Higher Mortality Rates Found in Patients with Parkinson’s Dementia, Lewy Body Dementia, Study Shows

AUGUST 15, 2018  BY DIOGO PINTO IN NEWS.

Patients diagnosed with Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) were found to have a mortality rate more than three times higher than the general population, according to researchers in Sweden.

The 10-year follow-up study, titled “Relative survival in patients with dementia with Lewy bodies and Parkinson’s disease dementia,” was published in the journal PLOS One.

DLB is a neurodegenerative disorder caused by the accumulation of alpha-synuclein protein clumps, leading to physical and cognitive damage.

The alpha-synuclein protein clumps and associated symptoms are also found in a large group of patients with Parkinson’s disease who develop dementia.

Years of research identified a link between the diagnosis of dementia and increased mortality. But the mortality levels greatly depend on dementia type, gender, and study design.

In the general population with dementia, late diagnosis, male gender, the existence of multiple coexisting conditions (comorbidities), and functional disability have been linked to shorter survival.

A research team from Skåne University Hospital in Malmö, Sweden, studied the survival of patients with PDD and DLB compared with the general population. To better understand survival in these groups, the team identified predictors of excessive mortality.

Researchers retrospectively studied 177 patients diagnosed with PDD or DLB from 1997 to 2014 at the Memory Clinic in Malmö. Data collected included demographics, time of first visit, time of diagnosis, comorbidities, apolipoprotein E (APOE) genotyping — a test used to assess a person’s susceptibility for Alzheimer’s disease — and the mini-mental state examination score at the time of diagnosis.

Of the 177 patients included in the study, 131 had DLB, while 46 were diagnosed with PDD. All these patients had at least one comorbidity due to the diagnosis of dementia.

A total of 143 patients (81%) had died by the time of follow-up, with a median survival of 4.1 years.

At a five-year follow-up, the mortality ratio — the ratio between the number of PDD/DLB patients’ deaths over the number of deaths in the general population — was 3.02, and at 10 years, it was 3.44, indicating that PDD and DLB patients have mortality rates more than three times higher than the general population.

Researchers also found that survival was worse if the patients were diagnosed at a younger age, were female, and showed lower scores on the cognitive test.

A more detailed analysis revealed higher mortality in DLB patients who were positive for the APOE test, but not in PDD patients who tested positive in APOE.

This retrospective study demonstrated a higher mortality rate in patients with PDD and DLB compared with the general population 10 years after the diagnosis of the disease.

Also, younger patients, females, and those who tested positive for APOE are linked to excess mortality.

“In conclusion, mortality in patients diagnosed with Lewy bodies and Parkinson’s disease dementia is over three times higher in patients during a ten-year follow-up, compared to persons in the general population unaffected by the disease,” the researchers wrote.

“Excess mortality is found primarily in younger patients, females and carriers of APOE. Further research is required regarding survival and possible interventions, including disease-modifying treatments, to improve care and prognosis for these patients,” they added

https://parkinsonsnewstoday.com/2018/08/15/higher-mortality-rates-found-parkinsons-dementia-lewy-body-dementia-patients/

TV presenter Claire McCollum tells of brave dad's struggle with Parkinson's

August 15, 2018

Presenter Claire McCollum with her dad Sam

Journalist Claire McCollum has had the opportunity to meet some of the greatest sporting legends over the years.

Among them was Muhammad Ali, considered one of the most charismatic boxers of all time.

And while interviewing Ali was a career highlight, the mum-of-two had no idea that she would one day have something in common with one of the most famous names in the world.

Nine years ago, her dad, 77-year-old Sam McCollum, was diagnosed with Parkinson's disease - the same degenerative condition that Ali battled for decades.

It is why 44-year-old Claire is now a passionate supporter of Parkinson's UK and why she is opening up about the devastation wreaked on families affected by the condition.

Currently, there is no cure for Parkinson's disease, a condition in which parts of the brain become progressively damaged, with the three main symptoms being a tremor, slow movement and stiff and inflexible muscles.

In the case of Claire's father, signs that he had the neurological condition came in the form of slowed movement and problems with co-ordination.

"I think he just didn't feel right," said Claire, mum to 11-year-old Samuel and nine-year-old Rosa.

