I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.
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The six skaters who skated all 24 hours at this year’s UNMC Skate-a-thon for Parkinson’s “chill out” on the UNMC Ice Rink after completing their marathon skating effort.
OMAHA, Neb. —
A record total of 640 skaters participated in the seventh annual UNMC Skate-a-thon for Parkinson’s, as the 24-hour skating event concluded at 2 p.m. Saturday afternoon at the UNMC Ice Rink.
This marked the third consecutive year the event has topped 500 skaters, and the first time it has exceeded the 600 mark.
The event is held in memory of event founder Colleen Wuebben, who was diagnosed with Parkinson's in 2005 at the age of 52 and died in 2013 at the age of 60.
Jenny Knutson, daughter of Ted and Colleen Wuebben and one of the event coordinators, said early estimates look very promising, as more than $11,000 were collected at the registration tent alone. She said online proceeds, pledges for skaters, and corporate sponsorships are yet to be processed.
“I know the Creighton Prep hockey team exceeded its $800 goal, and that’s not included in the $11,000 total,” she said.
When the final total is calculated, Knutson said she is confident that the seven skate-a-thons at UNMC will have netted more than $170,000 in proceeds. The total after the 2016 skate-a-thon was more than $155,000.
Proceeds go toward clinical and basic science Parkinson's research at UNMC as well as Parkinson’s Nebraska, an organization started by the Wuebben family to provide affordable exercise, education and services to improve quality of life for persons with Parkinson's.
“We are just overwhelmed with the response,” Knutson said. “This event just keeps getting bigger and better every year. It’s very encouraging for the future.”
Six skaters – Chris Rush, Mike Schoch, Ronnie Stark, Eric Winner, Abby and Jim Janicki – skated all 24 hours. This marked the fourth consecutive year that Rush has skated all 24 hours. In skating all 24 hours, it is estimated that each of the marathon skaters logged more than 16 miles. In addition, a Parkinson’s patient, Suzanne Arney, participated in the opening ceremonies.
Templederry student Joanne Shanahan was recently awarded a PhD in Philosophy from the University Limerick after she completed a thesis on Parkinson's disease.
A past pupil of St Joseph's College, Borrisoleigh, Joanne of Gurteen, Templederry, titled her thesis: 'Dancing for fun, Dancing for health, getting active: Increasing quality of life for people with Parkinson’s disease'.
In summarising her thesis, Joanne pointed out that the benefits of exercise for people with Parkinson’s disease are well established. But many people do not get enough exercise or dislike the exercise options available to them.
Set dancing has a rich cultural heritage in Ireland and is a popular social and cultural activity. Little is known about the benefits of set dancing for people with Parkinson’s disease. Therefore, the aim of Joanne's project was to investigate the feasibility and benefit of Irish set dancing for people with Parkinson’s disease in Ireland.
Her research involved inviting people with Parkinson’s disease to participate in eight weeks of set dancing classes. The aim of this was to determine the feasibility of set dancing for people with Parkinson’s disease. Participants were assessed before and after the eight weeks of set dancing classes. The results found the set dancing classes offered were safe and enjoyable, and improvements in quality of life and motor function were identified.
In order to better understand the potential benefits of set dancing for people with Parkinson’s disease in Ireland, a small randomised controlled trial was conducted. In this study, participants were randomly allocated to one of two groups.
One group continued with their usual care and participated in 10 weeks of set dancing classes. The other group continued with their usual care only. Again, participants were assessed at the start and end of the study. The results of this study also identified important information to inform the methods of larger projects.
A major part of this research involved developing an educational resource for set dancing teachers teaching set dancing to people with Parkinson’s disease in their local communities. The resource: 'Set dancing for people with Parkinson’s disease: an information resource for Irish set dancing teachers', is freely available and can be accessed through the University of Limerick Institutional Repository.
“This project gave me great satisfaction as I got the opportunity to involve people with Parkinson’s disease and their families in a fun and social activity,” Joanne said.
“Delivering the set dancing classes was thoroughly enjoyable as I observed people dancing, laughing and enjoying the social company. For this research to be meaningful, it must impact the lives of people with Parkinson’s disease. Moving forward, it is important to ensure that set dancing teachers have access to the educational resource and sufficient help available to help them deliver set dancing classes to people with Parkinson’s disease.”
