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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
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Thursday, June 1, 2017

Brain Trust Neurologist Panida Piboolnurak focuses on care of patients with movement disorders

June 1, 2017

s NHRMC Physician Group’s first neurologist specializing in Parkinson’s disease and movement disorders, PANIDA PIBOOLNURAK is glad Wilmington-area patients with these conditions no longer need to travel to other parts of the state to received specialized care.

Piboolnurak joined NHRMC Physician Group-Neurology in December.
While Piboolnurak says researchers in her field are likely years away from finding a cure for Parkinson’s and other neurological disorders, there are ways to help patients and families.
“Although we cannot find the root cause of Parkinson’s or a treatment that could help stop the progression, we have a lot of new technology to help the patient feel better while we look for a cure,” she says.
She usually sees about ten to fifteen patients a day, five days a week, as well as completes the necessary paperwork. These patients have a wide range of neurological issues. She advocates for a multidisciplinary team approach to treatment.

Aside from working with her neurology colleagues with specialties such as multiple sclerosis, muscular disorders, and stroke, she believes social workers, physical therapists, and others can help treat the entirety of a patient’s needs.
“It’s not just medication,” says NHRMC neurologist and Parkinson's disease specialist Panida Piboolnurak about the treatment for disorders that many see as “a shaking problem or a walking problem.”
In fact, patients with Parkinson’s disease and movement disorders can also have anxiety and depression and other issues that are nonmotor symptoms.

Her CV is like a travelogue along a circuitous neurological pathway: She received her medical degree with honors from Chulalongkorn University in Bangkok and later completed an internship in Springfield, Illinois; a residency at Cornell University in New York; and fellowships at Columbia University in New York and the University of Toronto.

Certified by the American Board of Psychiatry and Neurology, Piboolnurak has published in more than a dozen journals that address neurology.
She has studied topics such as brain stimulation for movement disorders, clinical motor physiology of movement disorders and Parkinson’s disease, and movement disorders and neurodegenerative diseases.

Her professional experience has been in Thailand, New York, Rhode Island, and – just before moving to Wilmington – Hawaii, where she served as director of the Hawaii Parkinson’s Disease, Movement Disorders and Neurodegenerative Diseases Center at Hawaii Pacific Neuroscience in Kailua.
“I’m glad I found a place where I can help serve the community,” she says of her move to Wilmington, which wasn’t already saturated with specialists in Parkinson’s and movement disorders. “Before they (patients and their families) had to drive a few hours to go to Duke or UNC for their needs, and now we can fill that gap.”

Piboolnurak says it’s important to include family members and caregivers in the care of patients with Parkinson’s and other movement disorders. She likes to sit with them all to discuss the patient’s disorder and the options for care.

Wilmington’s geography played a role in her decision to move to the area.
“I’m driven by the ocean,” she says.
She recalls how, when working at Cornell, she took the opportunity on good weather weekends to take the Long Island Rail Road to the beach.

“But I wanted way more than that, so I looked at where else I could practice neurology and be close to the ocean,” a move that took her to Rhode Island. After Rhode Island, she went back to Thailand for family reasons and later found another job near the ocean, this time in Hawaii. Affordable housing close to the beach was hard to find, so between her work schedule and the distance to the ocean, she didn’t get there often.

The opportunity in Wilmington allows the perfect blend of more reasonable housing near the ocean and the opportunity to make a positive impact on those with neurological disorders. Her parents, after visiting other area beaches selected Wrightsville Beach, live with her.

Asked if she had anything else to say about her life, Piboolnurak replies, “No, my life is so simple.”
There are probably a lot of people who would disagree.

Is Parkinson’s Hereditary?

June 1, 2017  BY ERUM NAQVI

Parkinson’s disease may be either hereditary, meaning it is caused by genetic factors, or sporadic, meaning it iscaused by environmental factors. In most cases, Parkinson’s is not hereditary nor directly inherited, and only 15 to 25 percent of Parkinson’s patients have a family history. In large population studies, researchers found that those with a family history of Parkinson’s have a 4 to 9 percent higher risk of developing disease than the general population.
Genes linked to the development of Parkinson’s are classified as either “‘causal genes” or “associated genes.”

