L-DOPA INHALER RAPIDLY IMPROVES PARKINSON’S DISEASE

6th January 2018 - New research

Background : The L-dopa inhaler CVT-301 is presently being assessed for its use in Parkinson’s Disease. It is designed to deliver a precise dose of a dry powder formulation of L-dopa. Inhaled L-dopa enters the body through the lungs and then reaches the brain far more quickly by bypassing the digestive system.

For more information go to : http://www.acorda.com/products/research-development/cvt-301 

Methods : Patients used the L-dopa inhaler CVT-301 up to 3 times per day for OFF episodes. After 2 weeks, the study-drug dose was increased from 35mg to 50 mg. The patients were assessed after 10, 20, 30, and 60 minutes. Results: The L-dopa inhaler was used at an average of 2.1 times per day. The UPDRS Part III score (Parkinson’s Disease symptoms) clearly improved. A treatment effect was already evident after only 10 minutes.

Adverse effects : The most frequently reported adverse events in those using CVT-301 were dizziness, cough, and nausea, each in 7% of patients.

Conclusion : As the effect was already seen after 10 minutes, which is the shortest time assessed, the effect could be even quicker. Consequently, CVT-301 could become of widespread use in Parkinson’s Disease for when a quick effect is needed.

Reference : Movement Disorders [2016] 31 (9) : 1356-1365 (P.A.LeWitt, R.A.Hauser, D.G. Grosset, F.Stocchi, M.H.Saint-Hilaire, A.Ellenbogen, M.Leinonen, N.B.Hampson, T.DeFeo- Fraulini, M.I.Freed, K.D.Kieburtz)

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/27090868 

http://www.viartis.net/parkinsons.disease/news/180106.pdf

They're using music to shine the Light of Day on Parkinson's

BY ED CONDRAN   January 5, 2018

Notable rockers Joe Grushecky and Willie Nile, among others, will hit the stage to help raise funds for the Light of Day Foundation

"There’s always great energy in Philly," said Joe Grushecky.

When Joe Grushecky took part in the initial Light of Day show at the Stone Pony in 2000, the gritty Pittsburgh singer-songwriter never expected the event to turn into a festival.

“But it happened and it’s for a great cause,” Grushecky said while calling from his Pittsburgh home. 

“It’s great that it’s still going on since we’re not where we need to be yet.”

Grushecky, 69, is managed by Bob Benjamin, who founded the Light of Day Foundation 17 years ago. The Foundation raises funds and awareness of Parkinson’s Disease and related disorders, including amyotrophic lateral sclerosis, known as ALS or Lou Gehrig’s disease.

“Bob [Benjamin] has been suffering [from Parkinson’s Disease] for 19 years,” Grushecky said. 

“He has always been about helping others with the disease. It’s time to help him and the best way for me is to get out there and perform at Light of Day shows.”

Grushecky never expected Light of Day to reach Philadelphia, but he’s excited about the gig since it’s an altruistic endeavor and he hasn’t been to the City of Brotherly Love in three years.

“We used to come and play the North Star Bar in Philly,” Grushecky said. “I miss it there. There’s always great energy in Philly.”

Expect Grushecky to preview songs from his forthcoming album, “More Yesterdays Than Tomorrows,” when he performs Saturday at World Cafe Live. 

“It’s a straightforward rock-and-roll record that will be out soon (February),” Grushecky said. “It’ll hit you right in the gut.”

Grushecky’s son, Johnny, who plays guitar in his backing band, the Houserockers, urged his dad to up the sonic ante.

“He said to me, ‘I expect more out of you,” Grushecky recalled. “You have to write better songs.’ I thought, ‘Well, I’ll show him. I made a straightforward rock-and-roll record.”

Grushecky’s longtime pal Bruce Springsteen has played in 11 of the last 16 Light of Day festivals. It appears that the Boss’ current run on Broadway will preclude him from performing at any of the 2018 events.

“Bruce is pretty tied up,” Grushecky said. “The cool thing is that he comes out when he has time.”

Grushecky has often shared a stage with Springsteen. “It’s really special,” Grushecky said. “It’s like playing baseball with Mickey Mantle at Yankee Stadium, or in my case, Roberto Clemente at Forbes Field. When Bruce does your songs, it’s phenomenal. Bruce is like my brother from another mother.”