"His movement was slow, although not as slow as it would be now, his co-ordination just started to be not as good as it would have been.

"He'd had wonderful hand-eye co-ordination and he would have built model airplanes all his life, but we noticed that his co-ordination wasn't as good.

"He would have been sliding his feet along when he was walking, although it wasn't really pronounced.

"Mum would have noticed it the most, she was living with him, so she would have picked up on things that maybe the rest of us didn't notice," said Claire "I obviously knew about (actor) Michael J Fox and Muhammad Ali, who I had the privilege of meeting, but Parkinson's wouldn't have been in my consciousness other than that, so it was a real shock when dad was diagnosed."

Her dad Sam is now on medication to try and slow down the progression of the disease, as well as manage his symptoms.

Despite this, the effects of the Parkinson's disease are felt by Sam and his wife of 49 years, 73-year-old Margaret, on a daily basis.

Claire struggles to talk about her dad's ailing health without becoming emotional, but she is constantly inspired by her parents.

"I could sit here and say it would be better if he didn't have this, but it is what it is and dad is wonderful, he carries it so well, he's brilliant with it," said Claire.

"He's a very quiet man and what he says matters, he is wonderful and I feel most calm about everything when I'm with him.

"Mum lives with it constantly and is going through it as much as dad is, so I feel for them both. I have to keep telling myself they'll be fine.

"There's actually no point in wishing it was any other way and we're lucky that we have dad and he and mum have such a wonderful partnership."

Claire describes her parents as "a real old fashioned, lovely couple", describing how they are completely devoted to each other.

"They care for one other, dad is very much mum's rock, although mum is doing a lot of caring for dad now," she added.

"She still needs him in so many ways and he is so much help on his good days.

"They work so well as a team, on his good days, dad gets up and does breakfast for mum and he lays the table properly, he doesn't just slap the dishes down on the table.

"They get out as much as possible, although it can be more difficult on his bad days."

She added: "His movement is definitely slower and his co-ordination is definitely becoming more compromised and there would also be the Parkinson's stare that some people talk about.

"That's where the expression on the face reduces, so even when dad is happy, you might not realise it.

"The thought processes are slowing down, too, so he might be saying something and will lose what he's trying to say.

"He knows what he's trying to say, the messages are in there, but the pathways are blocked and he can't get it out.

"It's definitely frustrating and it's becoming more of an issue."

Claire said they now have to keep a closer eye on what her father is doing.

She added: "Mum would have to watch him a bit more because when he isn't feeling so good, his balance and co-ordination would suffer and he has fallen a few times, which is distressing in itself.

"During the recent heatwave, dad would have been more prone to becoming dehydrated and that stops the medication from working as well.

"He isn't able to drive anymore, but we're thankful he made that decision himself because he realised his reactions weren't as quick as they once were. It's really been about dad learning his limits and learning to adapt."

For her part, Claire does as much as she can to help and support her parents - she moved closer to her childhood home in Jordanstown, where her parents still live, so she could help more.

Parkinson's UK has also played a crucial role in supporting the family, with Sam attending exercise classes, while Margaret spends time with other spouses and carers.

"They all know they're in the same boat and I think they get strength from that," continued Claire. "You can feel alone at times, but meeting up with other people affected with Parkinson's, it's a time when they feel they can talk about it.

"This disease is horrible, it isn't nice because it can take away so much of the person. I know dad is still in there, but it has compromised his life in so many ways.

"It would be wonderful if they could find a cure, but for now, we're just living with the moment, going with whatever way the Parkinson's is going and taking each day as it comes."

Claire has pledged her support for two upcoming events to raise funds for Parkinson's UK - Causeway Coast Challenge on September 8, starting from Carrick-a-Rede rope bridge in Ballintoy, and Parkinson's Does Strictly, being hosted by Claire, on November 2 at the Stormont Hotel in east Belfast. 