Causal genes

Causal genes are those which carry mutations that, when inherited, cause the disease. Parkinson’s caused by these mutations is very rare, accounting for only 1 or 2 percent of all patients. One example of a causal gene is SNCA, which encodes a protein called alpha-synuclein. At least five mutations of SNCA have been found to cause Parkinson’s. These mutations can be inherited and directly cause the disease.
The “Iowa kindred” or “Spellman-Muenter kindred” is a large family in Iowa. Researchers traced 200 members of this family with and without Parkinson’s and analyzed their entire genome to identify the genes associated with the disease. They discovered that mutations in the SNCA gene coding for alpha-synuclein was the causal gene for Parkinson’s in this family. Normally, SNCA is located on chromosome 4 as a single copy. However, members of this family carried three copies of the gene that caused them to develop the disease at a young age.

Associated genes

Mutations in associated genes do not directly cause Parkinson’s, but increase the risk of developing it. A person may have mutations in associated genes and never get Parkinson’s, but is more likely to develop it. The combined effect of associated genes and environmental factors may trigger the development of Parkinson’s.
Genes associated with Parkinson’s disease include PRKNwhich codes for the parkin protein;,PINK1which dodes for a protein found in the heart and skeletal muscles; LRRK2, which codes for a brain protein called dardarin; and PARK7, which codes for a brain protein called DJ-1.
Mutations in certain genes, including GBA (which codes for an enzyme called glucocerebrosidase) and UCHL1 (which codes for an esterase enzyme), also appear to increase the risk of developing Parkinson’s.
Mutations in the LRRK2 gene are common in people of North African, Basque, Portuguese, and Ashkenazi Jewish descent, but occur in almost all ethnic groups. Some people with LRRK2 mutations develop Parkinson’s disease as young as in their 30s while others develop the disease in their 80s, and others never develop it. There is great variability in the mutations that occur in the LRRK2 gene and the effects that these mutations have on the individual. Some people with LRRK2 gene mutations develop dementia, while others develop a form of Parkinson’s disease that shares features with amyotrophic lateral sclerosis (ALS). This variability, where some people develop certain disease features while others are protected, may provide clues about the underlying cause of Parkinson’s disease.
Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

Researchers Identify a Key Link Between the Brain’s Immune Cells and Neurodegenerative Disorders


Researchers at the University of California and the Salk Institute for Biological Studies have identified the mechanisms that make the brain’s immune cells different from all other immune cells
A finding with implications for Huntington’s disease was that genes associated with neurological illnesses have higher lessons of expression in microglia, or the brain’s immune cells, than in other brain cells. Expression is the process by which a gene creates a functional product such as a protein.
The results could help scientists uncover the role microglia play in several neurodegenerative and psychiatric conditions, including Huntington’s, Parkinson’s disease, schizophrenia, autism and depression.
The study, “An environment-dependent transcriptional network specifies human microglia identity,” was published in the scientific journal Science.
“These studies represent the first systematic effort to molecularly decode microglia,” Christopher Glass, a UC San Diego professor who was the senior author of the study, said in a press release. “Our findings provide the foundations for understanding the underlying mechanisms that determine beneficial or pathological functions of these cells.”
Microglia are responsible for maintaining the brain’s cell balance, which protects it from harmful invaders. They release pro- and anti-inflammatory signals in response to changes in the brain’s microenvironment, and ensure the health of the brain’s neuron network.
The researchers analyzed microglia cells in tissue samples from 19 people who had brain surgery for epilepsy, brain tumor, or stroke. They also looked at microglia cells in tissue from mice.
They found hundreds of genes more highly expressed in microglia than in other immune cells. They also discovered that the genes involved in microglia expression were different from those in other brain cells. And moving cells from tissue to a petri dish culture led to gene pattern changes, they learned.
They concluded that microglia cells have a unique gene expression pattern that changes when the  environmental changes. The adjustment was fast, they added. Within just six hours the level of expression in 1,957 genes had increased fourfold, and in more than 2000 genes it had dropped fourfold.
The researchers wondered if the genes that were highly expressed in microglia were associated with neurodegenerative or behavioral disorders, and if their surroundings impacted the level of expression. They found 146 human genes that were associated with neurodegenerative and psychiatric diseases whose expression depended on the surroundings.
But the gene expression in mice tissue differed from that in humans. This suggested that mice may be an unsuitable experimental model for some of these illnesses.
“A really high proportion of genes linked to multiple sclerosis, Parkinson’s and schizophrenia are much more highly expressed in microglia than the rest of the brain,” said Nicole Coufal, a pediatric critical care doctor at UC San Diego and a researcher at the Salk Institute. “That suggests there’s some kind of link between microglia and the diseases.”
More studies are required for a better understanding of microglia’s role in the development of neurological and psychiatric diseases, the team said.

