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I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.

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.

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Saturday, June 9, 2018

Diagnosised With Parkinson's Disease, Anthony Bourdain Decided to Quit Rather Than Fight

By Stan Geene  June 9, 2018



Anthony Bourdain arrives at the 65th Primetime Creative Arts Emmy Awards in Los Angeles, September 15.


Anthony Bourdain's suicide on June 8th followed his diagnosis with Parkinson's Disorder 3 or 4 months ago, according to multiple sources.

"3-4 months ago I posted that I thought Anthony Bourdain was showing signs of a neurological illness (Parkinson's) and may be why he committed suicide. So sad. Bourdain was a brilliant tv story teller," said one close associate on social media.



Like Robin Williams, Anthony Bourdain could not face a diagnosis of Parkinson's disease


According to Britain's NHS, early warning signs of Parkinson's disease include insomnia, loss of the sense of smell, constipation, dizziness and sweating. In addition to all these, Bourdain manifested a "Masked Face," starring off into the distance. The Northwest Parkinson’s Foundation says, “it’s easiest to recognize by a slowness to smile or frown, or staring off into the distance,” along with less frequent blinking. This had been noted about Bourdain in recent months

Depression and a diagnosis of Parkinsons often go hand in hand. Parkinson’s patients “tend to feel apathetic and generally disinterested in things they used to enjoy,” which are from the symptoms of sadness or helplessness that those with primary depression often feel. Robin Williams is now widely believe to have killed himself for the same reason.

There is an internet rumor that Bourdain's girlfriend actress Asia Argento had recently dumped Bourdain. It is possible that the breakup was a contributing factor.

Parkinson's disease (PD) is a long-term degenerative disorder of the central nervous system that mainly affects the motor system. The symptoms generally come on slowly over time. Early in the disease, the most obvious are shaking, rigidity, slowness of movement, and difficulty with walking. Thinking and behavioral problems may also occur. Dementia becomes common in the advanced stages of the disease

On June 8, 2018, Bourdain was found dead of an apparent suicide by hanging in his room at the Le Chambard hotel in Kaysersberg, France Bourdain was traveling with friend Éric Ripert who worried when he missed dinner and breakfast. Christian de Rocquigny du Fayel, the public prosecutor for Colmar, France, said "not much preparation and premeditation went into the act, and leads us more in the direction of an impulsive act," adding that, "at this stage, nothing suggests the intervention of a third party". He added that Bourdain's body bore no signs of violence, and that toxicology tests would determine whether drugs or medications were involved. Bourdain was working on an episode of Anthony Bourdain: Parts Unknown in nearby Strasbourg, France.

Anthony Michael Bourdain, 61 was an American celebrity chef, author, travel documentarian, and television personality who starred in programs focusing on the exploration of international culture, cuisine, and the human condition. He was considered one of the most influential chefs in the world by many commentators.

Bourdain was a 1978 graduate of The Culinary Institute of America and a veteran of numerous professional kitchens in his career, which included many years spent as executive chef at Brasserie Les Halles in Manhattan. He first became known for his 2000 bestselling book Kitchen Confidential: Adventures in the Culinary Underbelly. His first food and world-travel television show was A Cook's Tour, which ran for 35 episodes on the Food Network from 2002 through 2003. In 2005 he began hosting the Travel Channel's culinary and cultural adventure programs Anthony Bourdain: No Reservations (2005–2012) and The Layover (2011–2013). In 2013, he switched to CNN to host Anthony Bourdain: Parts Unknown.

Though best known for his culinary achievements and television presentations, along with several books on food and cooking and travel adventures, Bourdain also wrote both fiction and historical nonfiction.


Michael J Fox in contrast has made fighting Parkinson's disorder his career



http://www.smobserved.com/story/2018/06/09/news/diagnosised-with-parkinsons-disease-anthony-bourdain-decided-to-quit-rather-than-fight/3483.html

Apple Watch just got a lot better at tracking symptoms of Parkinson's Disease

June 9, 2018    


David Paul Morris | Bloomberg | Getty Images
Jeff Williams, chief operating officer of Apple speaks about Apple Watch during an event at the Steve Jobs Theater in Cupertino, California, on Tuesday, Sept. 12, 2017.