For more information, log on to www.parkinsons.org.uk

https://www.belfasttelegraph.co.uk/news/northern-ireland/tv-presenter-claire-mccollum-tells-of-brave-dads-struggle-with-parkinsons-37216580.html

Michael J Fox, 57, reveals he 'drank heavily' after his Parkinson's Disease diagnosis in 1991 and it damaged his marriage

By HEIDI PARKER FOR DAILYMAIL.COM  August 15, 2018

Admission time: Michael J Fox of Family Ties fame was diagnosed with Parkinson's Disease in 1991. And it was a hard pill to swallow for the energetic young actor who had made a fortune on his Back To The Future films he told People

Michael J Fox of Family Ties fame was diagnosed with Parkinson's Disease in 1991.

And it was a hard pill to swallow for the energetic young actor - he was only 30-years-old at the time - who had made a fortune on his Back To The Future films.

In the new issue of People, the 57-year-old star, who has been wed to actress Tracy Pollan since 1988, revealed that he took to drinking soon after he was handed the bad news about his health.

Parkinson's disease is a neurodegenerative disorder causing tremors and, when the disease has matured, the loss of motor skills.

Fox said that he was drinking heavily and hiding the wine bottles from his wife because he found it too hard to cope with his new illness.

It caused friction with Tracy, with whom he shares son Sam, 29, twin daughters Schuyler and Aquinnah, 23, and daughter Esmé, 16. 

'I was isolating myself from my family,' said the Teen Wolf star. 

Rough patch: He started drinking, which caused friction with Tracy, with whom he shares son Sam, 29, twin daughters Schuyler and Aquinnah, 23, and daughter Esmé, 16. Seen in 2017

Tracy added, 'It was scary because you just don't know how it is going to turn out.'

One morning when she found him passed out on the floor, she let him know she was over it. Instead of being angry, she looked 'bored' with it all, he said.

Tracy asked him, 'Is this what you want? Is this what you want to be?' She then walked out the door.

Michael cleaned up his act and decided his path was to help others so he launched his foundation to collect money for Parkinson's research. So far he has raised nearly $1 billion.

His big hit film: With co-star Christopher Lloyd in Back To The Future in 1985

He now believes that in five years doctors will be able to 'predict' Parkinson's.

As far as his long marriage to Tracy, he said they just clicked from the start because their upbringings were in line.

'Big families, middle children,' Fox said. 'Sense of humor. Both our families had that.'

'It was us against the world,' says Pollan of her own childhood. 'That's exactly what we've created.'

They met in the summer of 1985, when Pollan auditioned for Family Ties. Then in 1987 they worked on the film Bright Lights, Big City. They started dating, and a year later they wed. 

She said the trick to staying married is to 'just give each other the benefit of the doubt.' She added: 'He assumes I'm doing the best I can.'

And the Spin City actor also said: 'Find the best things about you and the best things about life and celebrate them.' 

Pollan said he has added 'so much' to her life.

'His optimistic worldview about everything is just so powerful. Michael doesn't worry about the future. I'm completely the opposite,' she admitted.

Fox then explained: 'It leaves a lot of work for other people sometimes because I'm like, "Oh yeah, don't worry about it. It'll be great!" I can do that because I know she's got it handled.'

http://www.dailymail.co.uk/tvshowbiz/article-6063291/Michael-J-Fox-57-reveals-drank-heavily-Parkinsons-Disease-diagnosis-1991.html

Changes in Glucose Regulation in Parkinson Disease

 Sheila Jacobs   August 14, 2018

Dysglycemia in Parkinson's may be a result of impaired adaptive insulin secretion because of dysautonomia.

Patients with Parkinson disease (PD) who are nondiabetic have impaired glucose control compared with healthy controls, according to the results of a controlled, cross-sectional study (ClinicalTrials.gov identifier: NCT01114321) that was conducted in the Movement Disorders Unit of the University Hospital of Clermont-Ferrand in France. Findings from the study were published in Parkinsonism and Related Disorders.

The investigators sought to detect changes in glucose regulation in patients with moderate to severe PD in response to oral glucose intake. Blood glucose levels and insulin kinetics were compared in 50 patients with PD and 50 healthy control patients during a 75-g Oral Glucose Tolerance Test (OGTT). Patients with PD and control patients were matched with respect to age, sex, and body mass index. 

A self-assessment questionnaire, the Scales for Outcomes in Parkinson's disease, Autonomic dysfunction (SCOPA-AUT), was used to analyze potential associations between changes in glucose kinetics and clinical parameters, including PD severity and autonomic function. 