Your nightmares might be a dementia warning sign


Thrashing and screaming in your sleep might be an early sign of a neurological disorder.
Scientists have discovered that patients who suffer from REM sleep behavior disorder (RBD) are more likely to be diagnosed with Parkinson’s or dementia later in life – suggesting that RBD could be an early indicator. This rare dream disorder causes strange, often violent dreams where sufferers scream, kick and thrash in their sleep, or even jumps out of bed in a rage.
John Peever, a neuroscientist at the University of Toronto, found that more than 80 percent of RBD patients eventually developed a neurological disease. Peever presented his team’s initial findings May 29 at the Canadian Neuroscience Meeting. They have not yet been published.
RBD is caused by a disrupted REM, or rapid eye movement, cycle. When we enter REM sleep our brain’s neurons fire like they do when we’re awake, but our body remains in a state of paralysis. This isn’t the case for people with RBD.
As part of his research, Peever discovered a group of cells in the brainstem that appear to be responsible for maintaining REM sleep. When he isolated the cells in mice, Peever could transition them between REM and non-REM sleep by turning the cells on and off.
But in RBD patients, Peever found that these cells were damaged.
“For some reason, the cells in the REM sleep area are the first to be sickened, and then the neurodegenerative disease spreads up into the brain and affects the other areas that case disorders like Parkinson’s disease,” Peever told Live Science. “REM Behavior Disorder is in fact the best-known predictor of the onset of Parkinson’s disease.”
Even though Peever’s study isn’t yet peer-reviewed, it’s not the first time researchers have noticed this link.
Two studies from 2013 found that more than 80 percent of RBD patients developed a disorder within a decade. And of 43 RBD patients observed in a 2010 study, 41 were eventually diagnosed with a neurological disease.
Further, a 2007 study of patients with multiple system atrophy (MSA) found that 90-100 percent of them suffered from RBD. MSA is a progressive neurodegenerative disorder that affects the part of the nervous system which controls your blood pressure, heart rate and bladder function.
Peever hopes that further research will help make way for protective medicines and therapies for RBD patients.
“Much like we see in people prone to cancer, diagnosing REM disorders may allow us to provide individuals with preventative actions to keep them healthy long before they develop these more serious neurological conditions,” he concluded at the conference.

If Air Pollution Causes Alzheimer’s, Dementia and Parkinson’s, Why Are We Still in Denial?