  • The Apple Watch is becoming a useful tool for medical researchers to track symptoms associated with Parkinson's. 
  • Now, it's gotten better at detecting tremors and shakes. 
  • Apple's new "movement disorder API" will accelerate research that's already underway, scientists say.

The Apple Watch will soon be able to track tremors experienced by Parkinson's Disease patients to help them manage their condition. 
Later this year, Apple will release a software update to make it easier for medical researchers to understand the difference between a random movement, and the shakes and dyskinesia that Parkinson's patients experience when they're getting treated with medications. 
Apple made the announcement this week at its developer conference, WWDC.
The new "movement disorder API" will accelerate research that's already underway in how wearable devices can be used to track the progression of Parkinson's, said Peter Schmidt, a Parkinson's researcher and vice dean of the Brody School of Medicine at East Carolina University, who has been advising Apple's health team.
About 60,000 people are diagnosed every year with Parkinson's in the U.S. alone and an estimated 10 million people have the disease globally. Not all of these patients will have access to an Apple Watch, or be able to afford one, but Apple is starting to work with health insurance companies like Aetna in figuring out ways to subsidize the cost. 
Eventually, according to Schmidt, if the results are promising, it could change how Parkinson's patients are treated, as long as doctors understand how to interpret data from wearable devices. 

Helping patients figure out when their meds are wearing off

Schmidt said one particularly exciting use of the Apple Watch could be for patients to pinpoint precisely when their meds are wearing off throughout the day.
As Schmidt explained, patients will typically ramp up their meds as the disease gets worse. Many will take them three times a day with every meal. But the time between lunch and dinner can sometimes stretch on, making the symptoms more pronounced at around 5 o'clock.
"Many patients don't know it's happening and they think they're getting tired or hungry and symptoms are returning," he explained. For those patients, taking an earlier dose of meds before dinner can be a big relief. "That small change could help make a big difference with their symptoms."

Schmidt said the research community is also exploring other uses for wearable devices to help Parkinson's patients, such as whether it can help diagnose the disease earlier.

Apple launched its ResearchKit software in 2015 to open up opportunities for medical researchers to launch iPhone-based studies. Since then, some of the most compelling studies with the most promising results have been aimed at Parkinson's. 
Academics immediately saw an opportunity to study for the first time how patients functioned outside of the clinic, particularly on weekends and evenings. People with the disease carry their phones and other devices with them everywhere, but many only go to the doctor every three to six months. 
Apple's movement disorder software makes these studies easier, as the algorithms have been designed to report back data that is known to be correlated with a tremor, as opposed to the motion from being on a bicycle, for instance. "With ResearchKit, we saw a set of numbers that represent movement but now we'll see a set of numbers that represent Parkinson's," Schmidt explained. 
Apple isn't the only technology company that sees opportunities for its consumer hardware to help people with movement disorders. Verily, Alphabet's life sciences unit, has a product called Liftware that sells spoons and other utensils that are designed to stabilize tremors and shakes.
https://www.cnbc.com/2018/06/09/apple-watch-adds-tech-to-track-parkinsons-disease.html

Trio fighting Parkinson’s with golf tourney


Jun 8, 2018 



SOUTH BERWICK, Maine  Michelle Richards, 48, went through a lot of stress with family deaths and everyday life challenges. As she walked her child to Central School, years ago, her leg gave out on the way home.

I thought, ‘that is weird,’ but Ive always been kind of clumsy, and I got tall really quick when I was young,said Richards. Five years before that, I was a banker and loved it, but I had issues with my arm and we thought it was just from banking. It wasnt. She had Parkinsons disease at 41.

Ralph Hyson, an avid golfer, and Kittery letter carrier for more than 30 years, is 55 and found out last year that he had Parkinson’s. I had tremors in my right hand and I was dragging my right leg. My wife noticed some changes and said I should get it checked out. My dad had Parkinsons for 16 years, but we dont know if its hereditary; a very few percentage of people have Parkinsons thats hereditary,Hyson said.