All participants had to drink the 75-g solution used in the OGTT within 5 minutes. After this, blood glucose and insulin levels were measured at 30 minutes (T30), 60 minutes (T60), 90 minutes (T90), 120 minutes (T120), 150 minutes (T150), and 180 minutes (T180). Blood glucose levels were significantly higher at T90 (P =.04) and T150 (P =.01) among patients with PD vs healthy control patients. 

In addition, the total area under the curve for blood glucose concentrations was significantly greater in patients with PD compared with healthy control patients (1187±229 vs 1101±201 mmol/min/L; P =.05). At the same time, there was no significant increase in insulin levels observed among patients with PD compared with control patients. 

Higher blood glucose levels were significantly associated with higher body mass index (P <.001), female sex (P <.033), longer duration of PD (P =.001), higher SCOPA-AUT scores (P =.017), and lower dose of dopaminergic agents (P =.023). 

The investigators concluded that the impairment in glucose control observed among patients with moderate to severe PD who do not have diabetes is the result of an impairment in their adaptive insulin response, which may be a novel nonmotor result of PD-associated dysautonomia. A major limitation of the current study is the fact that level of physical activity, which is known to play a large role in the regulation of glucose metabolism, was not evaluated.

Reference

Marques A, Dutheil F, Durand E, et al. Glucose dysregulation in Parkinson's disease: Too much glucose or not enough insulin? [published online May 31, 2018]. Parkinsonism Relat Disord. doi: 10.1016/j.parkreldis.2018.05.026

https://www.neurologyadvisor.com/movement-disorders/glucose-dysregulation-parkinsons-disease-insulin/article/788138/

Apomorphine Infusions Improves Off Time Associated With Parkinson Disease

Neurology Advisor Contributing Writer   August 14, 2018

Continuous infusion of apomorphine may allow for a reduction in required concomitant oral dose of antiparkinsonian medications.

Apomorphine infusions increased off time (the amount of time medications do not impact Parkinson disease symptoms) by reducing uncontrolled motor fluctuation in patients with Parkinson disease, according to a study published in Lancet Neurology.

The researchers of this double-blind, placebo-controlled trial randomly assigned 106 patients with Parkinson disease, who experienced motor fluctuations currently not managed with other medications, into a subcutaneous apomorphine infusion group or a placebo group. The apomorphine infusion group received apomorphine at a rate of 3 to 8 mg/hour for an average of 16 hours per day. The control arm received a placebo saline infusion for 16 hours per day. The first 4 weeks consisted of the titration period where the dosage was slowly increased to 8 mg/hour or to the highest tolerated dose. The next 8 weeks consisted of the maintenance phase where the dosage remained consistent.

Patients completed hospital visits at baseline, 2, 3, 4, 6, 8, 10, and 12 weeks where vital signs, standard blood tests, and adverse events were assessed. Patients completed diaries at home containing information on motor control and sleeping patterns. The primary endpoint was efficacy shown through a change in off time recorded in patient's diary. Secondary endpoints were changes in quality of life and adverse events.

The mean apomorphine dose was 4.68 mg/hour (SD 1.50), and 12 patients in the intervention arm and 23 patients in the control arm discontinued treatment before the end of the 12 weeks. The apomorphine infusion significantly reduced off time by -2.47 hours per day (SD 3.70) and -0.58 (SD 2.80) hours per day for the placebo group, for a total treatment difference of -1.89 hours per day (95% CI, –3.16 to –0.62; P=.0025).

Apomorphine infusions also significantly decreased time of dyskinesia (treatment difference 1.97 hours per day, 95% CI, 0.69-3.24; P=.0008), improved Patient Global Impression of Change scores (P<.0001), and improved self-evaluated general health in 71% of the patients. Oral levodopa doses decreased significantly in the apomorphine infusion from baseline to 12 weeks (P=.0014). Adverse events occurred in 93% of the patients receiving the apomorphine infusion, and most of these were mild or moderate. Skin reactions, nausea, and somnolence were the most common adverse events.

Severe adverse events were noted in 5 patients.

