Speech treatment for Parkinson’s comes to area

November 4, 2017  Alyx Arnett

Newly-implemented program through St. Vincent only one offered in area

Richard Szep exercises his voice alongside Courtney Wisher, M.S., CCC-SLP, during a speech therapy session.

When Richard Szep was diagnosed with Parkinson’s disease in 2006, he already had begun to notice one of the symptoms some patients experience: reduced voice loudness.

His once-loud voice now was meek, monotone, and people were having trouble hearing him, which was frustrating to the former Delco engineer. But this year, 11 years into his diagnosis, he found some relief.

Szep was the second patient to partake in St. Vincent Kokomo’s recently-implemented LSVT Loud therapy program, an evidence-based speech therapy treatment for individuals with Parkinson’s disease. Upon completion, the results left him smiling and his wife able to hear him from the other room at home.

“It helped me hear myself, and the fact of the matter is when we speak we speak quite low. It’s not that we want to; it’s just what happens,” said Szep, 77.

Four days a week for four weeks, Szep sat down with Courtney Wisher, M.S., CCC-SLP, at St. Vincent’s rehab facility and went through the intensive program that required him to do voice exercises into a microphone. The microphone was connected to a program that tracked his volume and how many seconds he could hold saying “ah.”

He went through various other exercises, including one called “functional phrases” that required Szep to give Wisher 10 sentences he said on a daily basis. One of them was, “Where are my glasses?” By practicing those phrases in a loud voice, Wisher said it would internally cue him to use his “loud voice” at home or in a social environment.

“The program is all about the patient self-calibrating their loudness and changing the way they perceive their loudness. To you and me, it’s like, ‘You’re not talking loud enough.’ But to a patient with Parkinson’s, it’s like, ‘I am talking loud.’ They’re not, so it’s re-cueing their internal monitor,” said Wisher.

The program is focused on a single goal: to speak loudly.

The program also required Szep to complete homework by practicing the exercises at home. Szep’s wife, Susan, said when she’d hear Szep saying “ah” in the other room, she would shout it back at him.

“He said it made it more fun to know someone was hearing him,” said Susan.

At the end of the program, data showed great improvement from Szep. When he started, his baseline measurement for loudness was 63.5 dB SPL (decibel sound pressure level), and he tracked 4.4 seconds for a sustained “ah.” At the end of the program, his dB SPL was 83.4, and he finished with 8.6 seconds for a sustained “ah.”

“A two-decibel loudness increase is huge, and he doubled his time,” said Wisher. “He did amazing.”

In addition to helping with loudness, the program also is said to be an effective treatment for problems such as diminished facial expression and impaired swallowing. With the program being new to the area, Wisher said she’s looking forward to helping other Parkinson’s patients improve their quality of life.

However, Wisher noted the program isn’t for all Parkinson’s patients. Studies indicate the therapy is most effective for those in the mid to moderate stages of Parkinson’s. She encouraged patients who are interested to come in for an initial voice evaluation.

Susan said there’s a noticeable difference in Szep’s audibility following the program. Szep also attends the Rock Steady boxing program at the YMCA, and Susan said it was heartwarming to be able to hear him over all of the other boxers last week in his session.

“I could hear him about all the others. It was really great,” she said. “I just love the way this program is coming to help physically, mentally, in so many different ways.”

For more information on LSVT Loud, call Wisher at 765-236-8500. For information on the local Parkinson’s support group, call Susan, who facilitates the group, at 765-438-3508.

http://kokomoperspective.com/kp/lifestyles/speech-treatment-for-parkinson-s-comes-to-area/article_93a8f704-be61-11e7-9ac3-6339ef659968.html

HERE’S WHAT WE THINK ALZHEIMER’S DOES TO THE BRAIN

NEUROSCIENCE NEWS   NOVEMBER 4, 2017

Summary: A new paper explores different findings about the development of Alzheimer’s and considers how personalized treatments may help combat this complex disease.

Source: The Conversation.

One of the difficulties of diagnosing Alzheimer’s is that we’ve no reliable and accurate way of measuring this protein build-up during the early stages of the disease. In fact, we can’t definitively diagnose Alzheimer’s until after the patient has died, by examining their actual brain tissue. NeuroscienceNews.com image is adapted from The Conversation article.

Around 50m people worldwide are thought to have Alzheimer’s disease. And with rapidly ageing populations in many countries, the number of sufferers is steadily rising.