Gary Parmley is 66 and doesnt have tremors, but he does have Parkinson’s disease. Since Parmley doesnt shake, people often think he doesnt have it.
Its embarrassing for me,said Parmley. “I have trouble finishing sentences and forget things. I was diagnosed three years ago. I had a real bad spell where I just stood in the kitchen one night and shook all over. I couldnt stop. They took me to the hospital and they thought I was having a stroke. 

No one thought I had Parkinsons. It kept happening to me and I was shaking at one time, but not much. I finally went to this other neurologist and he said I had it. The secret was he had me hold my hands up and he just barely touched me and I fell over backwards.
The three have more than a disease in common. They all live in South Berwick and are working together to put on a golf fundraiser to help people. The golf tournament called Putts Fore PD is a Team Fox event benefiting the Michael J. Fox Foundation for Parkinsons Research and is being held at the Links at Outlook Golf Course in South Berwick June 24.

Parkinson’s affects Richards, Hyson and Parmley differently, as it does with all people who have it. There is no cure, but there is aggressive research being done, especially with the help of the Fox Foundation. That organization gets support from Team Fox events such as Garys Putts Fore PD. Local grassroots community fundraisers all over the world, such as this one, raise money for research and possible treatments.

When the trio was asked whether they went through depression when diagnosed, they said depression and anxiety were big, but everyone deals with it differently.
Its a pride thing with all of us, I think,” said Richards.From what I know about New Englanders, you pull yourself up by your bootstraps and dont have a pity party. You just keep going.

Parmley had a real challenge after his diagnosis. They took my license away from me,he said. That about killed me. The only time I really have trouble right now is when I sleep. I dream and I act those dreams out. Just recently I had one and I was standing at the edge of the bed and I was getting ready to take a nose dive. We move pillows all around for when I jump out of bed.

It bothers me when people dont think I have the disease because I dont have the same symptoms as others. I walk 8 to 10 miles a day,said Parmley.
Thats so important to stay active,” Hyson said. “This whole Putts Fore PD is a metaphor. When you get diagnosed you are told to keep moving. Youre also told to not set yourself in a corner to be socially inactive because you need to keep your mind active. The disease can take your whole self worth away
Hyson said he had done golf fundraisers before for local youth groups and after his father died, he knew he wanted to do something.

The golf tournament of 144 players is sold out. We want to get this word out to keep people moving,said Hyson. “Wed like to see people with Parkinsons come down and have a class or something; get connected physically and socially. Eventually, Id like to see this thing grow nationwide and not be just a local effort
Parmley touched on the support he has had. “I dont really talk to people about this and dont know many people who have it, but I have a large family and they are right there for me. Ive gone off the deep end a few times and theyve been right there.

For information about Putts Fore PD, visit www.facebook.com/events/231471294287959. Want to Maine residents with Parkinson’s disease? Recycle through Maine Parkinsons Societys Clynk Program. For details, visit www.maineparkinsonsociety.org/clynk-bags/.

http://www.seacoastonline.com/news/20180608/trio-fighting-parkinsons-with-golf-tourney

Friday, June 8, 2018

Human midcingulate cortex sustains the execution of difficult or boring tasks, study finds

June 8, 2018, Ghent University



A breakthrough in brain research has promising implications for health and may lead to new answers about depression, attention-deficit hyperactivity disorder (ADHD) and Parkinson's disease. In a recent study, University of Victoria cognitive neuroscientist Clay Holroyd—with post-doctoral fellow José Ribas-Fernandes and Ph.D. student Danesh Shahnazian from UVic, and colleagues Tom Verguts and Massimo Silvetti from Ghent University—brings researchers one step closer to a better understanding of a mysterious area of the brain located deep in the cerebral cortex.

