total of nine patients withdrew from the study, including two who had been assigned to the placebo, three who had been assigned to receive the lowest dose of Tasigna, and four who had been assigned to receive the highest dose of the medication. From these, two withdrew from the study due to serious adverse events.

Tasigna was considered reasonably safe and well-tolerated, with most adverse events being mild or moderate in severity. The most common non-serious adverse events included falls, and musculoskeletal, respiratory, and skin conditions. Gastrointestinal and heart problems were less common.

In a secondary exploratory analysis of biomarkers, the investigators found that patients treated with Tasigna experienced a reduction in the levels of two toxic proteins that are considered hallmarks of Parkinson’s disease: a 20% decrease in alpha-synuclein and 30% reduction in tau.

In addition, they discovered that those taking Tasigna had an increase of more than 50% in the levels of dopamine (the brain chemical missing in those with Parkinson’s disease), suggesting that reducing the levels of toxic proteins could help the brain to use dopamine more effectively.

Those taking Tasigna performed better on motor tests and tended to have better scores in the PDQ-39 questionnaire (a measure of quality of life) compared to those treated with the placebo.

“We see that subjects on nilotinib performed better overall on motor testing and had a better quality-of-life measurement during the study than the placebo group. These are important observations suggesting that nilotinib stabilized the disease — a potential disease modifying effect that we haven’t observed with any other agents,” Fernando Pagan, MD, medical director of the GUMC Translational Neurotherapeutics Program and principal investigator of the study, said in a press release.

“These clinical findings need confirmation through larger studies with more diverse populations,” added Pagan, who also directs the Movement Disorders Clinic at MedStar Georgetown University Hospital.

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Gosuranemab Fails to Show Efficacy in Phase 2 Progressive Supranuclear Palsy Trial

clinical trial fails

Gosuranemab failed to meet its primary and key secondary goals in a Phase 2 study evaluating its use in treating progressive supranuclear palsy, an atypical parkinsonian disorder, its developer, Biogen, has announced.

Based on these results, Biogen will cease the clinical development of gosuranemab for this and other neurodegenerative diseases characterized by the buildup of toxic tau protein aggregates, collectively known as tauopathies.

“We are disappointed with the efficacy results of the Phase 2 PASSPORT study,” Alfred Sandrock, executive vice president of Research and Development and chief medical officer at Biogen, said in a press release.

“We remain unwavering in our commitment to advancing therapies that have the potential to address the significant unmet medical needs of people with neurodegenerative diseases,” he added.

Parkinson’s disease and progressive supranuclear palsy have similar disease manifestations, including slow movements and difficulties with gait. However, the hallmark of Parkinson’s is the toxic accumulation of misfolded forms of the alpha-synuclein protein within nerve cells, and tau for progressive supranuclear palsy.

Gosuranemab, previously known as BIIB092, aims to treat diseases where formation of toxic clumps (aggregates) of the tau protein occurs. This antibody is designed to bind to a specific part (N-terminal) of the tau protein, which would reduce the spread of the abnormal form of this molecule within nerve cells, potentially slowing  disease progression.

Different doses of the therapy were found safe in a previous Phase 1 study (NCT02658916) in progressive supranuclear palsy patients.

Based on these findings, Biogen opened the placebo-controlled, safety and efficacy Phase 2 study (NCT03068468) of gosuranemab, called PASSPORT, in April 2017.

The study recruited 490 people with progressive supranuclear palsy, who were given 50 mg/ml of gosuranemab intravenously (into the vein) or a placebo once every four weeks for 48 weeks. All participants, including those in the placebo group, were then set to be treated with gosuranemab at 50 mg/ml once a month from week 52 up to week 208.

PASSPORT’s primary goal (endpoint) was to assess the therapy’s efficacy using the progressive supranuclear palsy rating scale (PSPRS), a 100-point scale that helps to measure disease progression.

But topline results from week 52 showed no statistically significant changes in PSP scale.