We know that Alzheimer’s is caused by problems in the brain. Cells begin to lose their functions and eventually die, leading to memory loss, a decline in thinking abilities and even major personality changes. Specific regions of the brain also shrink, a process known as atrophy, causing a significant loss of brain volume. But what’s actually happening in the brain to cause this?

The main way the disease works is to disrupt communication between neurons, the specialised cells that process and transmit electrical and chemical signals between regions of the brain. This is what is responsible for the cell death in the brain – and we think its due to a build up of two types of protein, called amyloid and tau. The exact interaction between these two proteins is largely unknown, but amyloid accumulates into sticky clusters known as beta-amyloid “plaques”, while tau builds up inside dying cells as “neurofibrillary tangles”.

One of the difficulties of diagnosing Alzheimer’s is that we’ve no reliable and accurate way of measuring this protein build-up during the early stages of the disease. In fact, we can’t definitively diagnose Alzheimer’s until after the patient has died, by examining their actual brain tissue.

Another problem we have is that beta-amyloid plaques can also be found in the brains of healthy patients. This suggests the presence of the amyloid and tau proteins may not tell the whole story of the disease.

More recent research suggests chronic inflammation may play a role. Inflammation is part of the body’s defence system against disease and occurs when white blood cells release chemicals to protect the body from foreign substances. But, over a long enough period, it can also cause damage.

In the brain, tissue-damaging long-term inflammation can also be caused by a build-up of cells known as microglia. In a healthy brain, these cells engulf and destroy waste and toxins. But in Alzheimer’s patients, the microglia fail to clear away this debris, which can include toxic tau tangles or amyloid plaques. The body then activates more microglia to try to clear the waste but this in turn causes inflammation. Long-term or chronic inflammation is particularly damaging to brain cells and ultimately leads to brain cell death.

Scientists recently identified a gene called TREM2 that could be responsible for this problem. Normally TREM2 acts to guide microglia to clear beta-amyloid plaques from the brain, and to help fight inflammation within the brain. But researchers have found that the brains of patients whose TREM2 gene doesn’t work properly have a build-up of beta-amyloid plaques between neurons.

Many Alzheimer’s patients also experience problems with their heart and circulatory system. Beta-amyloid deposits in the brain arteries, atherosclerosis (hardening of the arteries), and mini-strokes may also be at play.

These “vascular” problems can reduce blood flow in the brain even more and break down the blood-brain barrier, a structure that is critical for removing toxic waste from the brain. This can also prevent the brain from absorbing as much glucose – some studies have suggested this may actually occur before the onset of toxic proteins associated within Alzheimer’s disease within the brain.

Personalised treatment

More recently, researchers have been looking deeper into the brain, specifically at the precise connections between neurons, known as synapses. A recent study published in Nature describes a process in the cells that may contribute to the breakdown of these synaptic communications between neurons. The findings indicate that this may happen when there isn’t enough of a specific synaptic protein (known as RBFOX1).

Thanks to this kind of research, there are now many new drugs in development and in clinical trials that could target one or more of the many brain-wide changes that occur with Alzheimer’s disease. Many researchers now believe that a more personalised approach to Alzheimer’s patients is the future.

This would involve a combination of drugs tailored to target several of the problems mentioned above, much like current treatments available for cancer. The hope is that this innovative research will challenge and pioneer a new way of treating this complex disease.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Anna Cranston – The Conversation

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image adapted from The Conversation article.

http://neurosciencenews.com/alzheimers-brain-7873/

Living with Parkinson's in Whanganui

November 3, 2017   By: Emma Russell

Community Educator Sue Tait has helped Kevin Speer continue doing what he loves. Photo/ Stuart 

As Kevin Speer zooms around Whanganui in his nifty golf cruiser it is hard to believe he suffers Parkinson's.

A condition he knew nothing about when he was diagnosed five years ago - but one he has learnt to live with thanks to Parkinson's Wanganui.

The 69-year-old still manages to play golf twice a week with his wife and uses specially designed walking poles to manage a lap around the block as often as he can.

But the movement disorder has dramatically impacted his lifestyle.

For Kevin it's his legs that have become the most stiff which makes it a challenge to mow the lawns, complete household chores for his wife and walk the golf course.

"But I haven't let it rule my life and getting out and about helps....so does my golf cruiser."

Kevin said he can get very lazy at times and it's easy to lose motivation but "I know it's good for me".

"Sometimes when I play golf I get tired in the sun and suddenly get very agitated and just need to be left alone...stress makes Parkinson's worse you see."

He said there needed to be more awareness about the condition because most people find out about it only after they or their loved one has been diagnosed.