The function of the human midcingulate cortex (MCC) has remained elusive to researchers despite decades of investigation and debate. The MCC appears to help sustain the execution of difficult or more mundane tasks, such as doing homework or balancing a budget, and without it, people might choose to do something easier or more enjoyable. But isolating exactly what it does is difficult to identify since the MCC is activated by most events in most tasks.

"This question has been called a 'holy grail' because, despite 25 years of study, no one really knows what this critical area of the brain actually does," says Holroyd. "Our study illustrates a promising new way to understand what the MCC does, which is important because dysfunction of this brain area is implicated in a variety of neurocognitive disorders including Parkinson's disease, ADHD and depression."

The researchers used a computational model to predict the functions of the MCC while people performed a series of daily tasks on a computer, such as making tea or coffee, while their brains were scanned using neuroimaging. The results of an innovative data analysis technique showed that the MCC tracks the progression of a task during its execution, which is encoded as complex patterns of activity across the  area.

Holroyd infers that when the MCC is engaged, people stay on task and avoid temptation or distraction.

More information: Clay B. Holroyd et al. Human midcingulate cortex encodes distributed representations of task progress, Proceedings of the National Academy of Sciences (2018). DOI: 10.1073/pnas.1803650115


https://medicalxpress.com/news/2018-06-human-midcingulate-cortex-sustains-difficult.html

Virtual Brain Gives Insights Into Memory Deficits in Depression

June 8, 2018
Source: RUB.

Researchers have developed a new computational model of major depressive disorder. The model reveals older memories, as well as short term memories, are affected by major depressive disorder. Researchers say how long the memory deficits go back depends on how long the depressive episode lasts.

The computational model not only showed deficits in recalling current events, it also struggled with memories that were collected before the depressive episode. NeuroscienceNews.com image is in the public domain.


During a depressive episode the ability of the brain to form new brain cells is reduced. Scientists of the Ruhr-Universität Bochum examined how this affects the memory with a computational model. It was previously known that people in an acute depressive episode were less likely to remember current events. The computational model however suggests that older memories were affected as well. How long the memory deficits reach back depends on how long the depressive episode lasts. 

The team around the computational neuroscientist Prof Dr Sen Cheng published their findings in the journal PLOS ONE on 7th June 2018.

Computational model simulates a depressive brain
In major depressive disorder patients may suffer from such severe cognitive impairments that, in some cases, are called pseudodementia. Unlike in the classic form of dementia, in pseudodementia memory recovers when the depressive episode ends. To understand this process, the scientists from Bochum developed a computational model that captures the characteristic features of the brain of a patient with depressions. They tested the ability of the model to store and recall new memories.

As is the case in patients, the simulation alternated between depressive episodes and episodes without any symptoms. During a depressive episode, the brain forms fewer new neurons in the model.

Whereas in previous models, memories were represented as static patterns of neural activity, the model developed by Sen Cheng and his colleagues views memories as a sequence of neural activity patterns. “This allows us not only to store events in memory but also their temporal order,” says Sen Cheng.

Impact on brain stronger than thought
The computational model was able to recall memories more accurately, if the responsible brain region was able to form many new neurons, just like the scientists expected. However, if the brain region formed fewer new brain cells, it was harder to distinguish similar memories and to recall them separately.
The computational model not only showed deficits in recalling current events, it also struggled with memories that were collected before the depressive episode. The longer the depressive episode lasted the further the memory problems reached back.

„So far it was assumed that memory deficits only occur during a depressive episode,” says Sen Cheng. “If our model is right, major depressive disorder could have consequences that are more far reaching. Once remote memories have been damaged, they do not recover, even after the depression has subsided.”

About this neuroscience research article

Funding: Deutsche Forschungsgemeinschaft, Bundesministerium für Bildung und Forschung, Stiftung Mercator funded this study.
Source: Sen Cheng – RUB 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “The reduction of adult neurogenesis in depression impairs the retrieval of new as well as remote episodic memory” by Jing Fang, Selver Demic, and Sen Cheng in PLOS ONE. Published June 7 2018.