Physical Therapist Jamie Graves leads the Grays Harbor Parkinson’s Support Group in chair exercises using a ball and a towel. (BETSY SEIDEL PHOTO)
The Grays Harbor Parkinson’s Support Group invites the public to attend a screening of “Present Moment,” an eight-minute film that shares a perspective on the chronic illness and the impact it has on an entire family.
The showing takes place Tuesday at 6 p.m. in the Hoquiam Timberland Library, 420 7th St., in the downstairs meeting room.
Parkinson’s disease is a movement disorder that results from loss of dopamine-producing cells in the brain. It has four main symptoms: tremor, rigidity, slowness of movement and impaired balance and coordination. As the symptoms progress, patients may increasingly struggle to walk, talk, carry on a normal life and take care of themselves. Parkinson’s usually strikes after individuals reach the age of 60, occurring subtly and gradually. It progresses at different speeds in different people.
In 2012, Hoquiam resident Bob Martin was diagnosed with Parkinson’s, but the closest support group was in Olympia. So he and his wife decided to create a local group in Hoquiam. The Grays Harbor Parkinson’s Support Group has been meeting monthly on the last Tuesday of every month from 6 to 7 p.m. at the Hoquiam library.
Guest speakers, exercise and group discussion are all on the agenda. The support group meets for dinner and social time at a local Hoquiam restaurant prior to the gathering at the library. There are 30 members who attend each meeting, but there is always room for more.
The Jan. 31 event is sponsored by Hoquiam Timberland Library and the Northwest Parkinson’s Foundation. NWPF’s mission is to establish an optimal quality of life for the Northwest Parkinson’s community through awareness, education, advocacy and care. The NWPF team will be on hand at this meeting to answer questions and to share information about Parkinson’s. For more information about NWPF, please visit www.nwpf.org.
Aimie Vallat, the film’s creator, will be attending the screening as well. Vallat owns Reel Witness Productions in Seattle with Noah Dassel, which focuses on advocacy filmmaking. Their award-winning documentary film, “Present Moment,” has played on PBS affiliate KCTS9 and screened at 23 film festivals around the world.
Researchers have identified more than 300 genes that influence alpha-synuclein’s toxicity, and among them are many known to predispose individuals to Parkinson’s disease (PD), researchers said. The finding provides new insight into what mechanisms lead to the disease.
The hallmark of Parkinson’s disease is the formation of alpha-synuclein protein aggregates, which are toxic to neurons and promote the loss of brain function, but the disease may also be caused by several gene mutations.
Two studies in the journal Cell Systems have tackled that issue.
“In the first paper, we used powerful and unbiased genetic tools in the simple Baker’s yeast cell to identify 332 genes that impact the toxicity of alpha-synuclein,” Vikram Khurana, the studies’ first author, said in a news release. “Among them were multiple genes known to predispose individuals to Parkinson’s — so we show that various genetic forms of Parkinson’s are directly related to alpha-synuclein. Moreover, the results showed that many effects of alpha-synuclein have been conserved across a billion years of evolution from yeast to human.”
“(F)or the first time, we were able to visualize the protein’s location, at minute scale, under physiologic conditions in an intact brain cell,” said Chee Yeun Chung, senior author of the studies.
Together, the works showed that alpha-synuclein interfered with the rate of protein production in the cell, as well as the transport of proteins between cellular compartments.
“These interactions can explain connections between different Parkinson’s genetic risk factors,” the researchers wrote.
The team had to develop computational tools to find patterns of protein interaction in both yeast and humans, and to make predictions about which human genes could be associated with alpha-synuclein’s toxicity.
“We now have a system to look at how seemingly unrelated genes come together to cause Parkinson’s and how they are related to the protein that misfolds in this disease,” Khurana said.
Researchers confirmed their results using generated neurons from Parkinson’s patients with different mutations. The protein interactions they had predicted allowed them to identify abnormal mechanisms shared among the patients.
“We believe these methods could pave the way for developing patient-specific treatments in the future,” Khurana said.
“This award recognizes our company’s successes in developing technologies which enable clinicians and clinical trial sponsors to profile brain health through the analysis of the brain’s electrical activity (EEG) during sleep and wake,” ABM chief executive officer and co-founder Chris Berka said in a press release.