"When I step on to the bus, nobody seems to have any idea that there is anything wrong with me."

Because Parkinson's affects the muscles, sufferers often don't show a lot of facial expressions and that can be difficult in social situations, Kevin said.

"They call it the mask of Parkinson's."

For the first week of November it's Parkinson's Awareness Week, aimed to educate the community and support those who are suffering.

The awareness week is being marked in Whanganui with a street appeal on Thursday, November 2 and Friday, November 3 from 10am till 4pm.

Collectors will be at Countdown at Trafalgar Square and Victoria Ave, New World on Victoria Ave and Mitre 10.

Parkinson's Wanganui community educator Sue Wilson said 2017 marked 200 years since Parkinson's was recognised as a medical condition.

"This awareness week we want to acknowledge 200 years of progress in understanding and treating Parkinson's but we also want people to know that 200 years is too long to wait for a cure."

There will also be a produce stall at the Rivercity Markets on Saturday and volunteers will be dressed in red.

Donations will be given to the local Parkinson's non-profit organisation to help the 70 people who suffer Parkinson's in Whanganui and their families.

What is Parkinson's?

A progressive neurodegenerative condition that affects the movement of the body. While it cannot be cured, it can be treated.

Who gets Parkinson's?

Around one in 500 New Zealanders have the condition. It is most common with older age groups - the average age being 59. People under 60 with Parkinson's are considered to have "early-onset Parkinson's".

What are the symptoms?

Symptoms for Parkinson's are characterised by both motor and non-motor.

Motor: Tremor, stiffness, slowness of movement.

Non-motor:
depression, fatigue, disturbance of normal sleep, lack
of sense of smell, constipation, trouble swallowing or speaking,
skin sensations and pain.

http://www.nzherald.co.nz/wanganui-chronicle/news/article.cfm?c_id=1503426&objectid=11939569&ref=rss

Scratching the surface of mature monocytes... and coming up with CXCR7

November 3, 2017

New research published online in the Journal of Leukocyte Biology showed for the first time that mature monocytes (a specific type of white blood cell) express the CXCR7 receptor on their surface. This receptor may be a therapeutic target for controlling inflammation in the brain associated with diseases like multiple sclerosis, Parkinson's and AIDS.

"Since mature monocytes appear to be the only white blood cells that primarily use CXCR7 to respond to the CXCL12 brain stimulus, we may have hit upon a novel method to block inflammation and HIV infection in the brain," said Mike Veenstra, a researcher involved in the work from the Departments of Pathology, and Microbiology and Immunology, at Albert Einstein College of Medicine in Bronx, New York. "We hope our findings spur further research and development of targets against the receptor so that novel treatment for NeuroAIDS and other diseases can become readily available."

To conduct the experiment, Berman and colleagues obtained cells from the peripheral blood of HIV-negative and HIV-infected individuals. Within these cells, the researchers examined the surface receptors CXCR4 and CXCR7 that were expressed on mature monocytes. They then performed blocking studies with pharmacological agents against each of the receptors using a tissue culture model of the human blood brain barrier to determine which of the surface receptors was used to enter the brain.

"Migration of blood monocytes to the brain can be involved in many diseases, including autoimmunity and spread of infections like HIV to the brain," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "These new findings might provide a novel approach to prevent these 'Trojan horses' in the cases of HIV from transporting their payload to the brain."

More information: Mike Veenstra et al. Frontline Science: CXCR7 mediates CD14 + CD16 + monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS, Journal of Leukocyte Biology (2017). DOI: 10.1189/jlb.3HI0517-167R 

Journal reference: Journal of Leukocyte Biology 

Provided by: Federation of American Societies for Experimental Biology

https://medicalxpress.com/news/2017-11-surface-mature-monocytes-cxcr7.html

Depression treatment needs overhaul

November 3, 2017 by Tess Redgrave

The way depression is diagnosed and treated needs a major overhaul, say authors of a new review article in the scientific journal Brain, Behavior, and Immunity.

This is because current treatment of depression is ineffective and lacks a plausible, coherent theoretical basis, they claim.

A new theory for depression and its treatment is proposed in the article "Depression subtyping based on evolutionary psychiatry: Proximate mechanisms and ultimate functions," authored by Markus J. Rantala, from University of Turku in Finland; Severi Luoto, from the University of Auckland in New Zealand; Indrikis Krams from the University of Tartu in Estonia and University of Latvia; and Hasse Karlsson from the University of Turku.