Key clinical secondary endpoints were also not met, including changes in the Unified Parkinson’s Disease Rating Scale Part II (which assesses motor experiences of daily living), the Clinical Global Impression of Change (measuring symptom severity), the Repeatable Battery for the Assessment of Neuropsychological Disease Severity (evaluating cognition), and the Progressive Supranuclear Palsy Quality of Life scale.

The treatment’s safety profile in the PASSPORT study was similar to that observed in previous studies.

Gosuranemab is continuing to be studied for Alzheimer’s, in the Phase 2 safety and tolerability TANGO trial (NCT03352557) in 654 people with mild Alzheimer’s disease with or without mild cognitive impairment.

Alzheimer’s is marked by the toxic aggregation of a protein called amyloid-beta.

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Immunotherapy Reduced Alpha-synuclein Clumps, Improved Dopamine Levels in Parkinson’s Mouse Model

antibodies and alpha-synuclein

Antibodies that selectively target the misfolded form of the alpha-synuclein protein — that which underlies the development of Parkinson’s disease — reduced the formation of alpha-synuclein clumps and improved dopamine levels in a mouse model. 

The study with that finding also provided a framework for screening  antibodies (immunotherapies) that target alpha-synuclein to identify those with the best therapeutic properties.

The study, “Characterization of novel conformation-selective α-synuclein antibodies as potential immunotherapeutic agents for Parkinson’s disease,” was published in the journal Neurobiology of Disease.

Nerve cell damage in Parkinson’s disease is caused by the build-up of toxic forms of the protein alpha-synuclein that forms clumps of misfolded proteins known as Lewy bodies.

Studies have found that reducing misfolded alpha-synuclein may be an effective therapeutic strategy for treating the disease. 

One idea is to create antibodies that specifically target misfolded alpha-synuclein, avoiding the problems associated with reducing the levels of properly folded, fully functioning alpha-synuclein.

This was the approach taken by a group of researchers at the University of Pennsylvania in Philadelphia. Their first step was to create and isolate antibodies that were highly selective for misfolded alpha-synuclein, then test the best candidate in a Parkinson’s mouse model to find out if the antibody had therapeutic potential. 

To create these antibodies, mice were injected with misfolded alpha-synuclein and the antibodies generated during the immune response were isolated and screened to find the best candidate. 

Brain sections from Parkinson’s patients with high numbers of Lewy bodies first were used to identify antibodies that selected pathological (disease-associated) alpha-synuclein.

The team hoped these antibodies may be used in humans, so those that bound to both mouse and human alpha-synuclein were preferred. 

Further testing found antibodies that bound to only the misfolded form of alpha-synuclein, but not the normal form. 

The final screen was to identify a candidate that prevented the development of alpha-synuclein pathology in neurons. Mouse neurons were treated with the previously selected antibodies and were exposed to toxic forms of human alpha-synuclein protein. The highest performing antibody, named Syn9048, reduced pathology [disease manifestation] by 97%.

As antibody treatments for Parkinson’s are likely to be given after symptoms emerge (when brain disease is already established), a mouse model was chosen to test the effectiveness of Syn9048 to reduce disease and rescue nerve cell function. 

Mice were injected with misfolded alpha-synuclein, which triggered nerve cell loss in the same areas of the brain as seen in Parkinson’s patients. Then they were given Syn9048 or a control antibody every week for six months.  

All mice gained weight in a similar manner, showing that the therapy was well-tolerated.

Examination of the mouse brains showed that Syn9048 reduced the aggregation of alpha-synuclein in areas related to Parkinson’s disease. 

Although Syn9048 was not successful in rescuing cells responsible for producing dopamine (dopaminergic), it increased dopamine levels in the brain, which suggested that the reduction of alpha-synuclein pathology may improve the function of remaining dopamine-producing neurons.

“Our study suggests that immunotherapy will not likely reverse existing pathology, but may halt the spread of pathology through the brain, preventing further motor and cognitive decline,” the researchers wrote.