Willie Nile

Grushecky and Springsteen, who met in 1980, are close in age, both grew up blue collar and are revered songwriters.

“We speak the same vocabulary,” Grushecky said. “We laugh at each other’s jokes. Bruce came to see us play back in the day and we just hit it off.”

Grushecky and the Houserockers won’t share a stage with Springsteen in Philly but will most likely jam with some of the other artists on the bill. 

“Who knows what will happen,” Grushecky said. 

“I love Ben Arnold and Willie Nile. This is going to be fun. The great thing about the Light of Day shows is that they are all different. Some are totally transcendent and others are really good. The only way to know how it will go is to come out and experience one or more of these shows.”

Light of Day is slated for Saturday, Jan. 6 at World Cafe Live, 3025 Walnut St., Philadelphia. 

Tickets are $15 upstairs, $20 downstairs and $30 for both. Show time is 7 p.m. Joe Grushecky and the Houserockers, Willie Nile & Band, Ben Arnold & Band, Joe D’Urso and the Stone Caravan and Remember Jones are downstairs. Jim Boggia, Graham Alexander, Isabella Rose, Vini Lopez, Lisa Bouchelle, Nalani and Sarina and John Byrne will perform.

http://www.phillyvoice.com/theyre-using-music-to-shine-the-light-of-day-on-parkinsons/

Minnesota photographer, painter to have works on display

by Tad Johnson  Jan 6, 2018 

The new Rosemount Steeple Center Gallery exhibition will feature Apple Valley photographer Rusty Fifield and Red Wing watercolor artist Dan Wiemer from January through March.

A free opening reception will be held at the Steeple Center on Wednesday, Jan. 17, from 6-8 p.m., with artist talks at 7 p.m. Refreshments will be served. The exhibit and reception are being organized by the Rosemount Area Arts Council.

Fifield is a longtime financial analyst with companies such as Springsted, Ehlert and Associates and currently as managing director and municipal strategist at Northland Securities.

He said he has been taking photographs for a long time, but only recently has dedicated more time to his craft.

“Some of the impetus came from turning 60 and thinking about the next chapter in my life,” he said.

Fifield was diagnosed Parkinson’s disease several years ago, but he says that so far, the changes in his life have not been significant.

“It does add a few new wrinkles to ‘still’ photography,” he said of living with the condition of the nervous system that affects movement and causes tremors.

“Parkinson’s is a constant reminder to embrace every day,” he said. “Photography helps me do that. I relish heading out in the dark hoping to find a spectacular sunrise to share.”

Many of the images in the show are those of Fifield’s favorite places; several of them are in Dakota County.

“There are amazing images all around us,” he said. “We just have to slow down, look and take the picture.”

Fifield wrapped up a daily-photo-for-a-year project on his SmugMug website this summer. Many of the images are of landscapes, downtown Minneapolis and his family.

“Like many others, I am trying to figure out what to do with my photography,” he said. “It lies somewhere between a hobby and a vocation. This project is part of the journey.”

He said the challenge in photography is to capture an interesting image that people will want to see again.

Fifield also tries to take the viewer to places or a perspective that they might not have seen otherwise.

More is at rustyfifield.com.

Wiemer is an award-winning artist and illustrator who was trained as a graphic designer and has painted in watermedia most of his life.

A graduate of Iowa State University with a bachelor of arts degree in graphic design, he has gathered some of his favorite works together for this show.  

“My work is a reflection and response of my love of the natural world,” he said. “I want my painting to reflect an energy and directness.”

He said he considers himself a landscape artist with most of his work created in watermedia.  

“I see firsthand the endless variety of ways to handle watermedia, and this excites me,” he said.

He is a past president of the Minnesota Watercolor Society and has taught classes and workshops for 20 years all over Minnesota.

“I play with the shapes and textures of the landscape,” he said. “I try to find rhythms in the scene that translate into exciting motifs. I combine acrylic and watercolor in a unique way to stylize my landscapes.”

Through an artist exchange program, Wiemer has had two extended stays in China — painting, teaching and exhibiting. In addition to painting in China, he has created paintings outside in nature in Puerto Rico, Scotland, Canada and throughout the U.S.  

More of his work can be seen at danwiemer.com.