"We argue that depression is not a single disease; it is a heterogeneous syndrome, with patients differing remarkably in symptom profile, pathophysiology and treatment responsiveness," says Severi Luoto, a PhD candidate in evolutionary psychology at the University of Auckland

"The evidence that major depressive disorder is a group of separate syndromes comes from the observations that patients not only have many hundreds of unique symptom profiles, but many of the symptoms often have opposite features such as insomnia or hypersomnia, or an increase or decrease in appetite," he says.

The review article classifies depressive episodes into 12 subtypes based on evolutionary psychiatry. Using an evolutionary lens, the authors have observed patterns in the existing literature that haven't been previously identified. 

"With the help of the 12 depression subtypes, it will be easier to find more effective treatments for depression," says Adjunct Professor Rantala, a member of the Turku Brain and Mind Center in Finland. "This is because the focus will be on treating the underlying reasons (triggers) of depression instead of merely focusing on the symptoms, which is how traditional psychiatry treats depression.

"We argue that the occurrence of symptoms (or patterns of symptoms) depends on the subtype of the depressive episode. The particular manifestation of depressive symptoms may have more to do with what triggered the depression (i.e. the proximate mechanisms) than the personality of the patient."

The 12 subtypes are induced by:

1. infection, in which sickness behaviour to combat pathogens and parasites may lead to symptoms such as loss of appetite, sleep disturbances, anhedonia, impaired concentration;
2. long-term stress which is known to activate the immune system, causing an increase in proinflammatory cytokine levels that influence mood;
3. loneliness;
4. traumatic experience;
5. hierarchy conflict where events such as unemployment, exclusion from a social group, bullying at school or professional hierarchy conflicts may trigger a depressive episode;
6. grief;
7. romantic rejection;
8. postpartum events which lead to depression in 10-15% of women;
9. the season, where Seasonal Affective Disorder (SAD) affects the individual at the same time each year;
10. chemicals such as alcohol and cocaine;
11. somatic diseases such as Alzheimer's, Parkinson's, migraine, epilepsy, stroke and traumatic brain injury; and
12. starvation which is known to reduce mood and, when prolonged, can lead to apathy and social withdrawal.

Using these 12 subtypes, the authors go on to ask: How does a certain depressive state benefit the organism – what "ultimate function" does it have? For example, starvation-induced depression can be an adaption to save energy in order to increase the odds of surviving through a famine.

But not all proximate mechanisms that trigger depression end up producing adaptive responses.

For example short-term low mood is an adaptation to adverse life events in the majority of cases. However, Rantala and Luoto argue that an adaptive state of low mood may turn into pathological clinical depression when the patient's symptoms do not serve the purpose that natural selection has shaped them to serve.

"Chronic clinical depression is what we could call an evolutionary novelty that arises from a mismatch between our current environment and our ancestral environment," says Luoto.

He adds that major depressive disorder constitutes one of the leading causes of disability worldwide: "Modern lifestyles – including a sedentary lifestyle with a diet high in energy and low in micronutrients – increase susceptibility to inflammatory dysregulation and chronic stress. These in turn increase the amount of proinflammatory cytokines in peripheral blood, leading to low mood and sickness behaviours characteristic of depression.

"If a depressive episode appears to be a response to an adverse life event, clinicians should evaluate whether the symptoms are adaptive or whether the depression episode has exacerbated into pathological depression," says Rantala.

"Some depressive responses to adverse life circumstances can be beneficial to the patient," adds Luoto. "So understanding the psychological and physiological underpinnings of depression is important and might remove some of the stigma around it. 

"Future depression treatments should employ an analysis of symptom patterns together with an in-depth interview and a blood test to reveal inflammation and stress hormone levels."

The review article further argues that subtyping depression episodes based on the original triggers of the mood change will help to find the best customised interventions for each patient. For example, in the case of depression induced by chronic stress, "interventions should seek to reduce stress levels either by using cognitive psychotherapy, exercise or medication that alleviates stress. Depression induced by loneliness in which stress hormone levels are elevated should focus on reducing loneliness, thus alleviating the stress."

"The focus of a treatment regime based on evolutionary psychiatry focuses on an individual's long-term mental and physical well-being instead of myopically fixating on the short-term alleviation of symptoms," say the authors.

They conclude by stating their hope that "the present subtyping based on an evolutionary and immunological approach to depression will prove its practical utility on a vast scale, helping to develop more effective therapeutic treatments and drugs that are targeted to the specific subtypes of depression."