When you think of factors that increase the risk of Alzheimer’s, dementia and Parkinson’s disease you probably think of genetics or traumatic brain injury. Even if you created a lengthy list of factors, you might never list air pollution—but more and more research shows that air pollution is involved in these brain diseases, which now affect 6 million Americans and 50 million people worldwide.
While we have known for years that air pollution increases the risk of asthma, lung infections and lung cancer, we are discovering that it is also linked to heart disease, depression, obesity and brain diseases. In a study published in the medical journal Environmental Health Perspectives, researchers assessed the effects of black carbon—a marker of traffic-related air pollution—on cognitive function and the central nervous systems of male study participants. The scientists found that there was a significant link between air pollution levels and a reduction in cognitive function, a worrisome result given our growing air pollution emissions.
Research also shows that coarse pollution particles tend to settle in the upper lungs, making them a threat to respiratory health, while fine and ultrafine pollution particles actually travel through the nostrils along neural pathways into the brain. That’s a scary thought…that smell of diesel or gasoline fumes we’ve become so accustomed to can actually be accessing our brains where they can do serious damage. Fine pollution particles can travel thousands of miles and ultrafine particles travel up to 6 miles, so what happens on one side of the planet can affect people on the other side.
It is no surprise that President Donald Trump’s decision to pull America out of the Paris Climate Accord will have far-reaching and longstanding results. Even major corporationsthat aren’t exactly known for their commitment to clean air (like ExxonMobil, Chevron, Dow Chemical Company, DuPont and even the much-hated Monsanto) are asking The Donald to stay committed to the Paris climate accord, and for good reason: the health of humans and other species on the planet depends on clean air.
Aren’t we already seeing enough signs of the damage? Respiratory illnesses, heart disease, brain disease, depression and other illnesses linked to air pollution are at record levels. And the effects of pulling out of the climate pact aren’t only health-related; the National Resources Defense Council, an environmental group, estimates that pulling out of the agreement will cost the United States close to $2 Trillion every year by 2100.
The Paris Climate Accord was a landmark decision made by representatives of 195 nations in December 2015 to commit to reducing climate change and ensure the health of future generations.
While Trump makes his decision, the effects of air pollution are already having disastrous consequences. Research in the Journal of Alzheimer’s Disease found a link between air pollution exposure and the brain inflammation and amyloid plaques involved in Alzheimer’s disease in both children and adults.
So what can you do? In addition to signing a petition urging the governor of your state to stay in the Paris climate accord, according to the California Environmental Protection Agency Air Resources Board there are other things you can do, including:
  1. Reduce travel on days with poor air quality.
  2. Avoid vigorous physical activity on days that have poor air quality.
  3. Avoid using your wood stove and fireplace on days that have poor air quality.
  4. Avoid using leaf blowers and other dust-producing equipment.
  5. Drive slowly on unpaved roads and other dirt surfaces.
  6. Get involved with air quality improvement programs in your community.
  7. If you own or operate an industrial source of PM10, comply with local rules that apply to your operation. Work with local agencies to develop strategies that will further reduce PM10 emissions.
Additionally, I would add:
  1. Encourage your employer to allow more teleworking or working from home.
  2. Turn off your vehicle engine immediately after arriving at your destination—don’t leave it idling while you check your phone.
  3. If your community doesn’t have an anti-idling bylaw encourage them to pass one.
  4. Eat a nutrient-rich diet and supplement with the vitamins that protect DNA against air pollution. Learn which vitamins play this critical role in my blog “The Vitamins that Protect Your DNA against Air Pollution.”
  5. Contact your government representative asking for the removal of Scott Pruitt from the Environmental Protection Agency before he totally dismantles the agency responsible for improving air quality and the environment.

These Lifestyle Hacks Will Help Anyone With a Chronic Illness


If you have a chronic illness, you know just how much energy it takes to complete your daily chores and common household tasks. In this video from newlifeoutlook, Jennifer shares some practical tips to help make life a little easier for anyone suffering from a chronic illness.

Jennifer looks at ways chronic illnesses sufferers can conserve energy and save time when they’re in the kitchen, along with hacks for personal grooming, getting dressed, cleaning, and shopping. The suggestions are designed to help patients avoid lifting heavy items, standing for too long, moving around a lot, or doing too much in one day.
Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

Antipsychotics to Treat Parkinson’s Psychosis Need Further Research, Report Says


The antipsychotics Clozaril (clozapine, or CLZ) and Nuplazid (pimavanserin, or PIM) are potential treatments for Parkinson’s disease psychosis (PDP) in patients with idiopathic Parkinson’s disease (iPD), whose cause is unknown. However, their use is currently limited and further research is necessary, according to a review of various trials.
Results of a meta-analysis of studies of antipsychotics used to treat PDP were shared in a letter titled, “Antipsychotics for the management of Parkinson’s disease psychosis,” published in the International Journal of Geriatric Psychiatry last April.
Up to 40% of patients with iPD develop PDP. Psychotic symptoms include visual hallucinations and delusions. PDP causes severe distress and agitation, which makes it harder for caregivers to provide care for these patients and often requires admission to nursing homes.
Antipsychotics are one of the options for treatment of PDP, but many antipsychotics cause deterioration in motor function. The letter reported on studies of antipsychotics that do not affect motor function in treating PDP.
Seroquel (quetiapine, or QTP) has often been used without demonstrated effectiveness, and over 50% of patients dropped out of trials because of adverse effects including somnolence and orthostatic hypotension, a drop in blood pressure when a person suddenly stands up from a lying or sitting position. Seroquel was not shown to reduce psychotic symptoms in PDP and neither was Zyprexa (olanzapine), even though they do not affect motor function.
Clozaril did reduce psychotic symptoms in these patients, but because it requires regular blood tests, it is inconvenient for elderly patients. Nuplazid, which is approved by the FDA in the U.S., but is not approved in the U.K., appears to be as effective as Clozaril in reducing psychotic symptoms, and neither therapy appears to cause deterioration in motor function.
In the U.K., Clozaril is recommended for managing PDP, but many neurologists have little experience with the drug, and collaboration between neurology and psychiatric services is required to make sure patients are safely treated.
“A standard therapy has yet to be determined for PDP. Despite its widespread use, QTP has not demonstrated efficacy or tolerability. CLZ and PIM are promising treatments; however, their use is currently limited. Further research, including adequately powered clinical trials and naturalistic cohort studies, with uniform outcome reporting are required to assess the efficacy, tolerability and access of these agents,” the letter stated. “These studies also need to investigate adherence issues, the impact of physical illness, quality of life measures and transition to nursing home placement.”