“Future studies assessing brain-wide spread patterns could help predict the maximal possible benefit of immunotherapy and could be used to determine when during disease progression immunotherapy would need to be administered to be most efficacious,” they added. 

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Weight Loss and Parkinson’s Disease

weight loss

Dad used to tell us that he has two sets of clothes: a normal set and a set of “skinny clothes” that emerge when he gets sick.

Dad was diagnosed with ulcerative colitis in his 30s, and the illness caused him to lose a startling amount of weight. He was thin to begin with, but the disease found ways to take more away.

Ulcerative colitis became more manageable for my dad as time moved forward. He put on a healthy amount of weight and chose his food based on desire rather than necessity. With the help of my mom and his friends, he was able to nurse himself back to health.

But for the next 34 years, his two sets of clothing would hang in the corner of his bedroom closet because he never was certain when his health might change. Today, Parkinson’s disease is back to challenge this strategy. And Dad’s skinny clothes are making an appearance.

Causes of weight loss in Parkinson’s disease

Weight loss in relation to Parkinson’s disease can occur for a number of reasons. Decreased appetite, additional energy output, and changes in digestion can slow your food intake. And this ultimately can cause a shift in body weight.

It makes sense, really. Dad’s tremors cause him to expend energy 24 hours a day. That’s a substantial amount of time that is spent in motion. And the body needs fuel to maintain this motion.

Dad seems to eat about the same amount, but what he chooses to eat has changed. My little sister makes sure there’s a constant supply of densely packed foods, such as avocados. They juice every morning, squeezing the nutrients out of a shocking amount of produce.

Sometimes I giggle to see him eating a midnight bowl of ice cream or a handful of chocolate. Weight loss almost seems like an opportunity to eat his favorite treats. Dad looks thin, but his doctor seems to think his weight is stable.

Combating weight loss

In a society where weight loss ads litter social media platforms, it is easy to think that weight loss is a good thing. And it can be. But when uncontrolled, one risks becoming nutritionally deficient. And this ultimately prevents the body from using the building blocks it needs to keep healthy.

According to Parkinson’s News Today‘s Patricia Inacio, extreme weight loss can cause dementia, increased dependency care, and a shorter life expectancy. A study Inacio highlighted evaluated several Parkinson’s patients and found that weight loss might be able to point doctors toward an early PD diagnosis. Furthermore, counteracting weight loss might lessen disease-related outcomes.

Whatever doctors continue to discover, managing weight loss appears to be an important element of Parkinson’s. And it’s a common one, too!

Dad’s skinny clothes

More than six years have passed since my dad’s Parkinson’s diagnosis. The journey has been choppy, inconsistent, and filled with color. New challenges always seem to emerge. The disease never slows, but my dad is just as quick to fight back. His adaptability and determination are unmatched.

Today, his pants hang a bit loose around his skinny legs. But the muscles still ripple. His normal clothes have been collecting dust in the back of his closet for a while.

Christmas might be a time when those sizes shift completely, making skinny the new normal. But he’s strong. He spends three days of every week at Rock Steady Boxing, preparing himself to better challenge his disease.

During a recent visit to the gym, emotions bubbled to the surface. I had never seen him so committed to tackling an obstacle. And with great effort comes great change.


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 Gene Therapy Delivery Method May Open BRAVE New World in Parkinson’s Research

BRAVE gene therapy method

A new method allows researchers to develop adeno-associated virus (AVV) — commonly used as the vehicle for gene therapies — that accurately target and deliver genes to specific cells in the body.

This new technology may be suitable to target dopaminergic neurons that are damaged in Parkinson’s disease.

“We believe that the new synthetic [lab-made] virus we succeeded in creating would be very well suited for gene therapy for Parkinson’s disease, for example, and we have high hopes that these virus vectors will be able to be put into clinical use,” Tomas Björklund, PhD, Lund University, Sweden, said in a press release.

Björklund is lead author of the study “A systematic capsid evolution approach performed in vivo for the design of AAV vectors with tailored properties and tropism,” which was published in the journal Proceedings of the National Academy of Sciences. 