The awards seek to recognize and chronicle the individuals, departments and organizations, corporate and public, working tirelessly throughout the industry. Commenting on the awards, GHP Coordinator Naomi Douglas stated in a press release that “The healthcare and pharmaceuticals market is the lifeblood of our society, and therefore it is a true honor to put the spotlight on our deserving winners … ”
GHP stresses that its award winners are chosen solely on merit, in recognition and commendation of their ingenuity and hard work. For more information about GHP award winners, and insight into working practices of the health and pharma industries’ “best of the best,” you can access the winners’ supplemental information on the GHP website
As a leader in neuroscience application development of devices for measuring and interpreting brain function, detecting abnormal neuro-cardio respiratory response during sleep, improving sleep quality, and enhancing performance for 15 years, Advanced Brain Monitoring has received research funding from the National Institute of Health (NIH). That included the recent award of a $1.5 million grant to expand its database of awake and sleeping EEG in patients with neurodegenerative diseases.
ABM research also has been funded variously by the Department of Defense Advanced Research Projects Agency (DARPA) and other government agencies. The company’s research findings have been reported in more than 100 scientific journals and papers, and its discoveries have been granted 27 patents.
“The envisioned future is for routine brain health assessments during sleep and waking to be conducted in a manner similar to a mammogram or colonoscopy,” CEO Berka observed. “Ultimately, early detection will increase the likelihood that an intervention can be matched to the patient based on the presence of brain biomarkers and administered prior to the onset of cognitive decline.”
Six FDA-cleared, CE-marked ABM medical systems are currently distributed in North America, Europe, Asia, and Australia. ABM-designed medical devices have been used in assessing and treating more than 1.5 million patients worldwide.
Services offered by ABM include streamlined EEG acquisition, secure transmission via a cloud portal with rapid analyses and reporting. They also can provide proprietary functional Neuro-Electrophysiological Imaging (fNEI) that simultaneously measures EEG during resting state, with or without concurrent neurocognitive tests that activate neural circuits involved in brain functions such as attention, memory and emotion. Quantified data from these tests can be compared to a database containing results from more than 10,000 test sessions on both healthy and impaired individuals.
“Preliminary results indicate potential for estimating the severity of brain impairment for Alzheimer’s and Parkinson’s disease, mild cognitive impairment,
and Frontotemporal dementia,” said ABMs’ Chief Medical Officer, Philip Westbrook, a clinical professor of medicine at UCLA. Westbrook has been actively involved in professional organizations associated with sleep disorders, and has served as president of the American Sleep Disorder Association (ASDA).
ABM’s Sleep Profiler device monitors brain function during sleep and is able to detect biomarkers associated with neuro-degeneration and chronic diseases. Clinical applications of Sleep Profiler include objective assessment of prescription sleep aid effectiveness in patients with insomnia and the impact of anti-depressants andanti-hypertensive medications have on quality sleep. “Sleep Profiler biomarkers have also been associated with the brain patterns of intensive care unit (ICU) patients who had sepsis or died,” said ABM President Daniel J. Levendowski. “Sleep Profiler will soon enable real-time monitoring of abnormal sleep patterns in ICU patients.”
Advanced Brain Monitoring also offers clinical trial services, specializing in early phase investigations of neurodegenerative and psychiatric indications, and the company can provide a comprehensive suite of EEG based sleep and daytime assessment technologies for use in pharmaceutical, medical device and academic clinical trials. ABM’s expertise spanning a broad range of neurological disorders enables its neuroscience research team to deliver streamlined EEG acquisition, secure data integrity management, customized data analysis, and worldwide clinical support
SHARK antibodies have been used to make a HUGE breakthrough in the fight against Alzheimer’s and Parkinson's diseases.
Danish pharmaceuticals firm Lundbeck along with private US research firm Ossianix have been using shark antibodies to breach the brain-blood barrier in mice.
The brain-blood barrier is a layer of cells around cerebral blood vessels on the brain that protects it from being breached by toxins.
Researchers have struggled in their attempts to pass the barrier and as such have been unable to treat brain related diseases using medicine.
However, the team at the pharmaceuticals firm has discovered how it can attach therapeutic proteins to antibodies from sharks, which essentially tricks the brain into accepting the drug.
Nerve cells on the brain affected by Alzheimer's
The experts used antibodies derived from sharks as the fish has an immune system very similar to that of a human and they were the first species to develop antibodies – proteins that are used by the immune system to detect things like viruses and bacteria – 400 million years ago.
By attaching the therapeutic proteins to the antibodies, the experts could target specific parts of the brain which are affected by Alzheimer’s and Parkinson’s.