More information: Markus J. Rantala et al. Depression subtyping based on evolutionary psychiatry: Proximate mechanisms and ultimate functions, Brain, Behavior, and Immunity (2017). DOI: 10.1016/j.bbi.2017.10.012 

Journal reference: Brain, Behavior, and Immunity

Provided by: University of Auckland 

https://medicalxpress.com/news/2017-11-depression-treatment-overhaul.html

Researchers obtain chemical data from cerebral fluid to treat neurodegenerative diseases

 November 3, 2017 by Clara Marc

Perfusion microdroplet allowing the extraction of interstitial liquid using the system developed by EPFL researchers. Credit: Guillaume Petit-Pierre

Researchers at EPFL have developed a new device and analysis method that let doctors measure the neurochemicals in a patient's brain. The Microsystems Laboratory 4 (LMIS4)'s system involves collecting microdroplets of cerebral fluid and analyzing them to obtain chemical data that can help doctors diagnose and treat neurodegenerative diseases.

Neurologists often use electrical impulses to stimulate and read brain signals. But the chemicals that neurons produce in response to these impulses are poorly understand at this point, even though they can provide valuable information for understanding the mechanisms behind neurodegenerative diseases like Alzheimer's and Parkinson's. 

"Neurons can be read two ways: electrically or chemically," says Guillaume Petit-Pierre, a post-doc researcher at LMIS4 and one of the study's authors. "Reading their electrical behavior can provide some limited information, such as the frequency and pace at which neurons communicate. However, reading their neurochemistry gives insight into the proteins, ions and neurotransmitters in a patient's cerebral fluid." By analyzing this fluid, doctors can obtain additional information – beyond that provided by neurons – and get a complete picture of a patient's brain tissue metabolism.

Collecting information through microchannels

The EPFL researchers developed a system that can both collect a patient's neurochemical feedback and form electrical connections with brain tissue. Their device is made up of electrodes and microchannels that are about half a hair in diameter. Once the device is placed inside brain tissue, the microchannels draw in cerebral fluid while the electrodes, which are located right at the fluid-collection interface, make sure that the measurements are taken at very precise locations. 

The microchannels subsequently create highly concentrated microdroplets of cerebral fluid. "The microdroplets form directly at the tip of the device, giving us a very high temporal resolution, which is essential if we want to accurately analyze the data," says Petit-Pierre. The microdroplets are then placed on an analytical instrument that was also developed by scientists at the LMIS4 and the nearby University Centre of Legal Medicine which has expertise in this type of complex analysis. As a last step, the microdroplets are vaporized with a laser and the gas residue is analyzed. Both the researchers' device and their analysis method are totally new. 

"Today there is only one method for performing neurochemical analyses: microdialysis. But it isn't very effective in terms of either speed or resolution," says Petit-Pierre. Another advantage of the researchers' method is that it is a minimally invasive way to collect data. Currently scientists have to work directly on the brains of rats afflicted with neurodegenerative diseases, meaning the rats must be sacrificed to take the measurements. Their research was published in Nature Communications.

The neural probe enables the direct collection of neurochemicals from the brain. Credit: G. Petit-Pierre

For this study, the researchers focused primarily on the calcium, sodium, potassium and other ions in cerebral fluid. They worked with EPFL's Neurodegenerative Disease Laboratory to compare the measurements they took on rats with those reported in the literature – and found that the results were well correlated. The next step will be to develop a method for analyzing the proteins and neurotransmitters in cerebral fluid, so that their implications in neurodegenerative diseases can be further studied. 

"Doctors could measure neurochemical responses to help them make diagnoses, such as for epilepsy, when they use electricity to measure signals from a patient's cortex," says Guillaume, "or to improve the efficiency of treatments like deep brain stimulation (DBS) for Parkinson's disease." Their research could also soon find direct applications in other medical fields. Guillaume currently works on a start-up project to develop a catheter for patients affected by hemorrhagic stroke. Based on a similar technology, his catheter would let doctors treat a common yet serious complication of this condition and thereby reduce the risk of death.

The neural probe enables the direct collection of neurochemicals from the brain. Credit: G. Petit-Pierre

More information: Guillaume Petit-Pierre et al. In vivo neurochemical measurements in cerebral tissues using a droplet-based monitoring system, Nature Communications (2017). DOI: 10.1038/s41467-017-01419-1 

Journal reference: Nature Communications

Provided by: Ecole Polytechnique Federale de Lausanne 

https://medicalxpress.com/news/2017-11-chemical-cerebral-fluid-neurodegenerative-diseases.html

After 18 months of study, VA delays adding new Agent Orange illnesses

By TOM PHILPOTT | SPECIAL TO STARS AND STRIPES Published: November 2, 2017

A U.S. Huey helicopter sprays Agent Orange over Vietnam.U.S.  ARMY

After 18 months of review by his department, Department of Veterans Affairs Secretary David J. Shulkin awkwardly announced Wednesday that he plans to “further explore” adding ailments to the list of compensable conditions VA presumes were caused by exposure to Agent Orange and other herbicides used during the Vietnam War.

