4 Quotes That Help Me Better Accept My Chronic Pain Condition

July  2018

Many of us like quotes and may even use them at different times, but they are really of no practical use unless we apply them to our lives. Like most people, I have heard thousands of them and there are probably a dozen or so that I have embraced, four of which I want to share that have helped me cope with chronic pain from a neurological movement disorder called dystonia. I have had it for almost 20 years and these four quotes help me better accept my condition to make the most of my life

“Don’t try to understand everything, because sometimes it isn’t meant to be understood, but to be accepted.” – Unknown

I tried so hard for so long to try and understand everything about dystonia and why I have it. Being educated is helpful, but it can sometimes be system overload. I also learned that by virtue of living with it, I do “on the job” training all the time, so I need to give my search for answers a break. It can become a frustrating obsession. To this end, I have learned to better let go of trying to find the answers to everything and, to not sound corny, let the answers come to me. This is where the first quote above helps me stay grounded and reduce my tension and anxiety about my disorder to a minimum. Every time I read it, I feel a weight off my shoulders.

Letting go of trying to understand everything can be very liberating. We have to work hard every day to think about our life right now and not the life we once had. This is the way everyone should live, dystonia or not. The past is over and as much as we may miss our former self, we must let go and live in the present. Letting go or accepting doesn’t mean giving in. It means changing our perspective about the health condition we live with. It doesn’t mean giving up the fight. It means fighting in a different way. This is where the Michael J. Fox quote comes into play for me:

“Acceptance doesn’t mean resignation. It means understanding that something is what it is and there’s got to be a way through it.”

My rendition of this quote is “how do we make the best of a difficult situation?” This puts me in the role of an active participant rather than a spectator who is being tossed around by my condition rather than making the best decisions for myself. With this quote in mind, I am learning to better focus on things just as they are – not the way I think they should be. The changes that can come out of this acceptance are incredible. Taking each day one at a time and fully embracing even the most seemingly minor accomplishment is very important to our well-being.

Saying how much we hate dystonia or any other condition, won’t make it go away. I promise! If we can find a way to cohabitate with our health condition, we are better off. Too many of us want to fight against it. We have to learn to accept it because it is a part of us whether we like it or not. No amount of anger will ever take it away. This is where this third quote is most applicable for me:

“The pain will not go away by getting angry or bitter. It will go away when you learn to accept life’s challenges with grace and ease.” – Leon Brown

This has been one of the most important things I have learned (still learning) to better manage all of the symptoms that come with my dystonia – physical, mental and otherwise. I have to learn to live with it rather than fight against it, all the while still trying to find ways to manage my symptoms. The more I do this, the less power it has over me. This might sound counterintuitive, but it might be the best way for us to find peace and healing. Stop waging war on your dystonia or other health condition. You will only get worse.

I had years of ruthless symptoms where I could barely speak sometimes because of the breathtaking pain. I still deal with some pretty rough symptoms, but my mind is in a better place where I am more at peace with how things are. This reduces my tension and stress, which leads to greater acceptance and a greater ability to be more productive. I am not near as productive as I once was and would like to be, but beating myself up over this is a complete waste of time and energy. I would rather focus what energy I have on my abilities, rather than all that is wrong with me.

 I invite you to do the same. Accept what is rather than dwell in the past or on everything you can’t do. Focus on your abilities. Most of us do more than we give ourselves credit for. We need to take control and do what is best for us in order to better manage today, and just today. Tomorrow will take care of itself. With this in mind, my final quote:

“It is not what happens to us in life that defines us. It is what we do with it that defines us.” – Tom Seaman

https://themighty.com/2018/07/quotes-acceptance-coping-dystonia-chronic-pain/

Drug now in clinical trials for Parkinson's strengthens heart contractions in animals

July 20, 2018, Johns Hopkins University School of Medicine

A drug currently in clinical trials for treating symptoms of Parkinson's disease may someday have value for treating heart failure, according to results of early animal studies by Johns Hopkins Medicine researchers.