Cite This NeuroscienceNews.com Article

Abstract

The reduction of adult neurogenesis in depression impairs the retrieval of new as well as remote episodic memory
Major depressive disorder (MDD) is associated with an impairment of episodic memory, but the mechanisms underlying this deficit remain unclear. Animal models of MDD find impaired adult neurogenesis (AN) in the dentate gyrus (DG), and AN in DG has been suggested to play a critical role in reducing the interference between overlapping memories through pattern separation. Here, we study the effect of reduced AN in MDD on the accuracy of episodic memory using computational modeling. We focus on how memory is affected when periods with a normal rate of AN (asymptomatic states) alternate with periods with a low rate (depressive episodes), which has never been studied before.

Also, unlike previous models of adult neurogenesis, which consider memories as static patterns, we model episodic memory as sequences of neural activity patterns. In our model, AN adds additional random components to the memory patterns, which results in the decorrelation of similar patterns. Consistent with previous studies, higher rates of AN lead to higher memory accuracy in our model, which implies that memories stored in the depressive state are impaired. Intriguingly, our model makes the novel prediction that memories stored in an earlier asymptomatic state are also impaired by a later depressive episode.

This retrograde effect exacerbates with increased duration of the depressive episode. Finally, pattern separation at the sensory processing stage does not improve, but rather worsens, the accuracy of episodic memory retrieval, suggesting an explanation for why AN is found in brain areas serving memory rather than sensory function. In conclusion, while cognitive retrieval biases might contribute to episodic memory deficits in MDD, our model suggests a mechanistic explanation that affects all episodic memories, regardless of emotional relevance.

https://neurosciencenews.com/virtual-brain-depression-memory-9292/

First photoactive drug to fight Parkinson's disease

 June 8, 2018, University of Barcelona





An international team has designed the first potentially therapeutic photoactive drug, MRS7145, to fight Parkinson's disease, according to the new article in Journal of Controlled Release.

This compound, which proved effective in laboratory animals in vivo, has been carried out by a team led by Francisco Ciruela, from the Faculty of Medicine and Health Sciences of the University of Barcelona, and collaborators.

Optopharmacology: beyond the limits of conventional drugs
Parkinson's is the second most common neurodegenerative disease after Alzheimer's and it affects more than 1 percent of the population. This disease, which affects the central nervous system, affects more than six million people worldwide, figures that could go higher than twelve million by 2030, according to data from the World Health Organization (WHO). In this disease, the neurotransmitter that controls the motor activity, dopamine, is reduced due the progressive death of dopaminergic neurons.

The action of  is sometimes limited due several factors –lack of spatial specificity, slow and inaccurate distribution, etc.- which can reduce its therapeutic efficiency. Also, the efficiency of the traditional treatment on Parkinson's (levodopa) diminishes over time and it requires to increase the administration of the dose or to change the drug. The  of new drugs (uncontrolled movements in the body, motor fluctuations, etc.) are another common denominator in most patients.

Optopharmacology is an innovative discipline based on the use of light –with a certain wave length- to control the activity of drugs. Therefore, light-sensitive drugs can act with a higher spatial and time precision and without creating adverse effects in the body.

MRS7145: opening the way to treat neurodegenerative diseases
The MRS7145, the first potentially therapeutic photoactive drug to fight Parkinson's, is a photo-sensitive derivate from SCH442416, a selective antagonist of adenosine A2A receptor. In scientific bibliography, some A2A antagonist receptors came up as potential drugs to fight Parkinson's, since they take part in the involved mechanisms in controlling the movement.

This photoactive drug is an inactive chemical compound that gets activated with light from a visible spectrum (with a 405 nm wave length) which is not harmful for the body. A series of optical fibers –planted in the striated bodies of laboratory animals- provide the irradiation of this area in the brain, which is responsible for the control of motor activity.

Lecturer Francisco Ciruela says, "once the striated body is radiated with violet light the active drug is released and blocks the adenosine A2A receptor. The blocking of adenosine receptors has an administrating effect on the activity of dopamine (pro-dopaminergic action)."