Limitations of this study included a possible degree of attrition bias due to the number of patients who withdrew early from the study, adverse events due to oral dopamine agonists not completely discontinued, and complete trial blinding could have been compromised due to the quick and notable effects of apomorphine.

In conclusion, apomorphine infusions significantly reduced off time and provided patients with Parkinson disease who experienced uncontrolled motor fluctuations a treatment option that is effective and safe.

This study was supported by Britannia Pharmaceuticals Ltd. Please refer to reference for a complete list of authors' disclosures.

Reference

Katzenschlager R, Poewe W, Rascol O, et al. Apomorphine subcutaneous infusion in patients with Parkinson's disease with persistent motor fluctuations (TOLEDO): a multicentre, double-blind, randomised, placebo-controlled trial [published online July 25, 2018]. Lancet Neurol. doi: 10.1016/S1474-4422(18)30239-4

https://www.neurologyadvisor.com/movement-disorders-advisor/persistent-motor-fluctuation-subcutaneous-apomorphine/article/788498/

Communication Deficits in Parkinson’s Patients Caused by Motor and/or Cognitive Impairment

AUGUST 14, 2018      BY MARTA FIGUEIREDO 

Communication difficulties are caused by motor and/or cognitive impairment in people with Parkinson’s disease, a review study highlights.

An interdisciplinary approach to assess changes in patients’ daily communications may help detect and monitor motor and cognitive symptoms in this population.

The review, “Communication impairment in Parkinson’s disease: Impact of motor and cognitive symptoms on speech and language,” was published in the journal Brain and Language.

While the clinical diagnosis of Parkinson’s disease is based on the presence of characteristic motor symptoms like tremor, slowness of movement, and rigidity, cognitive impairment is a significant non-motor symptom of the disease.

Up to 90 percent of all Parkinson’s patients have impaired communication, which may develop in the early or late stages of the disease. These deficits have a great impact in patients’ quality of life and can lead to social isolation and depression.

Communication deficits in Parkinson’s patients include changes in voice and speech acoustics, comprehension and production of language, verbal fluency, the use of action verbs, and speech pauses. These deficits have the potential to be used as linguistic biomarkers of the disease.

However, the contribution of motor and cognitive deficits toward impairment in each of those areas of communication, along with the appropriate tools to assess them, are still unclear.

Researchers conducted a PubMed database search using the terms “Parkinson’s” and “language,” “speech,” “acoustics,” “voice,” “pause,” and “communication.” All studies that met the team’s criteria were reviewed to evaluate the relative roles of motor and cognitive impairment in Parkinson’s communication impairment.

Changes in voice and speech acoustic, such as decreased loudness, monotone speech, and impaired articulation, appear to be associated with motor impairment, including slowness and rigidity of the vocal apparatus.

Linguistic deficits, such as production and comprehension of complex grammar and syntax language, are more likely to be caused by cognitive impairment than motor dysfunction. Also, studies have shown that language processing is associated with attention and executive function and working memory.

However, the frequency of those deficits in Parkinson’s patients without dementia is still unclear, and no well-established tools to measure patients’ grammatical complexity are available. Thus, future development of objective measures may help identify these deficits and determine whether they occur early in the disease to make them useful markers.

While verbal fluency is one of the most tested communication skills in Parkinson’s patients, so far results have not been consistent, suggesting that verbal fluency may be “a less sensitive marker of language impairment in [Parkinson’s disease], or that other confounders need to be examined,” researchers wrote.

Parkinson’s patients show consistent difficulties in using action verbs, which appear to be more associated with motor dysfunction than with cognitive deficits. One of the possible explanations for this deficit is that the process of storing the meaning of a word that describes an action uses the same brain regions as the process of learning and executing actions, which also is impaired in these patients.

“…action verb deficits could thus be contrasted with grammar and syntax deficits (i.e. markers of cognitive function), to develop symptom-specific linguistic markers for improved disease monitoring,” researchers wrote.

The authors also found that the increased frequency of speech pauses in Parkinson’s patients is likely to be affected by both motor and cognitive impairment. Because it also is increased in other neurodegenerative diseases, further research is necessary to identify Parkinson’s-specific pausing patterns and develop appropriate assessment tools.