LIFE Shared This Remarkable Parkinson's Disease Story in 1959. A Lot Has Changed Since Then

June 1,  2017  Lily Rothman,Liz Ronk,Julia Lull

The great LIFE photographer Margaret Bourke-White was in Tokyo in 1952 when she first discovered that, in the middle of a physically demanding photojournalistic career, the dull pain in her left leg was becoming something more. Rising from a meal, she found herself, for a few steps at least, unable to walk.

As she would recount in an extraordinary LIFE story seven years later, it turned out — after years of misdiagnosis and confusion — that her brief stumble was a symptom of the onset of Parkinson's disease, against which she would fight with everything she had for nearly two decades until her death at 67. It was, as the introduction to that 1959 article noted, the toughest battle ever faced by a woman who had seen many — including literal battles in World War II, during which she served as the first woman accredited to cover the combat zones as a photojournalist.

LIFE photographers Alfred Eisenstaedt and Margaret Bourke-White in 1959. Alfred Eisenstaedt—The LIFE Picture Collection/Getty Images 

With photographs by her fellow LIFE photographer, some of which are seen above, the story offered up the personal reflections of the woman who had taken the image that appeared on the of the magazine.

When I opened some medical insurance papers one day and learned I had Parkinson's disease, the name did not frighten me because I did not know what in the world it was," she wrote, describing how she learned the name that her doctors had kept from her as they prescribed physical therapy for her unlabeled symptoms. "Then slowly a memory came back, of a description Edward Steichen once gave at a photographers' meeting of the illness of Edward Weston, 'dean of photographers,' who was a Parkinsonian. I remembered the break in Steichen's voice: 'A terrible disease... you can't work because you can't hold things... you grow stiffer each year until you are a walking prison... there is no known cure...'"
The knowledge was, unsurprisingly, devastating to Bourke-White.
But she set her mind to learn what she could, to look for anything she could do for relief. She learned, she wrote, that she was just one of three quarters of a million Americans with the disease — "often they appear to be struck down at their peak," she wrote — and that, despite this number and the fact that the symptoms had been observed for thousands of years, nobody knew what caused it or how to stop it. Though Bourke-White was an extreme devotee of her exercise routine and even underwent a then-cutting-edge  to "deaden permanently" part of her brain, she knew that the operation she'd received had only treated some of her disease and that there was no way to know how the symptoms would progress from there

Today, more than half a century later, as Parkinson's researchers and advocates mark 200 years since Dr. James Parkinson the disease (then known as "shaking palsy") that would come to bear his name, many of the questions that confronted Bourke-White remain frustratingly unresolved for those who receive the same diagnosis she did. Treatment options, however, have advanced significantly since Bourke-White's time — and new advances are offering the hope for something even better.

For one thing, says Dr. Rachel Dolhun, vice president of medical communications at the Michael J. Fox Foundation for Parkinson's Research, a person with Parkinson's disease in the 1950s had no effective options for medication. The most widely prescribed therapy used today, which temporarily addresses some Parkinson's-related loss of dopamine, a movement-regulating brain chemical — wasn't discovered until the late 1960s. 

It is now also understood in a way that it was not a few decades ago that many different brain chemicals and parts of the body are involved in symptoms linked to Parkinson's, not just dopamine and the brain. In addition, the operation that Bourke-White received to basically destroy part of her brain is largely obsolete today, and a patient who was a candidate for brain surgery now would likely instead receive, which uses wires or electrodes to stimulate parts of the brain. (The physical therapy that was prescribed for Bourke-White, however, is one thing that hasn't changed: exercise remains a key way to address symptoms.) 