Photo-sensitive molecules that improve patients' quality of life
Improving the spatial and temporary precision of the drug and strengthening the commitment of the patient to the therapy are some of the benefits of optopharmacology in Parkinson's. "A fine time-space precision will enable manipulating the neural circuits in detail and set the functioning of those with therapeutic and neuroprotective purposes," says Ciruela.

"Nowadays, in addition, there are treatments that are based on the implementation of electrodes in the brain of patients with Parkinson's to control the electric activity of neurons. In the same lines, optical fibers could make light getting to almost any part of the body (spatial resolution), and these organs would be radiated with light controlled by an electronic device that would regulate the intensity and length of radiation (time resolution).

Maintaining the commitment of patients to the set therapeutic guideline on the long run is a big challenge for chronic diseases. "With a slow release system from the photoactive drug, such as a coupled patch with a radiation system remotely controlled by a phone App, the doctor could control in a precise manner the release of the most efficient dose of the active drug in the place of action," says Ciruela.

Although the clinical application of this photoactive  in patients is still far, this pharmacological innovation could lead the way to a research on new therapeutical solutions for this chronic disease. The new article, published in Journal of Controlled Release, is therefore a step forward in the field of pharmacology to design new therapeutical strategies with photo-sensitive molecules and to set innovative clinical protocols to improve patients' quality of life.

More information: Jaume Taura et al. Remote control of movement disorders using a photoactive adenosine A 2A receptor antagonist, Journal of Controlled Release (2018). DOI: 10.1016/j.jconrel.2018.05.033

https://medicalxpress.com/news/2018-06-photoactive-drug-parkinson-disease.html

Scientists show that a key Parkinson's biomarker can be identified in the retina

 June 8, 2018, Asociacion RUVID



A study involving scientists from the University of Alicante and the United States notes that the accumulation of a protein known as alpha-synuclein in the retina is a key Parkinson's biomarker that could help detect the degree of severity of the disease.

The work has been published this month in Movement Disorders, a journal in the field of clinical neurology edited by the International Association of Parkinson's and Movement Disorders, and is part of a broader scientific project funded by the Michael J. Fox Foundation.
The main researcher of this project is Dr. Nicolás Cuenca at the University of Alicante at the University of Alicante. This worldwide study has been conducted with retinas from deceased Parkinson's patients donated to Sun Banner, a centre dedicated to the study of Parkinson's and Alzheimer's.
Cuenca and Ortuño Lizarán explain that they have studied in detail the alpha-synuclein protein as one of the main pathological marks that are usually analysed to determine Parkinson's , a neurodegenerative disease that affects seven and ten million people in the world.
Parkinson's patients present an accumulation of alpha-synuclein in the , a characteristic sign of this disease, which forms Lewy bodies, which proliferate as the disease progresses.
Cuenca and Ortuño Lizarán emphasise that the scientific relevance of their work is based on the fact that, for the first time, they have identified Lewy bodies in retinas of people with Parkinson's disease. This is the result of the study of the retinas sent by the Banner Sun Health Research Institute from deceased Parkinson's patients, whose clinical and pathological data of the brain are collected in this American institute.
Also, researchers have found a correlation—the greater the amount of alpha-synuclein in the retina, the more Parkinson's motor and clinical disturbances, and the more serious the condition.
The accumulation of this protein in the retina forming Lewy bodies is similar to that found in the brain in Parkinson's patients. "That is why we believe that alpha-synuclein is a helpful biomarker for Parkinson's; it can show the degree of severity of the disease and reflects, in some way, what is happening in the brain," Cuenca said.
Ortuño Lizarán stated that currently there is no technique applied in medicine to detect alpha-synuclein in the retina of a living person. The work reveals a second finding in that this protein not only appears in patients diagnosed with Parkinson's, but also in some who did not present the usual motor symptoms of tremors and slowness of movement, although their brains were already affected by this disease.
According to Ortuño, this indicates that  can also be an early biomarker, which could help detect Parkinson's before the clinical symptoms appear.
One aspect of this research work, which is not included in the study, is the death of dopaminergic cells found both in retina and brain.
Parkinson's disease is characterised by the degeneration of dopaminergic neurons, which release dopamine, a key neurotransmitter for motor function, and people who suffer from this disease often experience visual disturbances.
Both researchers emphasise that the  represents the ideal place to study Parkinson's, Alzheimer's and multiple sclerosis as it is an extension of the brain and part of the central nervous system.
More information: Isabel Ortuño-Lizarán et al. Phosphorylated α-synuclein in the retina is a biomarker of Parkinson's disease pathology severity, Movement Disorders (2018). DOI: 10.1002/mds.27392 
Provided by: Asociacion RUVID
https://medicalxpress.com/news/2018-06-scientists-key-parkinson-biomarker-retina.html