Parkinson’s patients also may have subtle comprehension and processing deficits of non-verbal and emotional aspects of communication, such as difficulties in recognizing affective tones in speech and/or emotional faces and gestures. Additional knowledge about how these deficits affect communication in Parkinson’s patients is necessary.

“With improved characterization of speech and language deficits, it may be possible to develop markers specific for motor and non-motor symptoms of PD,” researchers wrote.

They noted these potential communication markers should be studied further in the context of daily communication, and that mobile technology and automated speech analysis approaches may be powerful tools that can be used in patients’ daily life.

https://parkinsonsnewstoday.com/2018/08/14/researchers-identify-causes-communication-deficits-parkinsons-patients/

Study Reveals Alpha-synuclein’s Role in Parkinson’s, Lewy Body Dementia

AUGUST 14, 2018     BY DIOGO PINTO 

Alpha-synuclein (aSyn), a protein linked to Parkinson’s disease and dementia with Lewy bodies (DLB), exerts its harmful effects by disrupting the normal function of protein production, a study has found.

This sheds light on the involvement of the aSyn protein in Parkinson’s disease, confirming its potential as a therapeutic target.

The study, “Alpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function,” was published in the journal Neurobiology of Disease.

Alpha-synuclein plays a key role in both Parkinson’s disease and DLB. This protein is the major component of Lewy bodies — protein clumps that develop inside nerve cells and contribute to neurodegeneration.

Mutations in the gene that provides instructions for making aSyn protein, the SNCA gene, are linked to familial forms of Parkinson’s disease. This is especially true for a mutation known as A30P.

Numerous neurodegenerative diseases, including Parkinson’s, are thought to be triggered by dysfunctions in the endoplasmic reticulum and Golgi complex.

These cellular structures work together and function as the body’s “postal service” by targeting and “packaging” newly produced proteins. They make sure these are delivered to their proper destination.

To understand the impact of the A30P mutation on aSyn production and on other cell functions and structures, including the endoplasmic reticulum and Golgi complex, an international team of researchers used a mouse that harbored the A30P mutation in the SNCA gene.

This allowed researchers to compare the expression of several genes in this mouse with another one that produced the healthy version of the aSyn protein. Gene expression is the process by which information in a gene is synthesized to create a working product, like a protein.

Researchers found that the transcription — the first step in protein production (DNA to RNA) —  of several genes was deregulated in the mouse that had the A30P mutation.

In particular, the COL4A2 gene, which codes for collagen — a protein that gives form to some tissues, including the skin — was highly expressed in the A30P mouse model.

This trend was confirmed in human nerve cells that also carried the A30P mutation. Collagen is present in several membranes within the body, including the blood brain barrier, a semipermeable membrane that protects the brain from outside factors.

This overexpression was associated with lower levels of a particular molecule, called a micro-RNA, that specifically regulates and controls levels of the COL4A2 gene. These results suggest a crucial role for collagen-related genes and dysfunction in basement membranes such as the blood brain barrier in aSyn toxicity.

In human nerve cells, mutated aSyn also altered the structure of the Golgi complex and made the endoplasmic reticulum more vulnerable to stress conditions. Several studies have implicated endoplasmic reticulum stress in the development of neurodegenerative diseases.

The researchers said that he findings provide new insights “into the putative role of aSyn on transcriptional deregulation, thereby uncovering novel targets for therapeutic intervention in [Parkinson’s] and other synucleinopathies.”

https://parkinsonsnewstoday.com/2018/08/14/alpha-synuclein-disrupts-protein-production-parkinsons-lewy-body-dementia/

Magnetic gene in fish may someday help those with epilepsy, Parkinson's

August 14, 2018  MICHIGAN STATE UNIVERSITY

https://youtu.be/1kprpXbMvA0

According to Michigan State University researchers, glass catfish that swim based on the Earth's magnetic field, could one day hold the key to how the human brain works and how diseases such as Parkinson's and other neurological disorders function. In this video, a magnet is activated, sending electromagnetic waves through a tank, and a small school of glass catfish immediately change their swim pattern.

EAST LANSING, Mich. -- An aquarium fish that senses the Earth's magnetic field as it swims could help unlock how the human brain works and how diseases such as Parkinson's and other neurological disorders function.