The Steeple Center is located at 14375 S. Robert Trail.

https://www.hometownsource.com/sun_thisweek/community/apple_valley/minnesota-photographer-painter-to-have-works-on-display/article_2f3911a2-f2f3-11e7-9c46-038f59261a1f.html

New Microglial Model May Aid Genetic Studies, Drug Screening

05 Jan 2018

Human Microglia in a Dish? 

Monocyte-derived microglia-like (MDMi) cells (green) appear to mimic the brain-resident cells.  [Courtesy of Science Translational Medicine/AAAS.] caption

Emerging data suggest that much of the genetic risk of Alzheimer’s disease plays out in microglia, the brain’s resident immune cells. If true, then studying their gene expression might pinpoint functional disease variants and identify pathological mechanisms. Obtaining enough microglia for such studies has been hard, but an article in Science Translational Medicine last December 20 offers a solution. Researchers led by Elizabeth Bradshaw and Philip De Jager at Columbia University Medical School, New York City, generated microglia-like cells from circulating human monocytes, which are plentiful in blood samples. The resulting cells behaved like microglia and expressed key microglial genes, the authors report, suggesting they might serve as a model for these ephemeral brain cells.

• A new protocol for turning monocytes into microglia-like cells generates large enough quantities for genetic studies.
• The cells closely match the behavior and gene expression of brain-derived microglia.
• This model system could help identify functional genetic variants for AD risk genes.

The authors made microglia-like cells from a large cohort of healthy volunteers, then examined the cells for genetic variants that affected the expression of risk genes for AD and other disease. These types of variants are known as expression quantitative trait loci. The authors found 141 of these eQTLs, then compared those findings to eQTLs identified in their previous study of monocytes (May 2014 news). While most of the associations between polymorphisms and gene expression were the same in the two cell types, the authors found differences as well, with some associations only showing up in the microglial model. This highlights the importance of studying disease risk in the right cell type, Bradshaw noted. “The [cellular] context is crucial,” she said.

Terrence Town at the University of Southern California, Los Angeles, said the model impressed him. “The authors painstakingly characterized the cells. They have a robust system for evaluating genetic risk factors in human-derived microglia. I think it will be a valuable resource for the scientific community,” he told Alzforum.

Microglia have been grabbing headlines in AD research ever since the discovery of variants in the microglial receptor TREM2 as some of the strongest genetic risk factors for the disease. In fact, in 2017, geneticists reported that the majority of AD genes are controlled by a master regulator of microglial gene expression, suggesting these immune cells might be responsible for the lion’s share of AD risk (Jun 2017 news). Studying risk genes in microglia has been challenging, however. Isolated directly from the brain, the cells rapidly change in cell culture (Jun 2017 news). Although scientists have generated microglia from induced pluripotent stem cells, these procedures take months and produce few cells, prohibiting large-scale association studies (Jul 2016 conference news). 

Bradshaw wondered if using monocytes as starting material might work better. Some controversial research suggests that these cells can enter the brain during disease states and differentiate into macrophages that are then difficult to distinguish from resident microglia. First author Katie Ryan started with existing protocols that expose human monocytes to a cocktail of cytokines to induce them to become phagocytic cells. Combining two of the protocols, she found that the resulting monocyte-derived microglia-like (MDMi) cells resembled brain microglia more than they resembled monocytes or monocyte-derived macrophages (MDMs) generated in vitro. Intriguingly, MDMi turned up expression of signature microglial genes and responded to inflammatory stimuli in the way microglia do, for example by expressing the cytokine IL10 (Durafourt et al., 2012). Also like microglia, they lived longer in culture than did monocytes or macrophages (Aug 2017 news). 

The authors took advantage of recent microglia gene-expression studies to extensively characterize the MDMis (Jan 2016 news). Of the 368 genes that were turned up or down in MDMi cells compared to their baseline expression in human prefrontal cortex, 55 percent were also similarly regulated in microglia made from iPSCs, and 32 percent in microglia isolated from human brain (Muffat et al., 2016; Zhang et al., 2016). “The MDMi cells seem to be as good a model as the induced microglia,” Bradshaw said.