Lundbeck Senior Vice President of Global Research, Kim Andersen, said in a statement: “Ossianix has generated a world leading platform for delivering antibodies and potentially other drug agents into the brain with significant potential to benefit patients with diseases in the central nervous system.”
The team state that the technology is still several years from being sufficient enough for human use, but Ossianix CEO Frank Walsh told the Financial Times that it could be in use, at least for human trials, in as little as two years.
Inserting a metal rod into the brain, scientists have used deep brain stimulation to treat Parkinson's - Treatment is also being explored for use in Alzheimer's
Medical researchers have found that it is possible to treat Parkinson's by inserting a metal rod directly into the brain. This rod stimulates the brain and alleviates the symptoms of Parkinson's. Researchers believe this treatment might even help those afflicted with Alzheimer's, epilepsy, bipolar disorder and depression.
About Deep Brain Stimulation
Deep brain stimulation, also referred to with the acronym of "DBS" is intriguing because of its reanimation potential. This surgical technique involves the placement of a metal rod directly into the patient's brain. The end of the rod contains electrodes that are connected to a battery implanted within the chest cavity. Once everything is in the proper position, the device is flicked on and an electrical current is generated to stimulate the neurons in the portion of the brain tied to Parkinson's.
DBS is typically used on patients where traditional medication does not suffice. Once the switch is flicked, the patient transitions from shaking in an uncontrollable manner and hardly being able to move to being quite relaxed and nearly in full control of his body. The man responsible for this groundbreaking treatment, Dr. Andres Lozano, has also found that DBS can even also conjure up once-lost memories in certain patients.
Non-Invasive Techniques to Treat Parkinson's and Other Diseases
If the placement of a metal rod in the brain seems a bit obtrusive or slightly morbid, don't fret. Other less invasive treatment methods are also available. One such treatment, known as transcranial magnetic stimulation or "TMS", is currently under development. If successful, this treatment will eliminate the need for surgery. It involves the use of high-powered magnets attached to the outer portion of the patient's head to transmit an electromagnetic current to the target space. Initial results show this treatment boosts cognition by stimulating neurons within the affected space. However, TMS is still fairly new. It might take several months or even years before TMS becomes a mainstream treatment.
Another technique referred to as “Neural Lace”, is currently being perfected by a company led by none other than Elon Musk of Tesla Motors fame. This technique makes use of neuromodulation to improve cognitive abilities.
A Word About Neuromodulation
The treatments outlined above have trailbazed a path for the new branch of medicine referred to as neuromodulation. This field makes use of TMS, DBS and other treatment methods to boost all sorts of different cognitive abilities. It is possible that patients afflicted with such diseases will eventually be able to walk directly into a clinic, have a brain scan conducted to identify deficiencies and then have those deficiencies ameliorated on-the-spot with neuromodulation techniques.
Neuromodulation also encapsulates the brain's innate ability to move objects. Neural prostheses have been created that empower patients to move robotic limbs with their thoughts. This is quite the incredible feat. Neuromodulation specialists envision patients being able to control numerous objects within their home in a similar way at some point in the near future. This challenge will likely be ameliorated as the internet of things goes mainstream in the coming months and years.
Where Will Neuromodulation Take Us?
Perhaps the next “level” of neuromodulation will be a direct link between the brain and the world wide web itself. This is the foundation of Musk's forementioned Neural Lace. Musk and plenty of other Silicon Valley power brokers aim to directly connect human brains to the internet, providing us with immediate access to the treasure trove of information available to web users. Such a direct data connection would heighten intellect, improve efficiency in every regard and empower those saddled by otherwise crippling diseases and maladies.
Grab your winter jacket and your sharpest ice skates, the 10th annual Skate-A-Thon for Parkinson's is back.
What started as a fundraiser for Parkinson's research and exercise programs in a small backyard ice rink 10 years ago, has now turned into a unique challenge.
It's all in honor of Colleen Wuebben, an Omaha woman who was diagnosed with Parkinson's Disease at just 52 years old. The nervous system disease can make patients stiff, have tremors and can impact their mobility and balance.
During the course of Wuebben's treatment, most of which involved medication, she discovered some Parkinson's patients improved their conditions by exercising.
So Wuebben got thinking, what could she do that could raise money for Parkinson's research and programs while also getting in exercise?