The drug, a member of a class of compounds known as phosphodiesterase (PDE) type I inhibitors, shows promising effects on dog and rabbit hearts, as well as on isolated rabbit heart cells, most notably an increase in the strength of the heart muscle's contractions, the researchers say.

Human heart failure is a chronic condition often marked by weakening of the heart muscle and its subsequent failure to pump enough blood. Currently, dozens of drugs are available to treat or manage heart failure symptoms, but drugs that improve the strength of the heart muscle's contractions, such as dobutamine, carry the risk of dangerous complications such as developing an irregular heartbeat.

However, in their study, described in a report published in the journal Circulationon July 20, the Johns Hopkins researchers demonstrate that the new compound works differently than current drugs, suggesting its use may be a safer way to increase heart contraction strength.

Heart failure affects about 5.7 million U.S. adults, according to the Centers for Disease Control and Prevention, and contributes to an estimated one in nine deaths. Standard treatment includes diuretics that increase urine production to keep the heart from becoming enlarged; angiotensin-converting enzyme (ACE) inhibitors that lower blood pressure and reduce the workload on the heart; and beta blockers that protect against heart damage from high levels of the stress hormone adrenaline that are common with heart failure, and that help reduce the heart's workload. There is no cure.

"Our results are intriguing because so far it's been largely uncharted territory to come up with a way of increasing contractility that doesn't ultimately hurt patients," says David Kass, M.D., the Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine and principal investigator of the study.

The drug explored in the new study, ITI-214, inhibits the enzyme PDE1, which is part of the larger phosphodiesterase (PDE) family of over 100 such proteins. All PDEs work by breaking down one or both of two molecules: cAMP and cGMP, each of which serve as molecular messengers inside cells. Each PDE has very specific features, including the type of cell they exist in and their location inside that cell, allowing them to adjust cAMP and/or cGMP very precisely.

PDE inhibitors work by stopping the breakdown of cAMP and cGMP, causing these molecules to build up so they can influence proteins to alter the cell. In heart disease, PDE activity can limit the beneficial effects of cAMP or cGMP, so inhibitors have the potential to act as a therapy.

In mice, Kass notes, PDE1 inhibitors had been reported to shrink abnormally thick heart muscle caused by high blood pressure and dilate blood vessels. However, in mice the heart mostly has a different form of the PDE1 enzyme than found in humans, so PDE1 inhibitors likely affect mice differently than humans.

Dogs and rabbits, which this research focused on, have a PDE1 composition more similar to humans, Kass says.

For their experiments, the researchers used six dogs surgically outfitted with sensors and heart pacemakers, and tested ITI-214's effects on them before and after inducing heart failure by running the pacemaker rapidly for approximately three weeks. The drug was tested at different doses, both orally and intravenously. The dogs were given at least a day between tests.

When given at an oral dose of 10 milligrams for every kilograms via a peanut butter-covered pill, ITI-214 increased the amount of blood pumped out by the heart each minute by 50 percent in the healthy hearts and by 32 percent in the failing hearts. It did this, Kass says, by increasing the strength of the heart's contractions by almost 30 percent and by dilating the blood vessels. Intravenous administration of the drug resulted in similar, but more rapid, effects.

"We were pretty agnostic about what we would find and didn't necessarily expect anything that novel," says Kass. "To my knowledge, no study had reported increased heart contraction strength from a PDE1 inhibition before. But then, all of the prior studies where this might have been tested had used mice, and we knew that a different PDE1 form was found in larger mammals and humans. So, we just had to try it, and the results were very interesting."

In healthy dogs, Kass cautions, the drug also raised their heart rate by approximately 40 beats per minute on average, which can be dangerous for heart failure patients. However, the dogs with failing hearts had no significant difference in heart rate before and after the drug was given.