Is a 32 percent overlap of microglia-specific genes between MDMi and brain microglia good enough? Town said the gene-expression differences did not trouble him. He noted that gene expression in microglia varies with their activation state and environment, and that cultured cells might never completely mimic those in the brain (Jul 2016 conference news). Bradshaw and collaborators will culture the MDMi cells with induced neurons and astrocytes as well as in three-dimensional culture systems to see if that nudges gene expression closer to that of brain-resident cells (Oct 2014 news). 

In the meantime, the authors asked whether disease-associated genes were regulated differently in these MDMi compared with other cells. They generated MDMi from frozen blood samples donated by 95 healthy young people who had participated in a genotyping study. Then they searched for genetic variants that correlated with expression changes in 94 genes linked to either AD, Parkinson’s disease, or multiple sclerosis, turning up the 141 eQTLs. But do these variants actually cause disease? To test this, the authors ran a co-localization analysis with known risk SNPs at those loci. For six genes, an eQTL matched up with a known risk SNP, suggesting that the expression changes might drive risk.

Notably, for two of these genes, LRRK2 and PILRB, risk factors for PD and AD, respectively, the authors found eQTLs in the MDMi cells that did not turn up in their previous study on monocytes. This finding underlines the idea that the genetic risk may be microglia-specific, Bradshaw said. For both LRRK2 and PILRB, increased expression in the MDMi cells associated with SNPs for higher risk. For LRRK2, a major PD risk gene, the association appeared particularly robust, agreeing with previous findings from neurons that too much LRRK2 can harm cells (Jan 2014 news). 

The scientists plan to repeat this genetic correlation study in microglia isolated from brain tissue samples removed during surgery. If the eQTL/gene expression levels match, it will further validate the MDMi cells as a model. Bradshaw believes the cells could be useful for drug screening, and is starting a company to pursue this.

The authors will perform further gene-expression studies. They are obtaining blood samples from Parkinson’s patients to look for gene expression changes in the disease, which may be more informative than looking at healthy controls alone. Larger populations might also uncover more associations. TREM2 variants did not show up in this study, perhaps because they are rare and may not have been present in this small cohort, Bradshaw said.—Madolyn Bowman Rogers

https://www.alzforum.org/news/research-news/new-microglial-model-may-aid-genetic-studies-drug-screening

Caffeine May Help Diagnose Parkinson’s Disease in Early Stages

January 5, 2018

People with Parkinson’s disease have lower levels of caffeine in their blood than people without the disease, even if they consumed the same amount of caffeine, according to new research.

Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson’s disease. Image credit: Blausen Gallery 2014 / Wikiversity Journal of Medicine, doi: 10.15347/wjm/2014.010.

“Previous studies have shown a link between caffeine and a lower risk of developing Parkinson’s disease, but we haven’t known much about how caffeine metabolizes within the people with the disease,” said Dr. Shinji Saiki, a researcher at the Juntendo University School of Medicine in Tokyo, Japan, and co-author of the study, published in the journal Neurology.

The study involved 108 people who had Parkinson’s disease for an average of about six years and 31 people of the same age who did not have the disease.

Their blood was tested for caffeine and for 11 byproducts the body makes as it metabolizes caffeine.

They were also tested for mutations in genes that can affect caffeine metabolism.

The two groups consumed about the same amount of caffeine, with an average equivalent to about two cups of coffee per day. But the people with Parkinson’s disease had significantly lower blood levels of caffeine and nine of the 11 byproducts of caffeine in the blood.

The caffeine level was an average of 79 picomoles per 10 microliters for people without Parkinson’s disease, compared to 24 picomoles per 10 microliters for people with the disease.

For one of the byproducts, the level was below the amount that could be detected in more than 50% of the people with Parkinson’s.

In the statistical analysis, Dr. Saiki and colleagues found that the test could be used to reliably identify the people with Parkinson’s disease, with a score of 0.98 where a score of 1 means that all cases are identified correctly.

In the genetic analysis, there were no differences in the caffeine-related genes between the two groups.

“People in the study with more severe stages of the disease did not have lower levels of caffeine in the blood, suggesting that the decrease occurs from the earliest stages of the disease,” said Dr. David Munoz, from the University of Toronto, Canada, who wrote an editorial accompanying the study.

“If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson’s, possibly even before symptoms are appearing.”