"She knew she couldn't run a marathon, she knew she couldn't climb to the top of Mount Everest but she knew how to ice skate," Wuebben's daughter Jenny Knutson said. "As strange as it sounds for someone with Parkinson's, a mobility and balance disorder, when she was on skates her gait and her glide just came naturally to her on skates." Wuebben's husband, Ted, said they always had a skating rink in the backyard. Not long after Wuebben was diagnosed, she went to her husband with two goals.
"One day she comes outside to the ice rink and said, 'I want to meet Michael J. Fox, and I want to start an exercise program for people with Parkinson's and you figure out how to pay for it,'" Ted said. "So I'm sitting on the ice rink and the 24 hour Skate-A-Thon was born."
In the first few years, the family filled their little rink in the backyard. Some years the ice getting so soft by the end, only the kids could finish the 24 hour skate.
But between friends, family and even some strangers with big hearts, they worked toward Wuebben's goals.
Colleen Wuebben passed away in 2013, at 60 years old. But before she passed, she already left her mark.
Using the money she raised, she made a donation to Parkinson's research, which led her to her meeting with Michael J. Fox.
Seven years ago, the family began to work with UNMC to create a bigger event using their ice rink. In the seven years they've been there, they've raised more than $155,000.
"It's an amazing experience when you're here at night and the crowd is going, the DJ is here, people are skating, saying hi to friends you haven't seen in a year," Knutson said. "Then you're out here at night and you're thinking, 'wow do I have what it takes to do this for a few more hours?' And you look around and think, 'yes I do! We're here for a pretty important reason.' And then the sun comes up and it's an amazing time. We've made it, we've done it one more day and we're just filling ourselves with hope that we can go out there and continue the Parkinson's Nebraska experience."
The 2017 Skate-A-Thon is Friday, January 27th starting at 2 p.m. and goes until Saturday, January 28th at 2 p.m. It's just $10 for all you can skate, including skate rentals.
You can also make donations.
There's no requirement to skate the full 24 hours, though many will try to last that long. But the Weubben family is hoping the event will continue to grow and make an even bigger impact for local families suffering from Parkinson's Disease.
"She (Colleen) said to me when she was in hospice, 'this is going to be easy because all the people suffering with Parkinson's and their care givers that's gonna be hard.'"
There will be a DJ, games, prizes, food, hot chocolate and a warming tent for anyone stopping by just to catch a glimpse of the skaters. At 10 p.m. there is a pajama and pizza party.
And at 1 a.m., for those brave souls, there is a skivvy skating party. That's skating 20 laps in nothing but your bare essentials.
Video Link: http://health.einnews.com/article/363910246/1PhhRtr505G7E9nf?lcf=Hzf-KE6h-Xmcpvzwcdl3CuzbRmZ8XaTUdg3y3lN96pg%3D
In order to drive a car, you need a good balance between accelerator and brake. The same applies to a part of the brain - the striatum - that controls our movements. Research at Lund University in Sweden has led to new findings on the interaction between the "accelerator" and the "brake" in the striatum. These findings may guide the development of treatments for movement disorders such as those occurring in Parkinson's disease.
In the initial stage of Parkinson's disease, patients' movements are stiff and slow. This can be remedied with the drug L-dopa, but after a few years of treatment, patients usually develop uncontrolled jerking motions known as dyskinesias. Other diseases, such as Huntington's disease and several hereditary conditions, are also associated with movement disorders of this kind.
"We know that the striatum plays an important role in movement control. But which neural pathways are most important has been hotly debated", says Parkinson's researcher Angela Cenci Nilsson in Lund.
An innovative approach
The striatum has two principal types of cells forming distinct neural pathway, termed "direct pathway" and "indirect pathway", respectively. The research debate has centred on whether both pathways are equally important in all situations, and whether they need to cooperate or can work independently. To address this question, the Lund researchers applied a method called chemogenetics. Using a harmless virus, they introduced a new gene into one or the other type of striatal cell in laboratory mice. The gene coded for the production of a receptor protein activating the relevant neural pathway. However, the receptor became stimulated only when the animal was administered a particular substance whose effect lasted a couple of hours. Using this method, the researchers were able to control the activity of cells forming the direct or indirect pathway while studying the animals' behaviour. Studies were conducted on both normal mice and animals with a Parkinson's-like injury, and both with or without L-dopa.