Even with these promising results, there was a major concern. Other heart failure drugs designed to strengthen heart contractions have potentially fatal complications, such as developing wildly irregular heartbeats. Inhibitors of a different PDE, PDE3, including amrinone and milrinone, are especially infamous for this.

"This was the boogeyman in the room," says Kass. "The new drug produced many of the same heart and artery changes that PDE3 inhibitors do, so we naturally worried whether it worked in a similar way and might also have complications. So we tested them side by side."

When they compared the effects of ITI-214 to a PDE3 inhibitor in isolated muscle cells from 13 rabbit hearts, the way the two drugs acted looked different.

One of the major ways that PDE3 inhibitors are thought to work is by increasing the amount of calcium inside the muscle cell, which triggers key proteins to exert more force on the cell, and causes the cell to contract more strongly.

As expected, when the researchers applied a PDE3 inhibitor to the heart cells, calcium levels rose and the cells contracted more strongly than without the inhibitor.

By itself, inhibiting PDE1 had no effect on the muscle cells, but the researchers thought this might be because PDE1 activity is too low in a resting cell. So they used a drug to first slightly increase cAMP levels, and this increased PDE1 activity enough for them to observe ITI-214's effects.

With the added drug, ITI-214 caused the cell to contract more strongly. However, the cell's calcium levels didn't rise, strongly indicating that ITI-214 increases muscle contractions through a different mechanism than the PDE3 inhibitors.

"Our results show that inhibiting PDE1 produces different changes than blocking PDE3, and so we hope that we can bypass the calcium-mediated and potentially deadly arrhythmias that have plagued PDE3 inhibitors," says Grace Kim, a lead co-author and a postdoctoral fellow in Kass' lab. "We are anticipating similar positive benefits on heart function but with much less toxicity."

Kass says ITI-214 also appears to function differently than dobutamine, which strengthens heart contractions in people with heart failure but also can cause fatal irregular heart rhythms. Dobutamine works by stimulating the beta adrenergic system, the same system that is activated by adrenaline. Dobutamine acts on the same pool of messenger molecules that increase the cAMP that PDE3 degrades, so its heart effects are similar to those of a PDE3 inhibitor.

When the researchers blocked the beta adrenergic receptors in 11 healthy, anesthetized rabbits and then applied ITI-214, all of the effects—except for its impact on heart rate—remained. If ITI-214 were acting through the beta adrenergic system, blocking the receptors should have blocked its actions.

Instead, it appears the drug might be working on cAMP generated by a different signaling system in the heart that uses adenosine. When the researchers used a drug to block receptors in the adenosine system in a separate set of seven anesthetized rabbits, all of the effects of the drug, including increased heart rate, were eliminated.

Other studies have demonstrated that the adenosine pathway can have protective effects on the heart, Kass says. In the same issue of Circulation, other investigators at the University of Rochester also found that PDE1 controls the adenosine pathway, and that inhibiting PDE1 could protect the heart from toxicity of some cancer drugs.

ITI-214 is now in early clinical trials and is being tested in heart failure patients at Johns Hopkins Medicine and Duke University. It has already passed phase 1 safety trials in healthy individuals.

Journal reference: Circulation

Provided by: Johns Hopkins University School of Medicine

https://medicalxpress.com/news/2018-07-drug-clinical-trials-parkinson-heart.html

Ketamine for Parkinson's? Clinical trial in the works

July 20, 2018   By Maria Cohut

Researchers are planning a phase I clinical trial to test the dyskinesia-relieving effects of ketamine.

The drug used to manage some of the most salient symptoms of Parkinson's disease is known to expose patients to more motor issues, as part of its side effects. Researchers suggest that ketamine could be used to neutralize those side effects.

Parkinson's disease, a motor system disorder, is characterized by tremor, limb stiffness, impaired balance, and slowness of movement, as well as impaired movement coordination.

There is currently no known cure for this disorder, so treatments focus largely on managing the symptoms.