And Dolhun says that advances in genetic science in the last 20 years or so, by offering new insights into how the disease works, have opened up a new range of research angles — and hope for a real cure, rather than just a better way to address the symptoms. For example, experts are excited by the testing of possible therapies that would target a protein called “Right now, because of those understandings, the development pipeline is richer than it’s ever been," she says.

 Technology is also changing what's possible for researchers and scientists. The Michael J. Fox Foundation is running  in which patients can log on and tell researchers about what it’s like to live their experience of Parkinson's disease, Dolhun says, and devices like wearables and smartphones are providing new ways to track and communicate about the symptoms. For example, whereas it used to be that a doctor might observe a patient's tremor for 15 minutes at a time every couple of months, now an app or a watch can allow patients to log data that gives researchers a 24/7 look at information about those symptoms.

These new possibilities are particularly important when it comes to Parkinson's disease, since the experience of what it's like to live with and fight the symptoms is very individualized. “It’s a different journey for every single person who’s on it," says Dolhun. "That’s why we need the patient experience to inform us so much, and that’s why it’s so important for patients to be involved directly

That's also one reason why the openness of people like Margaret Bourke-White mattered in 1959 and continues to matter today. There can still be a stigma attached to telling others that you are experiencing something that might make them see you as weak or in need of assistance. But if those who have it keep their experiences to themselves, it's harder for researchers to make progress toward a cure — and harder for others with the diagnosis to feel that they're not alone

 For Bourke-White, as she described for LIFE's readers, her fight against Parkinson's was, to the fullest extent possible, a reminder to keep working and enjoying what her body could do for every second possible. Nowadays, she wrote in 1959 after the surgery that helped her do that longer than would otherwise have been possible, "my fingers are more and more often loading my cameras, changing their lenses, and turning their winding buttons as I practice the simple blessed business of living and working again."

"It’s not uncommon for people to feel shy about sharing their stories," Dolhun says. "For [Bourke-White] to share her story so publicly I think really speaks volumes. When we see people come forward with their story, it’s not an uncommon thing for them to say, 'I really wish I had shared it earlier.' They feel a burden lifted." 

Researchers discover new 'GPS' neuron

June 1, 2017

An international research team led by UvA researchers Jeroen Bos, Martin Vinck and Cyriel Pennartz has identified a new type of neuron which might play a vital role in humans' ability to navigate their environments. The discovery is an important step towards understanding how the brain codes navigation behaviour at larger scales and could potentially open up new treatment strategies for people with impaired topographical orientation like Alzheimer's patients. The team's results are published in the latest edition of Nature Communications.
Every day billions of people across the planet successfully navigate their environments, for example when they go to work or head home. Such journeys generally happen with little conscious effort and rest on the brain's ability to use overall knowledge of an environment to make estimates of where it finds itself. The ability to make fine grained assessments of location is seated in the hippocampus, a seahorse-shaped structure located in the temporal lobe. Research shows that the precise mechanism for navigation includes hippocampal place cells, which increase or decrease in electrical activity depending on one's location. However, when making their daily commute, people don't need very detailed representations of which houses they pass in which order. Instead, they can make due with more course information. Left at the museum and somewhere down the road right again at the supermarket, called topographical orientation.
Building on current research, the researchers investigated how large scale navigational knowledge is coded within the brain and whether this process indeed occurs in different structures within the temporal lobe. They did this by training rats to perform a visually guided task in a figure-8 maze consisting of two loops that overlap in the middle lane. During the experiment, the researchers measured electrical activity in the brain by using a novel instrument which allowed the researchers to simultaneously record groups of neurons from four different areas. They recorded from the perirhinal cortex, hippocampus and two sensory areas. Recordings from the perirhinal cortex revealed sustained activity patterns. The level of electrical activity clearly rose and fell depending on the segment the rats were in and persisted throughout that entire segment.
'We found a pronounced difference between the responses in the perirhinal cortex and responses in other areas of the brain', says Jeroen Bos, lead author and researcher at the UvA's Swammerdam Institute for Life Sciences. 'Units from the perirhinal cortex had sustained responses throughout the whole loop. By contrast, responses from hippocampal place cells were scattered across the maze and their fields were much smaller than the loops of the maze. We were surprised to see the perirhinal cortex's responses align so closely with the layout of the maze, primarily because the region is commonly associated with object recognition. This seems to be a new type of neuron, which we have informally dubbed the 'neighbourhood cell'. This neuron seems to enable the brain to specifically differentiate between distinct segments ("neighbourhoods") of the environment.'
The team's results offer a first glimpse on how the brain is able to code navigation behaviour at larger scales and could be especially relevant for people with an impaired capacity for topographical orientation. The large scale of perirhinal coding contrasts with the finer scale of hippocampal coding. 'It is known that patients with Alzheimer's disease or with damage to the temporal lobe have great difficulty finding their way, especially to remote goal locations', says fellow researcher and professor of Cognitive Systems and Neuroscience Cyriel Pennartz. 'Albeit new, our findings don't conflict with previous literature on this phenomenon, for example such as the long-time London cab driver who sustained hippocampal damage. Although the driver could still navigate through the city, he remained highly dependent on main roads and would frequently get lost when using side streets. It might be that he was using the perirhinal cortex for global orientation but could no longer make use of the fine-grained place fields normally found in the hippocampus.'
In addition to offering new insights into brain mechanisms for spatial navigation at different scales, the results may guide patients with Alzheimer's or other diseases in using other spatial strategies than the ones most severely affected. The findings point to the perirhinal cortex as a target for treatment. Finally, research on neural replacement devices and assistive robots may benefit from this study.
Article: Perirhinal firing patterns are sustained across large spatial segments of the task environment, Jeroen J. Bos, Martin Vinck, Laura A. van Mourik-Donga, Jadin C. Jackson, Menno P. Witter & Cyriel M. A. Pennartz, Nature Communications, doi: 10.1038/ncomms15602, published online 26 May 2017.