Thursday, June 7, 2018

Dying cancer patients get better hospice care than those with dementia or Parkinson's, finds study that also reveals the young receive more treatment

June 7, 2018  By Rosie Taylor


  • Dying patients said not get the best palliative care unless they have cancer
  • Patients with dementia and strokes receive half the care as those with cancer
  • Cancer patients referred 53 days before death, but 27 days if another disease
  • Other inequalities include the young getting more treatment than older patients


Dying patients do not get the best palliative care unless they have cancer, a study suggested


Cancer patients receive roughly twice the palliative care time that other incurable diseases receive, according to a new study.

Patients with progressive and incurable diseases like dementia, liver failure, Parkinson's and strokes typically spend around half as much time receiving end-of-life care in hospices than patients with cancer.

Leeds University researchers analysed information about 42,000 deaths in the UK in 2015 and found patients with cancer were typically referred to hospices 53 days before their deaths, compared to 27 days for other terminal patients.
Other inequalities in end-of-life care included younger people receiving more treatment than older patients, and southerners typically getting more care than northerners.

A February survey among NHS nurses found they felt the NHS was under too much pressure to provide the care that dying patients needed.
For instance, almost all nurses – 94 per cent – said they have witnessed a patient die in hospital who had made a request to die at home.

Patients not being referred for palliative care
Researchers found older patients aged over 75 tended to receive less palliative care, spending an average of 39 days at a hospice compared to 78 days for under 50s.

And there is a North-South divide in end-of-life care, with patients in the South and Midlands spending an average of 55 days in hospices compared to 35 days for patients in the North.

Previous trials have shown patients with terminal illnesses benefit most when they spend three to six months in a hospice before their death.
But patients can usually only be referred to hospices by GPs, hospitals, community nurse specialists or social workers.

Lead author, Dr Matthew Allsop, said: 'Palliative care is for any person diagnosed with a terminal illness, not just those with cancer. It aims to help patients and their families achieve the best quality of life through treating or managing physical symptoms, and helping with any psychological, social or spiritual needs.

'We know that people have a better quality of life if they are referred for palliative care early, but our findings suggest that this is not happening in a majority of cases. 

'A large number of patients are accessing palliative care in the last weeks of life.'
Co-author of the study, Dr Sarah Russell, of charity Hospice UK, said: 'Despite increasing evidence about the benefits of early referrals for hospice care, our research shows that many people who could benefit from inpatient and community hospice care are not being referred early in their illness.

'Palliative and hospice care is not just for people in the last days of life, it is there to provide support for anyone with life-limiting illnesses, and their families, to help them live well until they die.'

The authors of the study, published in the journal Palliative Medicine, suggested health professionals should consider making earlier referrals to hospices for people with dementia and other conditions.

Patients with diseases like dementia and Parkinson's get less treatment than those with cancer

NHS under too much pressure to perform 
A survey of NHS nurses taken in February found they felt that the NHS is under too much pressure to provide suitable care for dying patients.
Patients are being left stranded in hospitals rather than being allowed to die at home or in hospices, the survey claims.

Others are dying alone because staff are too stretched to spend time with them, the report found.
Almost all nurses – 94 per cent – say they have witnessed patients dying in hospital when they had expressed the desire to die at home, in a hospice or care home setting.