The results showed that all types of movements were controlled by both pathways, which proved to function as a sort of "accelerator" (the direct pathway) and "brake" (the indirect pathway), respectively. In Parkinson's mice treated with L-dopa, activation of the direct pathway produced faster movements but also more severe dyskinesias, mimicking both the advantages and the disadvantages of Parkinson's therapy. On the other hand, activation of the indirect pathway gave slower movements but also eased the dyskinesias caused by L-dopa.
"We interpret these results to mean that the pathways need to interact in all situations, even in Parkinson's-like conditions and upon L-dopa treatment. You can't have only acceleration and no braking, but must instead balance both functions in a precise manner", says Angela Cenci Nilsson.
The results could inform both basic and therapeutic research
She believes that L-dopa therapy gives complications when it "inactivates the brake" by strongly inhibiting the indirect pathway, while "pressing too hard on the accelerator" by overstimulating the direct pathway such that dyskinesias can occur.
These new findings could explain why it has been difficult to develop new drugs for Parkinson's disease. Drug development in recent years has been directed towards one or the other neural pathway, whereas this study points to a need to intervene on both pathways using either a drug that regulates both of them or two complementary drugs.
"Our results could be of great significance both for basic research and for therapeutic research", says Angela Cenci Nilsson.
Parkinson's disease (PD) and other "synucleinopathies" are known to be linked to the misfolding of alpha-synuclein protein in neurons. Less clear is how this misfolding relates to the growing number of genes implicated in PD through analysis of human genetics. In two studies published in the advance online edition of Cell Systems, researchers affiliated with Whitehead Institute and Massachusetts Institute of Technology (MIT) explain how they used a suite of novel biological and computational methods to shed light on the question.
To start, they created two ways to systematically map the footprint of alpha-synuclein within living cells. "In the first paper, we used powerful and unbiased genetic tools in the simple Baker's yeast cell to identify 332 genes that impact the toxicity of alpha-synuclein," explained Vikram Khurana, first and co-corresponding author on the studies. "Among them were multiple genes known to predispose individuals to Parkinson's—so we show that various genetic forms of Parkinson's are directly related to alpha-synuclein. Moreover, the results showed that many effects of alpha-synuclein have been conserved across a billion years of evolution from yeast to human," said Khurana, former Visiting Scientist at the Whitehead Institute.
"In the second paper, we created a spatial map of alpha-synuclein, cataloging all the proteins in living neurons that were in close proximity to the protein," explained Chee Yeun Chung, former Whitehead Institute Senior Research Scientist, who co-led both studies with Khurana. The mapping was achieved without disturbing the native environment of the neuron, by tagging alpha-synuclein with an enzyme—APEX—that allowed proteins less than 10 nanometers away from synuclein to be marked with a trackable fingerprint. "As a result, for the first time, we were able to visualize the protein's location, at minute scale, under physiologic conditions in an intact brain cell," noted Chung, who is now Scientific Co-founder and Associate Director at Yumanity Therapeutics in Cambridge.
Remarkably, the maps derived from these two processes were closely related and converged on the same Parkinson's genes and cellular processes. Whether in a yeast cell or in a neuron, alpha synuclein directly interfered with the rate of production of proteins in the cell, and the transport of proteins between cellular compartments. "It turns out the mechanisms of toxicity of the misfolded protein are closely related to which proteins it directly interacts with, and that these interactions can explain connections between different Parkinson's genetic risk factors," said Khurana, now a Principal Investigator within the Ann Romney Center for Neurologic Diseases at Brigham and Women's Hospital and the Harvard Stem Cell Institute.
Finally, the authors addressed two major challenges for any study that generates large data-sets of individual genes and proteins in model organisms like yeast: How to assemble the data into coherent maps? And how to integrate information across species, in this case from yeast to human?
Enter computational biologist Jian Peng, former Visiting Scientist at Whitehead Institute and postdoctoral researcher at MIT. "First, we had to figure out much better methods to find human counterparts of yeast genes, and then we had to arrange the humanized set of genes in a meaningful way," explained Peng, now Assistant Professor of Computer Sciences at University of Illinois, Urbana-Champaign. "The result was TransposeNet, a new suite of computational tools that uses machine learning algorithms to visualize patterns and interaction networks based on genes that are highly conserved from yeast to humans—and then makes predictions about the additional genes that are part of the alpha-synuclein toxicity response in humans."