This helps people maintain autonomy and quality of life, as much as possible.

One of the main drugs used to treat Parkinson's disease is levodopa, which can help with limb stiffness and slowness of movement. But there is a caveat: patients for whom levodopa does work begin to experience potentially debilitating side effects after a few years on the drug.

"The problem is levodopa works great for a few years — we call that the 'honeymoon' period — but then you start getting these side effects," notes Dr. Scott Sherman, a neurologist at the University of Arizona College of Medicine in Tucson.

So what happens to many patients who take levodopa? They develop dyskinesia, or involuntary and uncontrollable movements that can affect the limbs, the head, or even the entire body, to various degrees of severity.

Once an individual develops levodopa-related dyskinesia, it does not go away unless treatment with this drug is discontinued altogether — though this may mean that their symptoms will no longer be managed.

But is there anything that could counteract levodopa's side effects? Dr. Sherman and colleague Torsten Falk believe that the answer may lie with ketamine.

Ketamine's effect on dyskinesia

Dr. Sherman and Falk found the first clues about ketamine's potential in offsetting dyskinesia when they tested it as a pain-relieving drug for patients with Parkinson's.

Their trial led them to observe an unintended yet welcome effect: dyskinesia was ameliorated, or even disappeared completely for a few weeks in the case of individuals on levodopa who were also administered ketamine.

When the researchers tried to duplicate these findings in a rat model, they found that the dyskinesia-offsetting effects of ketamine held strong.

This has led them to plan a controlled clinical trial in the hopes of discovering how — or whether — ketamine might best be used in conjunction with levodopa to treat patients with Parkinson's disease.

Ketamine's best-known side effect is dissociation (also known as disassociation), in which a person feels as though they are perceiving the world from some place outside of their own bodies. This uncanny effect is also why ketamine has notoriously been misused as a "party drug."

"Disassociation is a sort of 'out-of-body' experience. When people describe it, they have told me that they feel like they are in fish bowl," explains Dr. Sherman.

Another common risk of taking ketamine is raised blood pressure. However, the scientists are strategizing to keep these possible effects in check by carefully calculating dosage.

According to Dr. Sherman, "We are going to monitor blood pressure closely to make sure it doesn't get high. And," he continues, "we know at what dosage ketamine causes this disassociation; we expect that the dosage needed in Parkinson's disease will stay well below that level."

Upcoming clinical trials to confirm effects

The scientists plan to launch the phase I clinical trial — in which they will work with 10 patients with Parkinson's disease — later this year at the University of Arizona College of Medicine.

The project would be funded by a 3-year grant of $750,000, which will be awarded by the Arizona Biomedical Research Commission.

These funds are also due to cover additional experiments on a rodent model, which will allow the researchers to gain a better understanding of the underlying mechanisms at play.

"We want to find out exactly what ketamine is doing to have this effect," says Dr. Sherman.

"Ketamine has been long overlooked. Now it could prove very useful for Parkinson's patients."

Dr. Scott Sherman

https://www.medicalnewstoday.com/articles/322524.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202018-07-20&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

New Chemical Probe May Shed Light on Role of Potential Biomarker in Parkinson’s, Study Suggests

 JULY 19, 2018 BY PATRICIA INACIO, PHD

A new chemical probe that binds to a protein called DJ-1 — a sensor of oxidative stress and a potential biomarker of Parkinson’s disease — may help researchers understand how the protein participates in disease progression, a study suggests.

The study, “A chemical probe to monitor the parkinsonism- associated protein DJ-1 in live cells,” was published in the ACS Chemical Biology journal.

Oxidative stress is caused by an imbalance between the body’s production of potentially harmful reactive oxygen species (ROS) and its ability to contain them.

The release of ROS by dopaminergic neurons is one of the underlying causes of Parkinson’s disease. Dopamine is a chemical essential for nerve cell communication and memory formation.