The decision to punt long-anticipated decisions on Agent Orange-related ailments will disappoint thousands of aging veterans with bladder cancer, hypothyroidism, Parkinson-like tremors and hypertension (high blood pressure). Veterans and survivors were hopeful some or all of those conditions would be added to VA’s presumptive list of ailments linked to wartime herbicides, based on the latest and final review of medical and scientific literature on Agent Orange from the National Academy of Medicine (formerly known as the Institute of Medicine).

Instead, on the Nov. 1 deadline date that VA itself had set for this packet of decisions, Shulkin issued a brief statement at 6 p.m. promising only more delay.

“After thoroughly reviewing the National Academy of Medicine(NAM)’s latest report regarding veterans and Agent Orange, and associated data and recommendations from [VA’s] NAM Task Force, I have made a decision to further explore new presumptive conditions for service connection that may ultimately qualify for disability compensation. I appreciate NAM’s work and the commitment and expertise of [my] Task Force, and look forward to working with the [Trump] administration on the next steps in the process.

A last sentence, not attributed to Shulkin, explained that the VA “will begin work with the administration to concurrently conduct a legal and regulatory review of these potential presumptive conditions for awarding disability compensation to eligible veterans.”

In the past, VA began a regulatory review only after the secretary approved new ailments for the list. Shulkin hasn’t named any new illnesses. In conceding that VA experts already had “thoroughly” reviewed the latest science, however, Shulkin seemed to signal that parties elsewhere in the Trump administration didn’t want a VA announcement at this time rejecting or embracing new conditions.

“We thought we were going to get a decision sometime today,” said Rick Weidman, executive director for policy and government affairs for Vietnam Veterans of America. “Obviously we were mistaken. What they issued, to quote [White House press secretary] Sarah Huckabee Sanders, is a Nothing Burger.”

“I am shocked and dismayed if this is the VA Secretary’s decision, to continue to delay,” emailed Carla Dean, who lost her husband, a Vietnam veteran, to bladder cancer last year. Now president of the Bladder Cancer Foundation of Florida, Dean said she remained hopeful that Shulkin will do the “right thing soon.”

One Vietnam veteran from Wisconsin who has fought bladder cancer since 2006 expressed “complete disappointment” with Shulkin’s statement. Asking that his name be withheld, he said he served at a “heavily sprayed” combat base in Quang Tri province. Lifelong residual effects of bladder cancer surgery, he said, include incontinence, impotence, severe weight loss and fatigue. He twice has been denied VA disability compensation because his cancer is not on the “presumptive” list.

“I have talked to many other vets and the general feeling is that if the VA delays long enough, there won’t be any veterans left to worry about compensating for Agent Orange, because we will all have passed,” he said.

A spokesman for Rep. Phil Roe, R-Tenn., chairman of the House Veterans’ Affairs Committee, said he is reviewing VA’s announcement. But Roe “believes veterans waiting for a final decision deserve certainty, and [he] hopes Secretary Shulkin will work quickly to finish the legal and regulatory reviews.”

Dr. Kenneth S. Ramos, associate vice president for Precision Health Sciences and a professor of medicine at the University of Arizona, chaired the committee of medical experts that produced the NAM report that Shulkin has deferred acting on. Ramos said his “gut reaction” to the statement “is that it’s positive. It’s very encouraging that the recommendations brought forth by the committee were thoroughly evaluated and are being considered for re-evaluation by the department.” Ramos added, “The tone suggests receptivity to the seed that the National Academy has provided … When you look at past experience, any change in compensation policies seems to take time moving through the system.”

NAM delivered its report, Veterans and Agent Orange: Update 2014, to VA in March 2016, after reviewing medical and scientific literature published from Oct. 1, 2012, through Sept. 30, 2014. NAM found evidence to support changing the strength of association between herbicide exposure and several ailments.

For bladder cancer and hypothyroidism, it found “limited or suggestive” evidence of an association to herbicide exposure, an upgrade from “inadequate or insufficient” evidence found earlier. For some ailments, including Parkinson’s and ischemic heart disease, limited or suggestive evidence has been judged strong enough to add the illnesses to the presumptive list. For other diseases, including hypertension, which is common in an aging population, it hasn’t been enough.