The adeno-associated virus (AAV) is a common, naturally-occurring virus, which has been shown to work as an effective gene therapy delivery vehicle for genetic diseases, such as spinal muscular atrophy. In gene therapy, scientists deliver a working version of a faulty gene using a harmless AAV that was modified and inactivated in the lab. This way the virus functions only as a delivery vehicle and does not have the capacity to damage tissues and cause disease.

While AAVs have a natural ability to penetrate any cell of the body and infect as many cells as possible, their usefulness as a potential therapy requires the capacity to specifically deliver a working gene to a particular cell type, such as dopamine producing-nerve cells. Those are the ones hose responsible for releasing the neurotransmitter dopamine and that are gradually lost during Parkinson’s disease.

A team of Swedish researchers have developed a new method — called barcoded rational AAV vector evolution, or BRAVE — that combines powerful computational analysis with the latest gene and sequencing technology to produce AAVs that can specifically target neurons.

To make AAVs neuron specific, the team selected 131 proteins known to specifically interact with synapses (the junctions between two nerve cells that allow them to communicate).

They then divided the proteins into small sequences, called peptides, and created a large library where each peptide could be identified by a specific pool of genetic barcodes (a short sequence of DNA that is unique and easily identified).

The peptide is then displayed on the surface of the AAV capsid, allowing researchers to test the simultaneous delivery of many cell-specific AAVs in a single experiment.

The team then injected these AAVs into the forebrain of adult rats and observed that around 13% of the peptides successfully homed to the brain. Moreover, 4% of the peptides were transported effectively through axons (long neuronal projections that conduct electrical impulses) toward the nerve cell’s body.

Researchers then selected 23 of these unique AAV capsids and injected them into rats’ striatum, a brain region involved in voluntary movement control and affected in Parkinson’s disease. Twenty-one of the new AAV capsids had an improved transport capacity within nerve cells than in standard AAVs.

One particular capsid, called MNM008, showed a high affinity for rat dopaminergic neurons. Researchers then tested whether this viral vector also could target human dopaminergic neurons.

The team transplanted neurons generated from human embryonic stem cells into rats’ striatum. Six months later, they injected either MNM008 or a control AAV capsid and found that MNM008 was able to target these specific cells and be transported into dopaminergic neuronal cell bodies through axons.

“Thanks to this technology, we can study millions of new virus variants in cell culture and animal models simultaneously. From this, we can subsequently create a computer simulation that constructs the most suitable virus shell for the chosen application — in this case, the dopamine-producing nerve cells for the treatment of Parkinson’s disease,” Björklund said.

Overall, researchers believe the BRAVE method “opens up the design and development of synthetic AAV vectors expressing capsid structures with unique properties and broad potential for clinical applications and brain connectivity studies.”

The team has established a collaboration with a biotech company, Dyno Therapeutics, to use the BRAVE method in the design of new AAVs.

“Together with researchers at Harvard University, we have established a new biotechnology company in Boston, Dyno Therapeutics, to further develop the virus engineering technology, using artificial intelligence, for future treatments,” Björklund said.

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Running Sprints Is Safe, Feasible for Those with Milder Parkinson’s, Study Finds

running sprints

Sprint running is a safe and feasible form of physical exercise for people with mild-to-moderate Parkinson’s disease.

That is the conclusion reached in the study, “Sprint exercise for subjects with mild-to-moderate Parkinson’s disease: Feasibility and biomechanical outputs,” was published in Clinical Biomechanics.

Physical exercise has been recommended for people with Parkinson’s disease because it helps to maintain balance, posture, mobility, and the ability to perform normal daily activities.

“Particularly for subjects with PD [Parkinson’s disease], a high-intensity multimodal exercise program and intensive training on a stationary bicycle were reported as feasible and safe,” the researchers wrote.

Sprint running is a type of high intensity exercise in which individuals run short distances in limited periods of time as fast as they can. In healthy individuals, sprint running increases muscle strength, physical endurance, heart and lung function and mental health.