It is no surprise then that patients with a loss of function of the DJ-1 protein — which senses and protects against ROS molecules — often experience an early-onset familial form of Parkinson’s disease.

DJ-1 senses oxidative stress through a specific amino acid, called Cys-106, which becomes oxidized when it comes in contact with reactive oxygen species. This led researchers to hypothesize that DJ-1 could be a biomarker for oxidative stress in Parkinson’s disease.

The problem with this biomarker is that researchers need to distinguish the different forms DJ-1 can take. And while many probes can determine if a cysteine residue is oxidized or reduced, none are specific for this protein, largely hindering its detection.

Researchers in this study investigated a new compound, called aminoepoxycylcohexenones (AECH), which had shown high specificity to a bacterial protein similar to DJ-1.

They examined seven AECH probes and their ability to monitor oxidized DJ-1 levels in live cells. Among them, four strongly bound the protein, and three were moderate inhibitors.

The strong inhibitors rapidly bound the protein, but they also bound it even when mutations were present. However, moderate inhibitors did not label the mutant protein, and one in particular, called FM247, was chosen for additional analysis.

They tested FM247 in two human cell lines from cervical and lung cancer patients, as well as in a cell line relevant for Parkinson’s disease.

In all the different cell lines, the probe showed a clear selectivity for the oxidized DJ-1.

These results support the usefulness of FM247 as a tool for monitoring oxidized DJ-1 levels, which could be an important biomarker for Parkinson’s.

“Furthermore, FM247 and tools derived thereof are promising for imaging of DJ-1 in live cells to obtain direct information of localization and oxidation states,” the researchers concluded.

https://parkinsonsnewstoday.com/2018/07/19/new-chemical-probe-may-shed-light-potential-parkinsons-biomarker-study/

Computer Model to Select Parkinson’s Patients Who Benefit Most from Deep Brain Stimulation

JULY 19, 2018 lBY IQRA MUMAL

Cleveland Clinic researchers have developed a new model that accurately predicts whether quality of life would improve in Parkinson’s disease patients after deep brain stimulation, a new study shows.

The tool may help select those who will benefit the most from the procedure, guiding patients and physicians in the decision-making process.

The study, “Quality of Life Improvement Following Deep Brain Parkinson’s Disease: Development of a Prognostic Model,” was published in the journal Neurosurgery.

Deep brain stimulation (DBS), an established treatment for Parkinson’s disease, is a neurosurgical procedure that involves implanting a medical device called a neurostimulator in the brain, which will send electrical impulses to specific brain regions.

While several studies have discussed the potential benefits of using deep brain stimulation, others have reported DBS-associated complications, making it hard for patients to decide whether they should undergo the procedure.

One of the most important markers of success after a surgical procedure is the evaluation of a patient’s quality of life (QoL). Researchers have become very interested in determining the factors that can best predict QoL improvements after DBS surgery.

Investigators attempted to develop a model that can help predict improvement in QoL after surgery for deep brain stimulation.

Specifically, they made use of preoperative patient characteristics and imaging data that would be available in most centers that regularly perform deep brain stimulation.

QoL was measured using the Parkinson’s Disease Questionnaire-39 (PDQ-39). Then, potential predictive factors — such as patient demographics, clinical presentation, imaging scans, and motor and psychological testing — were analyzed for their impact on QoL scores post-surgery.

Among the 67 patients in the study, 36 (53.7%) experienced an improved quality of life following surgery. Researchers discovered that there were five variables that significantly contributed to the QoL outcome.

The first was the number of years since the onset of symptoms. An analysis showed that for every additional year since symptoms onset, patients demonstrated an 11% greater chance of improvement in QoL.

The second variable was bilateral DBS implantation. Essentially, patients who underwent deep brain stimulation implants in both hemispheres of the brain were six times more likely to have an improvement in QoL compared to those who only underwent right-sided DBS.