The NAM review also looked again at cardiovascular conditions and herbicide exposure. It didn’t upgrade the link to heart ailments but it did affirm limited or suggestive evidence that hypertension is linked to herbicide exposure.

It also studied whether conditions with Parkinson’s-like symptoms should fall into the same limited or suggestive category as Parkinson’s disease itself. NAM found “no rational basis” for excluding Parkinson-like symptoms from the same risk category. Parkinson’s disease was added to VA’s presumptive list in 2010.

Under a law Congress let expire in 2015, the VA secretary had 180 days to consider a NAM report before deciding whether to expand the list of presumptive diseases to trigger automatic eligibility for disability compensation. Shulkin is under no such deadline. But a VA study group, followed by a VA task force, reviewed the NAM report. At one point a senior VA official predicted that by July 2016 then-VA Secretary Bob McDonald would have what he needed to decide on new presumptive ailments. Yet a year passed and McDonald opted to leave those decisions for the Trump administration. Shulkin had been McDonald’s top health official during the NAM review period.

By late summer this year, Shulkin promised a decision on new ailments to the presumptive list by Nov. 1. Weidman said he suspects the White House’s Office of Management and Budget blocked any plan to add new ailments to the list.

Weidman said members of Vietnam Veterans of America “are going to be really angry” with more delay, because “there is probably enough evidence now for the secretary to declare other ailments” as tied to Agent Orange exposure, “glioblastoma first among them.” And sailors and Marines who served aboard ship off Vietnam, the Blue Water Veterans, should have been deemed eligible like ground forces for compensation for presumptive ailments long ago, Weidman said.

“The ball is now in [President Donald] Trump’s court,” he added. “It’s not something now that [former President Barack] Obama did or did not do.”

Send comments to Military Update, P.O. Box 231111, Centreville, VA, 20120; email milupdate@aol.com; Twitter: @Military_Update.

https://www.stripes.com/after-18-months-of-study-va-delays-adding-new-agent-orange-illnesses-1.495773

New Version of CRISPR Edits RNA to Correct Mutations Without Impacting Genome

 NOVEMBER 2, 2017   BY IQRA MUMAL IN NEWS.

MIT researchers have developed REPAIR, a new version of the CRISPR/Cas9 gene editing system that can edit RNA instead of DNA — so as not to alter a person’s genome — and may one day be used to treat Parkinson’s and a variety of other diseases.

The findings are published in the study, “RNA editing with CRISPR-Cas13,” in the journal Science.

The classic CRISPR/Cas9 system involves a guide RNA (gRNA) and a protein called the Cas9 nuclease. The gRNA guides the Cas9 nuclease to a precise location in the genome, where Cas9 can cause a double stranded break. This prompts the cell’s repair machinery to fix the break, leading to mutations in the gene so as to cause it to not be expressed.

Researchers at MIT engineered a new system for mammalian gene editing, which targets the RNA sequence instead of the DNA sequence. DNA codes for RNA molecules, which then code for proteins. In this way, targeting  RNA can still change the gene product (a protein), but without making a change in the entire genome.

REPAIR — the RNA Editing for Programmable A to I Replacement — can change a single RNA nucleotide, potentially reversing some of the disease-causing mutations at the RNA level.

“The ability to correct disease-causing mutations is one of the primary goals of genome editing,” Dr. Feng Zhang, the study’s senior author and an associate professor in Brain and Cognitive Sciences and Biological Engineering departments at MIT, said in a press release. “So far, we’ve gotten very good at inactivating genes, but actually recovering lost protein function is much more challenging.

“This new ability to edit RNA opens up more potential opportunities to recover that function and treat many diseases, in almost any kind of cell.”

Much like DNA, RNA is made up of a sequence of letters, or nucleosides. In many human diseases, including Parkinson’s, there is often a mutation from the nucleoside G to A, and this single nucleoside change can lead to disease symptoms. REPAIR has the ability to recognize a specific A, and turn into a nucleoside called I (inosine). The I is read by cellular machinery as a G, which essentially turns back the A mutation to a G correction.

Unlike the Cas9 protein, the Cas13 enzyme targets and cuts RNA. Dr. Zhang’s research group discovered a Cas13 enzyme from the bacterial species Prevotella, called PspCas13b, which was found to be very effective at targeting RNA.