_____

Motoki Fujimaki et al. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology, published online January 3, 2018; doi: 10.1212/WNL.0000000000004888

David G. Munoz & Shinsuke Fujioka. Caffeine and Parkinson disease. A possible diagnostic and pathogenic breakthrough. Neurology, published online January 3, 2018; doi: 10.1212/WNL.0000000000004898

http://www.sci-news.com/medicine/caffeine-diagnose-parkinsons-disease-early-stages-05601.html

How Alzheimer’s Spreads Through the Brain

NEUROSCIENCE NEWS   JANUARY 5, 2018
Source: The Conversation.

Researchers investigate how toxic proteins associated with Alzheimer’s disease spread throughout the brain.

Harmful tau protein spreads through networks. NeuroscienceNews.com image is credited to Thomas E Cope.

Alzheimer’s disease is a devastating brain illness that affects an estimated 47m people worldwide. It is the most common cause of dementia in the Western world. Despite this, there are currently no treatments that are effective in curing Alzheimer’s disease or preventing its relentless progression.

Alzheimer’s disease is caused by the build-up of two abnormal proteins, beta-amyloid and tau. Tau is particularly important because it causes neurons and their connections to die, preventing brain regions from communicating with each other normally. In the majority of cases, tau pathology first appears in the memory centres of the brain, known as the entorhinal cortex and hippocampal formation. This has been shown to occur many years before patients have any symptoms of disease.

Over time, tau begins to appear in increasing quantities throughout the brain. This causes the characteristic progression of symptoms in Alzheimer’s diseases, where initial memory loss is followed by more widespread changes in thinking and behaviour that lead to a loss of independence. How this occurs has been controversial.

Transneuronal spread

In our study, published in Brain, we provide the first evidence from humans that tau spreads between connected neurons. This is an important step, because stopping this spread at an early stage might prevent or freeze the symptoms of Alzheimer’s disease.

This idea, called “transneuronal spread”, has been proposed before and is supported by studies in mice. If abnormal tau is injected into a healthy mouse brain, it quickly spreads and causes the mice to manifest dementia symptoms. However, it had not previously been shown that this same process occurs in humans. The evidence from mouse studies was controversial, as the amount of tau injected was relatively high, and disease progression occurred much more rapidly than it does in humans.

n our study, we combined two advanced brain imaging techniques. The first, positron emission tomography (PET), allows us to scan the brain for the presence of specific molecules. With this, we were able to directly observe the abnormal tau in living patients, to see exactly how much of it was present in each part of the brain.

The second, functional magnetic resonance imaging (fMRI), measures blood flow in the brain in real time. This allowed us to observe the activity produced by brain regions communicating with each other. For the first time, by scanning the same people with both methods, we were able to directly relate the connections of the brain to the distribution of abnormal tau in living humans with Alzheimer’s disease.

We used a mathematical technique called “graph analysis” to analyse brain connectivity. This technique involved splitting the brain up into 598 regions of equal size. We then treated the connectivity between regions like a social network, assessing factors such as the number of contacts a brain region had, how many “friendship” groups it took part in, and how many of a brain region’s contacts were also contacts of each other.

In a flu epidemic, people with a large number of social contacts are most likely to become infected and then to pass the infection on to others. Similarly, the transneuronal spread hypothesis predicts that strongly connected brain regions will accrue most tau. This is what we observed. This relationship was present within each brain network individually, as well as across the whole brain.

We were also able to exclude potential alternative explanations for the appearance of tau throughout the brain. It had previously been suggested that tau might appear at brain regions that were vulnerable because of high metabolic demand or a lack of support from their neighbours. While it is possible that these factors are important in neuronal death, our observations were not consistent with them being the primary drivers of the initial accumulation of abnormal tau.

In addition, by looking at patients with a range of disease severity, from mild cognitive impairment through to established Alzheimer’s disease, we were able to disentangle the causes of tau accumulation from its consequences. We showed that increasing amounts of tau in Alzheimer’s disease caused the brain to become less connected overall, and the connections that remained became increasingly random.

Long-range connections

Finally, we contrasted the findings in Alzheimer’s disease to a rarer condition called progressive supranuclear palsy (PSP), which affects approximately three in every 100,000 people. This condition is also caused by tau, but it remains confined to the base of the brain. We demonstrated that in PSP the evidence did not support transneuronal spread. This might be because of the different structure of abnormal tau pathology in the two diseases. In Alzheimer’s disease, tau is present in “paired helical filaments”, while in PSP it is in “straight filaments”.