The third was the UPDRS-III total score, which assesses the motor signs of Parkinson’s disease. Researchers showed that for every extra 1% “on” vs. “off” medication change in UPDRS-III total score, the odds of quality of life improvement increased by 4.5%.

“On” in UPDRS-III refers to patients who are receiving medication and have a good response, while “off” refers to times when patients have a poor response in spite of taking medications. Therefore, patients who are responsive to medication are more likely to experience an improvement in QoL after deep brain stimulation.

The fourth variable was the levodopa-equivalent daily dose. Results showed that for every every additional 100 units of levodopa-equivalent daily dose that a patient was prescribed preoperatively, the improvement in QoL increased by 12.4%

Finally, for every one-point increase in the preoperative PDQ-39 score — which indicates worse QoL — patients experienced a 7.3% increase in odds of improvement after DBS.

To develop the predictive model, researchers used three of these factors: change in PDQ-39, percent change in UPRS-III, and years since symptom onset. These three factors were able to collectively predict improvement in QoL after DBS with an 81% accuracy.

“Our data may serve as the foundation to further refine a clinically relevant prognostic tool that would assist the decision-making process for clinicians and DBS multidisciplinary teams assessing patient candidacy for surgery,” investigators wrote.

https://parkinsonsnewstoday.com/2018/07/19/computer-model-select-parkinsons-patients-benefit-deep-brain-stimulation/

Visual Hallucinations in Dementia and Parkinson Disease: Assessment of Patient, Caregiver Experiences

Emily Pond    July 19, 2018 

Researchers conducted in-depth interviews with 10 individuals with dementia and 11 individuals with Parkinson disease, all of whom experienced visual hallucinations.

Visual hallucinations are mediated by cognitive ability and level of insight, according to study results published in the International Journal of Geriatric Psychiatry. 

Researchers conducted in-depth interviews with 10 individuals with dementia and 11 individuals with Parkinson disease, all of whom experienced visual hallucinations. Interviews were also conducted with the informal caregivers of the participants with dementia (n=11) and Parkinson disease (n=9). An “inductive thematic approach” was utilized to analyze and qualify interview elements.

In the study, 3 primary themes were identified: (1) “insight and distress,” (2) “caregiver approach: challenging [vs] reassurance,” and (3) “normality and stigma.” Across interviews, “insight” was identified as a protective measure; if participants recognized their visual hallucinations as an element of their disorder, they were less likely to feel threatened or afraid. Caregiver approach to visual hallucinations was also identified as a significant influence; some challenged the existence of visual hallucinations, whereas individuals caring for more impaired individuals often “colluded” with the visual hallucinations in order to reassure the patient. 

Interviewees also highlighted the stigma associated with hallucinations, and patients who felt their situation was “abnormal” were less likely to seek help. This trend was more common in patients with Parkinson disease than patients with dementia, although both described feeling “embarrassed or ashamed.”

As a qualitative study, this research provides insight into patient experiences. Based on these data, the researchers suggested that therapeutic efforts focus on support “according to the level of insight and cognitive impairment,” and that the medical community provide an additional measure of support by working to destigmatize hallucinations.

Reference

Renouf S, ffytche D, Pinto R, Murray J, Lawrence V. Visual hallucinations in dementia and Parkinson's disease: a qualitative exploration of patient and caregiver experiences [published online June 28, 2018]. Int J Geriatr Psychiatry. doi:10.1002/gps.4929

https://www.psychiatryadvisor.com/geriatric-psychiatry/dementia-parkinson-disease-visual-hallucinations/article/782043/

Aggressive immune cells aggravate Parkinson's disease

July 19, 2018         University of Erlangen-Nuremberg

Parkinson's disease, formerly also referred to as shaking palsy, is one of the most frequent disorders affecting movement and the nervous system. Medical researchers have come across a possible cause of the disease - in the patients' immune system.