“Although positive effects of sprint running have been reported for mouse models of PD, healthy subject and middle-aged adults, and for people with major depressive disorders, no study has investigated safety and feasibility of sprint running for individuals with PD,” the researchers wrote.

A team of Brazilian scientists decided to investigate whether sprint running could be a well-accepted, safe and feasible form of training exercise for people with mild-to-moderate Parkinson’s.

They compared the performance, satisfaction and acceptance of 20-meter (about 22-yard) sprint running training sessions among 16 men with Parkinson’s and 21 men who did not have the disease (controls). Satisfaction and acceptance were evaluated with a self-administered questionnaire, while exercise performance was determined based on biomechanic parameters — force, velocity and power — that were measured on high-speed video recordings of the sprint training sessions.

Two individuals with Parkinson’s decided to withdraw from the study. The remaining 14 patients and all individuals from the control group completed the study. Each participant, after a warm-up period, ran two sprints.

Self-administered questionnaires revealed that all participants were satisfied and felt the sprint training sessions were feasible and acceptable.

Investigators found some differences between the two groups in certain biomechanic parameters. For instance, they discovered the sprint maximal force and maximal power outputs were higher among patients with Parkinson’s, while mechanical effectiveness was higher among controls.

The maximal force and maximal power outputs refer to the maximum amount of force exerted horizontally and to the maximal mechanical power during sprint acceleration, respectively; mechanical effectiveness measures a runner’s ability to apply force against the ground more horizontally.

“Interestingly, no difference in velocity capabilities and overall 20-m[eter] sprint performance was observed between groups, possibly explained by different mechanical strategies in both groups over the sprint accelerations,” the researchers wrote.

Statistical analyses also showed that mechanical variables are important predictors of exercise performance in individuals with Parkinson’s disease.

Overall, running sprints seems to be a feasible and well-accepted exercise for those with mild-to-moderate Parkinson’s disease. Importantly, the team believes these results “are clinically relevant since sprint running could be used as a type of high-intensity exercise to rehabilitate this population with a high degree of acceptance.”

However, additional studies are required to further explore this possibility, by assessing the effects of sprint running on muscle strength, cardiorespiratory capacity, locomotion, motor symptoms, and other psychological aspects.

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Higher Risk of Falls Linked to Longer Disease Duration and PIDG Subtype, Study Suggests

gene mutation cancer risk

In Parkinson’s patients, the risk of falls increases depending on disease duration and having the postural instability/gait disturbance (PIDG) subtype, but is not signficantly correlated with non-motor symptoms, a study suggests.

The study, titled “Falls in persons with Parkinson’s disease: Do non-motor symptoms matter as much as motor symptoms?,” was published in Arquivos de Neuro-Psiquiatria.

Falls can be a major problem for people with Parkinson’s disease, with some individuals being at greater risk of serious falls. However, identifying a person’s fall risk can be challenging because the risk is affected by a multitude of different factors that may or may not be related to Parkinson’s disease itself.

Intuitively, it may seem that the best predictors of falls are likely related to motor symptoms — after all, falling is associated with moving. But, previous studies have suggested that measurements of motor function aren’t good predictors of falls.

The researchers behind this new study set out to investigate whether including non-motor symptoms, in addition to motor symptoms, would help better predict fall risk in people with Parkinson’s.

To test this, the researchers assessed 179 people (average age of 64.6 years, mean disease duration of 10.4 years) with Parkinson’s who were seen at the National Institute of Neurology and Neurosurgery in Mexico City. The participants’ clinical history, including fall history in the past year, was taken.

Participants underwent a series of evaluations, including disease state using the Hoehn and Yahr scale, assessment of motor symptoms using relevant parts of the Movement Disorders Society Unified Parkinson’s Disease Rating Scale, as well as non-motor symptoms using the Non-Motor Symptoms Scale.

Overall, 16.8% had experienced a fall in the last year, with just over half of these having experienced more than one fall — the average was 2.5 falls per month. The researchers noted that this is a “very low” proportion of patients who experienced falls (“fallers”), which “could partially be explained by under-representation of advanced forms of the disease,” a limitation of the study.