Michigan State University scientists are the first to discover a navigational gene in glass catfish called the electromagnetic-perceptive gene, or EPG, that responds to certain magnetic waves. They've already developed a way to use it to control movement in mice. 

The implications of the federally funded study, published in the journal Scientific Reports, have the potential to revolutionize treatments for humans and help those who suffer from tremors related to Parkinson's and seizures associated with epilepsy.

"We've found a noninvasive way to activate this gene once injected in the brain cells of mice and regulate movement in their limbs," said lead author Galit Pelled, a medical bioengineering professor in MSU's Institute for Quantitative Health Science and Engineering. "It could work similarly in humans."

A person suffering Parkinson's disease tremors, for example, could have the gene injected into a specific location or subset of cells in the brain. A magnet that emits electromagnetic waves in an eyeglass frame could then activate the gene to help control, if not stop, the tremors. 

"Technology is getting better and better every year, so this magnet could be built into anything," Pelled said.

Currently, deep brain stimulation treatments for some Parkinson's patients' tremors involve highly invasive procedures such as drilling a hole in the skull and implanting electrodes. During this process, neurons and other cells can be damaged.

Pelled's co-author, Assaf Gilad, a professor of biomedical engineering and radiology, is taking their findings a bit further and is looking into engineering stem cells to express the gene.

"Stem cells are very good carriers of genes so if someone has Parkinson's, we can introduce these stem cells into the brain as a therapy," he said. "This type of treatment could not only help the brain, but could work in other parts of the body too, like the heart, and help those with heart issues."

The researchers said their next steps are to figure out what makes the electromagnetic-perceptive gene so sensitive to these magnetic waves.

"The mechanism of the gene is still unknown," Gilad said. "But once we understand how it really works, it could open the door to even more possibilities."

###

The study was funded by the National Institutes of Health.

Michigan State University has been working to advance the common good in uncommon ways for 160 years. One of the top research universities in the world, MSU focuses its vast resources on creating solutions to some of the world's most pressing challenges, while providing life-changing opportunities to a diverse and inclusive academic community through more than 200 programs of study in 17 degree-granting colleges.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2018-08/msu-mgi081418.php

FoxFeed Blog: 'American Ninja Warrior' and Team Fox Unite to Jump, Flip and Bounce toward a Cure for Parkinson's Disease

Allison Boiles,    August 13, 2018

On Sunday, August 5, joyful yelps, booming music and cheers of encouragement echoed inside the DojoBoom trampoline gym in Thousand Oaks, California where more than 450 guests and volunteers gathered to jump and flip at "Parkour 4 Parkinson's." The inaugural Team Fox fundraiser was the passion project of Akbar Gbajabiamila, Michael J. Fox Foundation (MJFF) Board member and host of NBC's television competition "American Ninja Warrior."

"I am blown away by the support that surrounded Parkour 4 Parkinson's. From the Ninjas flying in from all over the country, to the entire Fox Foundation" said Akbar. "Thank you to everyone who came out to this event -- I am so inspired by your support and know together we will find a cure!"

Mixed in with families from the Southern Californian Parkinson's community, more than 30 celebrity "Ninjas" from the famed TV show could be seen guiding children through obstacle courses, signing autographs and jumping on the gym floor. Between ticket sales and an onsite raffle, more than $65,000 (and counting!) was raised to help speed a cure for Parkinson's. As with all Team Fox events, 100 percent of funds raised will go directly to the high-impact research programs of MJFF.

But that's not all. "Parkour 4 Parkinson's" has gone virtual with an online auction that will have you jumping to bid at one-of-a-kind experience packages curated by Akbar himself. Now through August 15, visit michaeljfox.rallyup.com/akbar and outbid your friends for packages from Universal Studios Los Angeles, "American Ninja Warrior," the Los Angeles Chargers and "The Late Night Starring Jimmy Fallon." As a reminder, 100 percent of your winning bid will go directly to research to help us end Parkinson's disease. 

To view the gallery:

https://www.michaeljfox.org/foundation/news-detail.php?american-ninja-warrior-and-team-fox-unite-to-jump-flip-and-bounce-toward-cure-for