The survey of more than 600 nurses, conducted by Marie Curie and Nursing Standard journal, found most nursing staff believe it is now a 'common occurrence'.

One nurse said patients were dying in hospital because 'fast track services to get patients home where they want to die [are] not very fast'.
Carole Walford, chief clinical officer at Hospice UK said: 'Nurses continue to face huge barriers. Many hospices are already reaching out to hospitals to work together to improve end-of-life care in acute settings.' 

Following the worst flu season in seven years, nurses were also worried about the impact of this year's winter pressures on end-of-life care.
Almost eight in ten feel the winter crisis had a negative effect on the quality of care they are able to provide to dying patients. 

IS DYING PAINFUL? 

Many people fear death partly because of the perception they might suffer increasing pain and other awful symptoms the nearer it gets.
There is often the belief palliative care may not alleviate such pain, leaving many people to die excruciating deaths.
But an excruciating death is extremely rare.
The evidence about palliative care is that pain and other symptoms, such as fatigue, insomnia and breathing issues, actually improve as people move closer to death.
More than 85 percent of palliative care patients have no severe symptoms by the time they die.
Evidence from the Australian Palliative Care Outcomes Collaboration (PCOC) at the University of Wallongong shows that there has been a statistically significant improvement over the last decade in pain and other end-of-life symptoms.
Worldwide an estimated 40 million people are in need of palliative care, 78 percent of whom live in low and middle-income countries.
Only about 14 percent of people who need palliative care currently receive it.

http://www.dailymail.co.uk/health/article-5817013/Dying-patients-not-best-palliative-care-unless-cancer.html?ITO=1490&ns_mchannel=rss&ns_campaign=1490

New Biosensor May Shed Light on Molecular Processes Involved in Parkinson’s

 JUNE 7, 2018 BY ALICE MELÃO 





New sensors with increased sensitivity and specificity to detect interactions between proteins, fat molecules, and other biological elements, represent a powerful tool to investigate mechanisms linked to human diseases, such as Alzheimer’s or Parkinson’s.
The way biomolecules react and interact with each other is crucial to sustain normal cellular function, and to ensure all cellular mechanisms are properly working. This comprises mechanisms such as molecular signaling and transport in cells that require insertion of proteins with the cell lipid membrane.
Until now, available label-free techniques were not able to differentiate simple cellular processes such as protein insertion, chemical release and membrane disruption. As such, researchers had to rely on multiple experimental methods to analyze and understand the processes taking place within cells.
This not only made the experimental setting more complex, it also made it more difficult to integrate all data into single response models.
To overcome these challenges, a team led by researchers at Ecole Polytechnique Fédérale de Lausanne in Switzerland developed a new biosensor system.
The mid-infrared biosensor has the capacity to access the distinct chemical fingerprint information of proteins, lipids, or other biochemical compounds in complex biological samples while monitoring their dynamic interactions.
A major advantage of this new technology is that it allows scientists to preform complex analysis without destroying samples, in real-time, and with high sensitivity.
The team tested the potential of the biosensor to evaluate the molecular changes of cell membranes and tiny vesicles loaded neurotransmitter molecules (responsible for communication between brain nerve cells) upon exposure to melittin, the major toxic component of the honeybee venom.
The biosensor allowed researchers to monitor the disruptive mechanisms triggered by melittin in real-time and without requiring any additional process of molecule labeling.
The team could track the processes by which melittin induced membrane disruption and neurotransmitter cargo release from the vesicles.
“Our sensor opens up exciting possibilities for gaining new insights into biological processes such as signaling or transport in basic research as well as provides a valuable toolkit for bioanalytical and pharmaceutical applications,” researchers wrote.
These findings pave the way to apply this biosensor to several research fields, and investigate important mechanisms linked to human diseases, such as pore formation and membrane disruption induced by protein aggregates in neurodegenerative diseases.
https://parkinsonsnewstoday.com/2018/06/07/new-biosensor-targets-molecular-processes-involved-parkinsons/