The researchers constructed statistical models using several types of data that they had collected, with the aim of identifying factors that were significantly over-represented among the fallers — thus, being predictive of falling.

They found that the severity of motor and non-motor symptoms in the participants was not significantly linked with fall risk.

However, the study did find two factors that were linked with fall risk: the first was disease duration. Patients who had experienced symptoms for longer were more likely to fall — average disease duration was 12.8 years in the fallers group and 7.4 years in the non-fallers group.

The second risk factor was having the PIDG subtype (which accounted for 59.8% of the participants), one of the three groups into which Parkinson’s patients can be divided based on their most prominent motor symptoms. The PIDG subtype is associated primarily with difficulty standing and/or walking and is thought to be associated with rapid progression of disease and cognitive dysfunction.

While about half (53%) of the people in the non-fall group had the PIDG subtype, nearly all (93%) of those in the fall group had the subtype.

“Disease duration and the PIGD subtype were identified as relevant risk factors for falls in [people with Parkinson’s disease]. Non-motor symptoms appear to have a less important role as risk factors for falls,” the researchers wrote, adding that these findings suggest a need for a “more intensive approach in fall prevention” for people with this subtype.


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Fall Avoidance Workshops Well-received by Elderly Parkinson’s Patients, Study Suggests

fall avoidance strategies

Interactive sessions, including games that are intended to help elderly Parkinson’s patients learn strategies to avoid falling, are well-received, a small Brazilian study suggests.

The study, “Gerontotechnology for fall prevention of the elderly with Parkinson,” was published recently in Revista Brasileira de Enfermagem

Falling is a major health risk for older people, and Parkinson’s disease (PD) symptoms can increase an individual’s likelihood of falling. One way to promote fall prevention is for older people with PD to be aware of certain strategies that can limit the risk. Often, that requires just being cognizant of limitations and taking things slower than might feel normal.

In the new study, researchers wanted to create a gerontological intervention to help older people with PD learn skills that would help them avoid falling, as well as bolster skills such as memory that can be affected by PD.

Gerontotechnology is defined as “the study of technology and aging that seeks to ensure good health, seeking to meet the needs arising from the aging process,” the researchers wrote.

The intervention consisted of two workshops — lectures and  interactive memory games — to help provide information to participants.

Nine older people with PD participated in each of the workshops. The participants raged in age from 68 to 74 years, four were male, five were female, four were married, and five were widowed.

The first workshop lasted about two hours and was divided into two segments: a segment in which participants were exposed to the imminent risks of falls and their correlation with Parkinson’s; and a segment of interaction and socialization through application of the memory game.

The second workshop lasted about 90 minutes and also was divided into two segments: the presentation of some topics in a booklet (developed by the researcher) for fall prevention and Parkinson’s; and memory games that could be played in groups of two or three participants.

After going through the workshops, participants were interviewed in order to ascertain their feelings about it.  Overall, responses were positive:

“The experience was very good, the time passed quickly and I learned many tips,” one participant is quoted in the study. Another said, “These things help us, it’s important, I want this little book because for us it’s a document that helps a lot.” Another participant noted “it helped to improve my memory.”

The researchers grouped the responses into categories, to highlight factors that were valuable to participants, namely: “Avoiding and learning not to fall;” “Helping people to pay attention;” “I liked it because it reminds me of my childhood/a different thing;” and “Learning from the game.”

Many participants reported enjoying the feeling of playing a game in order to learn. For instance, one participant said it reminded him/her of playing with his/her children. Other common responses were that the workshops helped emphasize the active steps that need to be taken in order to avoid falling, such as moving more slowly and with more deliberation and care.

Broadly, the researchers described the participants’ responses as being that the intervention improved “self-care, empowerment and knowledge.”

The researchers noted that this is a very small and qualitative study, so further research will be needed to improve similar interventions and to determine their merit.

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