We showed that as PSP progresses, direct long-range connections are preferentially damaged, meaning that information had to take a more indirect route across the brain. This might explain why, when asked a question, patients with PSP usually respond slowly but correctly.

Overall, evidence of transneuronal spread in humans with Alzheimer’s disease provides proof of concept for exciting new treatment strategies to lock up tau pathology before it can cause significant damage.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Thomas E Cope receives funding from the Patrick Berthoud Charitable Trust and the Association of British Neurologists. The NIMROD study was funded by the National Institute for Health Research, Cambridge Biomedical Research Centre and Biomedical Research Unit in Dementia, PSP Association, the Wellcome Trust, and the Medical Research Council.

Source: Thomas E Cope – The Conversation

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Thomas E Cope.

http://neurosciencenews.com/neurology-alzheimers-spread-8277/

NFL gives $16.3 million for neuroscience research

Bob Hille, January 5, 2018

The NFL has allocated an additional $16.3 million toward research into the long-term effects of concussions and traumatic brain injuries, the league announcedFriday.

The funding — part of an original $30 million pledge that was part of a five-year agreement with the Foundation for the National Institutes of Health that ended in August — will go to three research projects focusing on neurodegenerative diseases, such as CTE, Parkinson's disease and ALS, all of which have been linked to repetitive brain injuries suffered by NFL players.

"These research initiatives represent important scientific projects, with proven track records of achievement that affect public health," the league said in a statement. "Each of these research programs receives substantial federal funding. Through this commitment, the League hopes to advance the understanding of concussion and other brain injuries, especially among athletes and veterans."

The league is donating $7.65 million to the U.S. Department of Defense's Concussion Assessment Research and Education Consortium Grand Alliance, which also involves the NCAA, and another $7.65 million to the NIH-funded Transforming Research and Clinical Knowledge in Traumatic Brain Injury initiative. The remaining $2.25 million will go to the National Institute of Aging.

http://www.sportingnews.com/nfl/news/nfl-neuroscience-research-money-funding-cte-als-parkinsons/11r8at43a1fff17httdo0yd6qn

The Future of Parkinson’s in the Palm of Your Hands

By maria.deleon—January 5, 2018 

After seeing, caring, and treating strangers, patients, and loved ones with devastating brain illnesses such as Parkinson’s, I felt compelled to help in whatever way possible to advance the knowledge and understanding of the brain….Thus, I began to participate in clinical studies in hopes of helping to find a cure for me, my patients, and my loved ones.

Decision to join

I have been involved in clinical research since my early twenties as a control, a patient, and a researcher. In just a couple of decades, my focus switched from volunteer control to researcher to patient. Thus, my needs changed. But throughout all my years of involvement in clinical research the notion of “paying it forward” remained – honoring those that sacrificed in the past and learning from previous mistakes to retain humanity and dignity of those suffering and needing care now and in the future. So for me, offering a new treatment or participating in one is about trying to find the ‘right‘ treatment that will improve the life of those with same symptoms.

Expectations

From years of experience, I know that there are always risks involved so it is important to be honest with yourself as to the motives of your participation and what your expectations are. For me, since I have discovered that I don’t do well with procedures or tolerate a lot of medicine changes as my disease has evolved, I limit my participation now to non-invasive procedures and drugs that we already have some information on. This was not always case keeping in mind that our bodies and circumstances change. Device evaluation and standardizing scales is an equally important job for a volunteer. Of course this is different for everyone and being truthful with yourself is paramount!

Pearls of wisdom

I have seen many things through my years in medicine. The one constant is that most people rarely consider the possibility of a negative outcome. This is not to say that there are a lot of positives like having a closer rapport with doctor, getting free medication and testing along with financial compensation at times. However, in the excitement of the moment or the urgent need to help with present symptoms many forget that Parkinson’s is a constantly changing one which will have to be dealt with in the future as well. Thus, one must keep in mind that sometimes participating in one trial can limit not only participation in future trials but also limit the established treatments offered as was the case for many, and a friend in particular who underwent a surgical procedure which proved ineffective. Yet, that individual is no longer able to receive known surgical treatments or participate in other trials despite fact that disease has advanced.