Parkinson's disease, formerly also referred to as shaking palsy, is one of the most frequent disorders affecting movement and the nervous system. Medical researchers at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) have come across a possible cause of the disease -- in the patients' immune system.

Currently, approximately 4.1 million people suffer from Parkinson's disease throughout the globe, in Germany alone more than 300,000 people are affected. Typical symptoms of the disease are slowness of movement, rigidity, frequent shaking and an increasingly stooped posture. The cause is the continuous death of nerve cells in the brain, which produce the messenger substance dopamine.

Scientists are working to gain insights into the mechanisms which lead to the loss of nerve cells that produce dopamine. Until now, little has been known about whether human immune cells have an important role to play in Parkinson's disease. The stem cell researchers Dr. Annika Sommer, Dr. Iryna Prots and Prof. Dr. Beate Winner from FAU and their team have made a major leap forward in research into this aspect of the disease. The scientists from Erlangen were able to prove that in Parkinson's disease immune cells from the immune system, so-called t-cells, attack and kill nerve cells which produce dopamine in the midbrain.

The FAU team based its research on a surprising observation: the scientists found an unusually high number of t-cells in the midbrain of Parkinson's patients. These cells are commonly found in the brains of patients suffering from diseases in which the immune system attacks the brain. During tests carried out in collaboration with the movement disorders clinic (molecular neurology) at Universitätsklinikum Erlangen (Prof. Jürgen Winkler), researchers discovered an increased number of certain t-cells, specifically Th17 cells, in Parkinson's patients, similar to patients with autoimmune diseases such as rheumatoid arthritis.

In view of these results, the researchers decided to develop a very unusual cell culture from human cells. A small skin sample was taken from affected patients and healthy test subjects. These skin cells were converted into stem cells, which can develop into any type of cell. The research team then further differentiated these cells into midbrain nerve cells specific to the patient. These midbrain nerve cells were then brought into contact with fresh t-cells from the same patients. The result: the immune cells of Parkinson's patients killed a large number of their nerve cells, but this did not appear to be the case with healthy test subjects. Another result gives reason for hope: antibodies which block the effect of Th17 cells, including one antibody which is already being used on a daily basis in the hospital to treat psoriasis, were able to largely prevent the death of the nerve cells.

'Thanks to our investigations, we were able to clearly prove not only that t-cells are involved in causing Parkinson's disease, but also what role they actually play,' explains Prof. Dr. Beate Winner. 'The findings from our study offer a significant basis for new methods of treating Parkinson's disease.'

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Story Source:

Materials provided by University of Erlangen-Nuremberg. Note: Content may be edited for style and length.

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Journal Reference:

1. Annika Sommer, Franz Maxreiter, Florian Krach, Tanja Fadler, Janina Grosch, Michele Maroni, Daniela Graef, Esther Eberhardt, Markus J. Riemenschneider, Gene W. Yeo, Zacharias Kohl, Wei Xiang, Fred H. Gage, Jürgen Winkler, Iryna Prots, Beate Winner. Th17 Lymphocytes Induce Neuronal Cell Death in a Human iPSC-Based Model of Parkinson’s Disease. Cell Stem Cell, 2018; 23 (1): 123 DOI: 10.1016/j.stem.2018.06.015

https://www.sciencedaily.com/releases/2018/07/180719094349.htm

STUDY: TOXIN USED TO CLEAN WATERWAYS CAUSES PARKINSON'S

July 18, 2018

https://youtu.be/HdxVD9_Niwk

Below is the closed-captioning text associated with this video. Since this uses automated speech to text spelling and grammar may not be accurate.

toxin used to clean lake-stngr-2 a study is showing a toxin being used to help clean waterways in our area could be causing a serious health disorder. k-i-m-t news three's brian tabick is at clear lake today talking to those swimming... brian - is that toxin used on the lake?xxx maplive:study: rotenone causes parkinson's clear lake, ia google earth 2018 google city beach.jpg amy those with the iowa department of natural resources say the toxin rotenone has never been spread over clear lake... but has been used on ventura marsh which is attached to the body of water. 