This analysis produced networks that mapped out how alpha-synuclein is related to other Parkinson's genes through well-defined molecular pathways. "We now have a system to look at how seemingly unrelated genes come together to cause Parkinson's and how they are related to the protein that misfolds in this disease," said Khurana. To confirm their work, the researchers generated neurons from Parkinson's patients with different genetic forms of the disease. They showed that the molecular maps generated from their analyses allowed them to identify abnormalities shared among these distinct forms of Parkinson's. Prior to this, there was no obvious molecular connection between the genes implicated in these varieties of PD. "We believe these methods could pave the way for developing patient-specific treatments in the future," Khurana observed.
Deep brain stimulation is a medical procedure that involves implanting electrodes permanently into the brain and using them to alter the functioning of specific neural networks. A battery inserted subcutaneously in the chest provides the device with power. One application of the technology is as a treatment for Parkinson’s Disease, a neurodegenerative condition that causes tremors and difficulties moving. While the treatment can bring about an impressive alleviation of symptoms, research suggests that Parkinson’s patients often struggle to adjust psychologically. Now a case study published in the British Journal of Health Psychology has provided some of the first insights into what it’s like for a patient to contemplate undergoing surgery for deep brain stimulation, and then to adjust in the immediate aftermath.
Psychologist Virginia Eatough at Birkbeck University of London and her colleague, nurse specialist Karen Shaw from UCL’s Institute of Neurology, interviewed Katherine (not her real name), a 72-year-old Parkinson’s patient, three times: three weeks prior to surgery for deep brain stimulation, then four and twelve weeks afterwards. After transcribing the interviews, the researchers identified three main themes, the first concerned how she made the decision to go ahead with the surgery after the idea was proposed to her by her consultant.
Understandably, Katherine was scared of the procedure. But while she was encouraged by medical staff to speak to her friends and family, she found that they were so worried that she kept her own concerns to herself. “Most people’s reaction has been one of slight horror,” she said, “so I’ve been spending my time reassuring them…”.
Katherine also said how she’d been provided with a lot of facts about the intervention by medical staff, but that what she really wanted was a human form of reassurance. “I was looking for confidence [from my consultant],” she said, “and he didn’t give it. He didn’t not give it but he didn’t give it”. Katherine also said repeatedly that she would have liked to speak to other patients who’d gone through the procedure, but that this wasn’t an option.
In the end, after being impressed by the warmth of surgeon she decided to go ahead with the surgery, in the hope of a breaking through the “dead end” she’d reached with her worsening illness.
The second theme was Katherine’s shifting emotions through the period before and after the operation. She spoke of her fear of her Parkinson’s “engulfing her”, but also her trepidation at the procedure. As it grew imminent, her fear gave way to relief and excitement. “I stopped feeling apprehensive, I sort of gave up, I decided to just let it go,” she said.
Then immediately after the surgery, not detecting any noticeable improvement in her symptoms, Katherine went through a phase of feeling feelings of failure, disappointment and anger. “I felt I’d failed,” she said, “the fact that I wasn’t immediately dramatically different made me feel I’d failed, I had a huge sense of failure.”
But eventually, after returning home, Katherine became more aware of her improvements, and she realised that her doctors, who were pleased with the outcome, hadn’t just been feigning their satisfaction with the outcomes. This realisation made her feel overjoyed, grateful and happy. At the same time, however, she began to feel “slightly cast adrift” and “frightened” at the lack of continuing support.
“The procedure had given rise to considerable emotional fragility,” the researchers said, “indicating the need for psychological support at all stages.”
The final theme concerned “the embodied meaning” of the procedure. Katherine saw it as “odd”, “spectacular” and “strange”, the stuff of fiction. “I’m worried about getting water in the holds in my head,” she said. “I felt my brain had been taken over and God knows what thoughts had been put in it and would I ever be in control of it again and would I know how to handle by new brain?”.
Later she began to adjust. “I try not to think about it,” she said. “… You could go fairly crazy trying to think about having sticks in your head, but then I’ve got two artificial hips and an artificial knee so why am I not worrying about that, it’s the same intrusion and it’s artificial.”
The researchers said their case study showed how the deep brain stimulation experience is “one of considerable emotional and cognitive turmoil”, indicating the importance of “patient tailored discussion, counselling and emotional support”. One practical suggestion they had is for the introduction of a buddy system in which prospective patients are paired with a patient who has already undertaken the procedure. The researchers also emphasised that the interviews demonstrated the need for medical professionals to go beyond providing factual advice. They need to “step outside of their professional role, no matter how briefly, and see how it looks from the perspective of someone like Katherine.”