Playing a POSITIVE role in research

Although as with anything, there are pros and cons. Review risks and benefits with your physician and don’t be afraid to limit your role in clinical trials as long as you remember to be honest with yourself and your doctor in order to find the right study that will suit your needs. This will not only maximize your success and well being but allow you to feel confident in helping yourself as well as future generations.

https://parkinsonsdisease.net/clinical/future-treatments-in-the-palm-of-your-hands/

Dance program aims to slow effects of Parkinson’s disease

By REBECCA LEFTWICH,    Jan. 05, 2018 

Judith Furlong simulates shooting an arrow at a target during warmups for a Dance for Parkinson’s class.

Over the years, many studies have shown dance to have therapeutic effects on mood disorders such as depression and anxiety, and now a dance program specifically targeted at slowing the effects of Parkinson’s disease is proving successful in Newnan as well.

At Southern Arc Dance Center, Paulo Manso de Sousa teaches two Dance for Parkinson’s classes a week. The classes are based on a program developed by Mark Morris Dance Group in New York, which built the program on the fundamental premise that “professionally trained dancers are movement experts whose knowledge is useful to people with (Parkinson’s disease).”

Parkinson’s disease (PD) is a neurodegenerative disorder that affects the brain’s production of dopamine. According to the Parkinson’s Foundation, symptoms of the disease – which has no known cause – develop slowly over a period of years and can include slowed movements, rigid limbs, and problems with gait and balance.

Treatment options include medication and surgery, but there is no known cure. Parkinson’s is not fatal, but complications from the disease are the 14th leading cause of death in the United States, according to the Centers for Disease Control and Prevention.

Exercise can relieve some motor symptoms of PD by modifying areas of the brain where dopamine signals are received, in addition to improving overall health, medical experts say. However, people with PD often are equally impacted by non-motor symptoms such as apathy, depression, constipation, sleep disorders, loss of sense of smell and cognitive impairment.

Dance for Parkinson’s was created to address aspects of both motor and non-motor symptoms of the disease, which was part of the appeal for Manso de Sousa, whose studio is one of only two in Georgia offering certified instructor-led Dance for Parkinson’s classes. Manso de Sousa – a world-renowned dancer and instructor – traveled to Brooklyn to train in Dance for Parkinson’s at Mark Morris Dance Company so he could bring the classes to Southern Arc Dance Center.

“I try to find opportunities for people to dance,” said Manso de Sousa, who has taught and choreographed for dancers of all ages and skill levels, including those confined to wheelchairs and missing limbs. “I did it as an art, and I was lucky to do it as a career. I believe everybody can dance, and really want to give something to the community.”

The program was developed after a former dancer was diagnosed with Parkinson’s and came back to take dance classes at the Mark Morris Dance Group to help with her symptoms instead of choosing more typical physical therapy. Dance for Parkinson’s classes specifically address balance, flexibility, coordination, isolation and depression by using narrative, imagery, music and socialization.

“Unlike therapy when they’re doing constant movement, and they are much more cognizant to the physical aspects, the class is poetic and musical and keeps their minds involved,” Manson de Sousa said. “When they’re in therapy, they’re curing their disease. When they’re in dance class, they’re having fun, joking with each other … it’s a social event.”

Don Chapman has attended classes at Southern Arc since Manso de Sousa began offering them last year.

“I very much enjoy the class and think Paulo is a great motivator for all of us,” Chapman said. “It keeps us moving and is not too strenuous, which is very good in my opinion. I highly recommend the class to anyone, not just us with PD.”

Southern Arc’s Dance for Parkinson’s classes are offered Mondays from 7-8 p.m. and Tuesdays from 10-11 a.m. Anyone interested can try one class for free and each class is $5 after that. “Care partners” are encouraged to participate in class at no charge, Manso de Sousa said. 

“If you’re a care partner, it’s not very exciting to just drop them off and sit around waiting for an hour,” he said. “We want you to come in and participate, to share the experience and have some fun.”

For more information, call Southern Arc Dance Center at 770-683-3724, email info@southernarcdance.org or visit the studio at 40 Greenway Court in Newnan.

http://times-herald.com/news/2018/01/dance-program-aims-to-slow-effects-of-parkinsons-disease

People Who Sleep Less Than 8 Hours a Night More Likely to Suffer Anxiety and Depression

NEUROSCIENCE NEWS    JANUARY 4, 2018
Source: Binghampton University.