brian live-lintro-2 but those i spoke with today say they aren't letting this news stop them from enjoying a day at the beach.xxx lowerthird2line:study: rotenone causes parkinson's clear lake, ia dave howlett and his granddaughter brandy spend a lot of their time at the beach and in the water. toxin used to clean lake-mpkg-1 natural sound he has never heard of rotenone. those with the iowa d-n-r say the chemical is used to kill off invasive species, carp in particular in ventura marsh. they say small amounts of rotenone will not have an impact on humans. but a study done on the toxin and its use by farmers has linked it to parkinson's disease, a disorder of the central nervous system.

howlett says it's not stopping him from enjoying the weather and the water. lowerthird2line:dave howlett clear lake, ia i haven't heard anything to that affect i mean if a guy is out there everyday swallowing it you know but just to be wading around in is swimming around, don't see a problem. / brian live-ltag-2 those with the iowa d-n-r say they have been using the compound since 19-30's. they use around 50 to 100 thousand dollars of each year in waterways throughout the state. in clear lake brian tabick k-i- m-t news three. / thank you brian. the d-n-r says the chemical is used in many of the lakes only contains around five percent of rotenone . /

http://www.kimt.com/content/video/488560691.html

How Michael J. Fox And Tracy Pollan Have Stayed Together For 30 Years Despite their hardships

KATE STREIT · July 18, 2018

Despite their hardships, the couple have gone on to have success in life, work and love.

Actors Michael J. Fox and Tracy Pollan have been married for an impressive 30 years. Although some relationships in Hollywood have stood the test of time, it’s no secret that a lot of romances that take off in Tinsel Town end up having a pretty short shelf life. But Fox and Pollan have weathered a lot together since they wed on July 16, 1988. They’ve had career ups and downs, parenthood, a harrowing period of time in which they received threats from a stalker and Fox’s journey with young-onset Parkinson’s disease, which he was diagnosed with in 1991 at just 29 years old.

Fox and Pollan met on the set of “Family Ties,” the hit 1980s sitcom in which Fox starred as Alex P. Keaton, a precocious and whip-smart young man who drove his liberal parents crazy with his conservative political beliefs. In 1985, Pollan was cast as Fox’s character’s girlfriend, Ellen Reed,  an equally intelligent dancer who could stand her ground in a battle of the wits with her love interest.

Although the two had great onscreen chemistry, they were both involved with other people at the time (Pollan with actor Kevin Bacon and Fox with “Facts of Life” star Nancy McKeon) and were just friends and colleagues during the time they played a couple on TV.

However, when they both found themselves single a short time later, they began to date. The couple got engaged in December 1987 after just seven months together. In 1989, Pollan gave birth to their first son, Sam Michael. They later welcomed twin daughters Aquinnah Kathleen and Schuyler Phyllis in 1995 and daughter Esme Annabelle in 2001.

Fox went public with his Parkinson’s diagnosis in 1998, and together the couple have made it their mission to raise funds and awareness for the disease through the Michael J. Fox Foundation, a 501(c)3 nonprofit. Fox acts as founder, and Pollan also sits on the organization’s Board of Directors.

Despite their hardships, the couple have gone on to have success in life, in work and in love. And after all these years, it seems like they are still pretty smitten with each other.

“He’s an amazing father,” Pollan gushed of her husband to People back in 2015, adding, “He’s one of the smartest people I know … and he’s pretty cute still!”

For his part, Fox says that his initial feeling that he and Pollan were meant to be turned out to be right.

“Let me put it this way — my instincts were proven out,” he said in a 2002 interview with Oprah Winfrey for O Magazine. “Tracy was the right person for me, and it has been amazing.”

Here’s to many more happy years together for this sweet couple!

https://www.simplemost.com/michael-j-fox-tracy-pollan-relationship/