Casualty actress launches film project for Parkinson's play Kinetics

June 1, 2017   BY

Sue Wylie seeks funding for film based on her play Kinetics

Sue Wylie and Steve Rollins in the play Kinetics
Actress Sue Wylie is launching a project to create a film based on her play about the life-changing disease she developed six years ago.
Sue, who used to teach drama in Dorchester, was diagnosed with early onset Parkinson’s at the age of 50 and turned her experiences into a play, Kinetics, which premiered last year.
Now she is building on the success of its tour of the south west by creating a film as a teaching resource to health professionals.
Sue said: “The diagnosis came as a big shock. I thought it was something only old people got and I had just turned 50.
“I found it difficult to tell people and realised how little was known about this chronic condition.”
She combined her experience with another real-life story based on a student she knew whose outlet from his problems was parkour, also known as free running - with the main characters coping with their desire to move.
Kinetics enjoyed support from Dorchester Arts and, following performances in the town’s Corn Exchange, went on to gain Arts Council funding for a tour last autumn.
Sue said: “We got letters and emails saying it should be seen by a wider audience and that’s when I thought about a film. It has a lot of potential as a resource for professionals as well and so I am launching a Kickstarter campaign to raise the money for it.
“We’re all ready to go and in the first few days we’ve already got £3,300 but we need about £30,000.”
A registered charity, DT2 Productions, has been set up to advance education about Parkinson’s with the film as an innovative resource.
The project has a production team lined up including director Tom Martin and they aim to complete filming in a week in August in Bristol.
Sue’s career under her Equity name of Sue Broomfield includes stage, radio and television work including Casualty and The Bill.
But she has eased that workload now to focus on Kinetics and to cope with the disease that often leaves her tired.
She said: “I feel frustrated about this condition because I can’t do things at the pace I want to. I find the enforced slowing down a challenge.”
Sue, who used to teach drama at the Thomas Hardye School in Dorchester as well as in Taunton, is also planning other projects related to Kinetics including a radio workshop with Bournemouth University students.
Donations can be made online at or by sending a cheque made payable to DT2 Productions to Sue at Wylye Croft, Martinstown, Dorchester, DT2 9JL. Or call 01305 889085 to find out more.
Mark Tattersall, Dorchester Arts artistic director, said: “We are hugely proud and really hope that the film comes off as it would be wonderful for Kinetics to play a role in changing attitudes towards Parkinson’s on an even wider scale than we managed with the recent tour.”