Binghampton University researchers report sleeping less than 8 hours a night can result in negative, repetitive thoughts associated with anxiety and depression.

These negative thoughts are believed to leave people vulnerable to different types of psychological disorders, such as anxiety or depression, said Coles. NeuroscienceNews.com image is in the public domain.

Sleeping less than the recommended eight hours a night is associated with intrusive, repetitive thoughts like those seen in anxiety or depression, according to new research from Binghamton University, State University of New York.

Binghamton University Professor of Psychology Meredith Coles and former graduate student Jacob Nota assessed the timing and duration of sleep in individuals with moderate to high levels of repetitive negative thoughts (e.g., worry and rumination). The research participants were exposed to different pictures intended to trigger an emotional response, and researchers tracked their attention through their eye movements. 

The researchers discovered that regular sleep disruptions are associated with difficulty in shifting one’s attention away from negative information. This may mean that inadequate sleep is part of what makes negative intrusive thoughts stick around and interfere with people’s lives .

“We found that people in this study have some tendencies to have thoughts get stuck in their heads, and their elevated negative thinking makes it difficult for them to disengage with the negative stimuli that we exposed them to,” said Coles. “While other people may be able to receive negative information and move on, the participants had trouble ignoring it.”

These negative thoughts are believed to leave people vulnerable to different types of psychological disorders, such as anxiety or depression, said Coles.

“We realized over time that this might be important — this repetitive negative thinking is relevant to several different disorders like anxiety, depression and many other things,” said Coles. “This is novel in that we’re exploring the overlap between sleep disruptions and the way they affect these basic processes that help in ignoring those obsessive negative thoughts.”

The researchers are further exploring this discovery, evaluating how the timing and duration of sleep may also contribute to the development or maintenance of psychological disorders. If their theories are correct, their research could potentially allow psychologists to treat anxiety and depression by shifting patients’ sleep cycles to a healthier time or making it more likely a patient will sleep when they get in bed.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Meredith Coles – Binghampton University

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Full open access research for “Shorter sleep duration and longer sleep onset latency are related to difficulty disengaging attention from negative emotional images in individuals with elevated transdiagnostic repetitive negative thinking” by Jacob A. Nota and Meredith E. Coles in Journal of Behavior Therapy and Experimental Psychiatry. Published online October 16 2017 doi:10.1016/j.jbtep.2017.10.003

Abstract

Shorter sleep duration and longer sleep onset latency are related to difficulty disengaging attention from negative emotional images in individuals with elevated transdiagnostic repetitive negative thinking

Background and objectives

Repetitive negative thinking (RNT) is often associated with disruptions in sleep and circadian rhythms. Disruptions in sleep and circadian rhythms may deal a “second hit” to attentional control deficits. This study evaluated whether sleep and circadian rhythm disruptions are related to the top-down control of attention to negative stimuli in individuals with heightened repetitive negative thinking.

Methods

Fifty-two community adults with high levels of transdiagnostic RNT and varying habitual sleep durations and bedtimes participated in a hybrid free-viewing and directed attention task using pairs of emotionally-evocative and neutral images while eye-tracking data were collected. Self-report and clinician-administered interviews regarding sleep were also collected.

Results

Shorter habitual sleep duration was associated with more time looking at emotionally negative compared to neutral images during a free-viewing attention task and more difficulty disengaging attention from negative compared to neutral images during a directed attention task. In addition, longer sleep onset latencies were also associated with difficulty disengaging attention from negative stimuli. The relations between sleep and attention for positive images were not statistically significant.

Limitations

A causal link between sleep and attentional control cannot be inferred from these cross-sectional data. The lack of a healthy control sample means that the relations between sleep disruption, attention, and emotional reactivity may not be unique to individuals with RNT.

Conclusions

These findings suggest that sleep disruption may be associated with a specific impact on cognitive resources that are necessary for the top-down inhibitory control of attention to emotionally negative information.

“Shorter sleep duration and longer sleep onset latency are related to difficulty disengaging attention from negative emotional images in individuals with elevated transdiagnostic repetitive negative thinking” by Jacob A. Nota and Meredith E. Coles in Journal of Behavior Therapy and Experimental Psychiatry. Published online October 16 2017 doi:10.1016/j.jbtep.2017.10.003

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