Marines who served there from '53 through '87 may be eligible for benefits if they developed Parkinson's disease or certain cancers linked to contaminated water
York County Department of Veterans Affairs is seeking local Marine Corps veterans who developed Parkinson's disease or certain types of cancer as a result of drinking contaminated water at Camp Lejeune between 1953 and 1987, according to a news release.
Marine vets, or their surviving spouses, may be eligible to receive compensation if the veteran served at Camp Lejeune in North Carolina from Aug. 1, 1953, through Dec. 31, 1987, and developed one of the following:
Aplastic anemia and other myelodysplastic syndromes
The new technique probes the neural pathways that cause these tremors, and also provides a way to map and troubleshoot other circuits in the whole brain.
A new circuit-mapping approach to probe the brain should help improve treatments for Parkinson’s disease. It also provides a methodology to identify, map and ultimately repair neural circuits associated with other brain diseases. (Image credit: iStock / D3Damon)
If a piece of electronics isn’t working, troubleshooting the problem often involves probing the flow of electricity through the various components of the circuit to locate any faulty parts.
Stanford bioengineer and neuroscientist Jin Hyung Lee, who studies Parkinson’s disease, has adapted that idea to diseases of the brain, creating a new way to turn on specific types of neurons in order to observe how this affects the whole brain. The work is described in the Jan. 26 issue ofNeuron.
Lee, who trained as an electrical engineer before becoming a brain researcher, wanted to give neuroscientists a way to probe brain ailments similar to how engineers troubleshoot faulty electronics.
“Electrical engineers try to figure out how individual components affect the overall circuit to guide repairs,” Lee said.
In the short term, her technique should help improve treatments for Parkinson’s disease. In the long run it provides a methodology to identify, map and ultimately repair neural circuits associated with other brain diseases.
Seeing the circuit
Lee’s circuit-mapping approach combines two experimental tools with a computational method. The first experimental tool is optogenetics. Pioneered by Stanford bioengineer Karl Deisseroth, optogenetics modifies specific types of neurons – the basic working parts of the brain – so they can be turned on in response to light. The second experimental tool is called functional MRI, or fMRI, which measures blood flow in the brain. Increased blood flow is associated with increased activity. Using optogenetics to turn on a specific type of neuron, and fMRI to observe how other regions of the brain responded, Lee then used a computational analysis to map the entire, specific neural circuit and also determine its function.
Controlling Parkinson’s tremors
One hallmark of Parkinson’s disease are uncontrollable tremors. Neuroscientists believe that these tremors are caused by malfunctions in the neural pathways that control motion. They know that different regions of the brain are constantly forming circuits to carry out tasks, whether motion or speech. However, prior to Lee’s technique, researchers had no way to show how activating a specific type of neuron might cause a specific circuit to form in the whole brain.
Testing her approach on rats, Lee probed two different types of neurons known to be involved in Parkinson’s disease – although it wasn’t known exactly how. Her team found that one type of neuron activated a pathway that called for greater motion while the other activated a signal for less motion. Lee’s team then designed a computational approach to draw circuit diagrams that underlie these neuron-specific brain circuit functions.
“This is the first time anyone has shown how different neuron types form distinct whole brain circuits with opposite outcomes,” Lee said.
Lee said the findings in this paper should help to improve treatments for Parkinson’s disease. Neurosurgeons are already using a technique called deep brain stimulation (DBS) to calm Parkinson’s tremors in their patients. DBS delivers tiny electric jolts to neurons thought to be responsible for the tremors. A more precise understanding of the how those neurons work to control motion could help guide more effective stimulation.
But more broadly speaking, Lee thinks that her technique – optogenetic fMRI combined with computational modeling – gives researchers a new way to reverse-engineer the functions of the many different types of neurons in the brain and the bafflingly diverse array of neural circuits formed to carry out different commands.
Other members of the Stanford team include Daniel Bernal-Casas, a postdoctoral scholar, and Hyun Joo Lee, a research scientist, both in the Department of Neurology and Neurological Sciences; and Andrew Weitz, a graduate student in bioengineering. This work was supported by the National Institutes of Health, the National Science Foundation, an Alfred P. Sloan Research Fellowship and an Okawa Foundation Research Grant Award.