They inactivated the cleavage activity of Cas13, so it would no longer cause a double-stranded break. Instead, they fused Cas13 to a protein called ADAR2, which changes the letter A to the letter I. This leads to a simple mechanism where Cas13 seeks out the target sequence of RNA, and ADAR2 makes the conversion from A to I, leading to the formation of the correct protein.

To further improve the REPAIR system’s efficiency, the researchers also created an upgraded version, called REPAIRv2, which succeeded at the targeted edit up to 51% of the time.

To demonstrate that REPAIR can work in a disease context, researchers treated human cells with single nucleoside mutations that cause Fanconi anemia and X-linked nephrogenic diabetes insipidus. Work showed that REPAIRv2 successfully edited the mutation at the RNA level.

“The success we had engineering this system is encouraging, and there are clear signs REPAIRv2 can be evolved even further for more robust activity while still maintaining specificity,” said Omar Abudayyeh, co-first author and a graduate student in Zhang’s lab.

The team  plans to continue to improve REPAIRv2 by manipulating the delivery system to improve its effectiveness when introduced into human cells.

https://parkinsonsnewstoday.com/2017/11/02/potential-parkinsons-treatment-seen-in-repair-rna-targerting-version-of-crispr-gene-editing-system/

NHS Greater Glasgow and Clyde launch Parkinson's drug alert tool to 'cut hospital stays'

November 2, 2017   Helen McArdle,  Health Correspondent

Dr Anne Louise Cunnington, Parkinson's specialist at Glasgow Royal Infirmary (Photo by Kirsty Anderson / Herald & Times)

A HOSPITAL warning system designed to prevent Parkinson's patients from skipping vital medication if they are admitted for unrelated emergencies such as heart attacks or falls has been rolled out in Scotland's largest health board.

The Parkinson's specialist who helped create the "dashboard" alert tool believes it will reduce the length of time patients spend in hospital and, if successful, offers a blueprint which could be rolled-out across NHS Scotland.

Under the system, any patients with Parkinson's from the Greater Glasgowand Clyde area are automatically flagged on the health board's 'Track' computer system with a yellow hazard triangle. When a hospital consultant or nurse sees the symbol, they can click on it for contact details for the patient's Parkinson's team. Meanwhile, Parkinson's consultants and nurse specialists across the region will also get an automatic alert on their work computer if any of their patients are admitted to a hospital in the Greater Glasgow and Clyde region, ensuring that they can contact the ward to check that the Parkinson's medication is being administered as required.

Dr Anne Louise Cunnington, who is based at Glasgow Royal Infirmary, worked with the health board's IT experts to design the system after a UK-wide Parkinson’s Audit of patients highlighted concerns over how quickly they were being given their medication on admission to hospital for unrelated conditions. Missing just a few doses of their regular drugs can have a very serious impact symptoms, such as tremors, speech and mobility.

Dr Cunnington said: “Patients with Parkinson’s, like any other patients, can be admitted to hospital for any number of reasons, such as a heart attack or serious infection, not necessarily because of their Parkinson’s. This means the focus of their treatment would be on the primary reason for their admission.

"If you look at patients' feedback they often are dissatisfied with the care they receive in hospital and it's often to do with medication. I suspect it's because staff are not necessarily familiar with Parkinson's and its complications, the drugs management, and maybe they don't always remember that for the vast majority of people with Parkinson's, medication is the only way of controlling their symptoms and that medication must be administered at fixed times every day."

Around one in 500 people in Scotland have Parkinson's disease. In a UK-wide audit of patients, half said they did not always get their medication on time while in hospital and 39 per cent said this led to a deterioration in their condition.

Analysis of hospital admissions among over-65s between 2009 and 2013 in England also indicated that those with Parkinson's averaged a longer length of stay than those without it.

Dr Cunnington said: "You can't necessarily put that down to not getting their meds, but we do know that they are twice as likely to have an unscheduled admission and cost the NHS three and a half time more and spend 73 per cent longer in hospital than the age-matched control group.

"What we want to see whether this dashboard does reduce length of stay."

The new system launched in mid-September and Dr Cunnington believes it is already making a difference.

She said: “It is very simple, but very effective. The dashboard has also helped raise awareness amongst staff and has brought this issue to the forefront of their mind.

“Not only does this improve things for the patients themselves, but it also saves money for the NHS as it’s proven that given the right medication, hospital stays will be shorter and beds will be freed up for other patients. It really is a win, win situation.”

http://www.heraldscotland.com/news/15633099.Parkinson__39_s_drug_alert_tool_launched_in_Glasgow___39_can_cut_hospital_stays__39_/