I Ask This Of You!

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.

I am not responsible for it's contents. I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish.

This is for you to read and to always keep an open mind.

Please discuss this with your doctor, should you have any questions, or concerns.

Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

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Saturday, August 22, 2015

Daughter honors former West Point chaplain father with weekly races after Parkinson's diagnosis

Reverend Richard P. Camp and daughter Kathy

Every weekend Kathy Camp laces up her sneakers, lines up at the start line and hits the pavement, competing in road races in honor of her athlete father who no longer can. Parkinson’s disease has stolen his physical gifts; Richard Camp was a life-long athlete who won running medals well into his 70s. Now, he struggles to get out of a chair.
“Seeing both his inability to be the person I knew him to be… and seeing how his athletic prowess have given him a really phenomenal long life and wanting that for myself… the combo of that created the path that I’m on now,” Kathy, 37, of Laurel, Maryland, told
For the first 18 years of her life, Kathy was raised at the United States Military Academy at West Point, where her father, Reverend Richard P. Camp, now 79, served as chaplain from 1973 to 1996.
In high school, Richard was a multiple-letter athlete and was recruited by Vince Lombardi to play football at West Point. He turned them down to attend Wheaton College in Illinois, where, his senior year, he was invited to camp for the Chicago Bears. Instead, he got his Master of Divinity degree from Gordon Conwell Theological Seminary in South Hamilton, Massachusetts.
At West Point, Richard played pick-up football with cadets and even coached at the end of the Vietnam War when staffing was slim.
In his 60s, he started running competitively in the USA Track & Field races. In his 70s, he was invited to run The Penn Relays, the first and oldest relay meets, started in 1985. He won the 100-meter in his age division and medaled several years in a row.
“His 23 years at West Point kept him going in his 40s, 50s, 60s… when you’re leading cadets to build their emotional, physical and spiritual muscles,” Kathy, a mother-of-one married to a Marine Corps officer, said. “Being a lifelong athlete helped him with Parkinson’s to stay off heavy drugs because his body is so naturally well-tuned.”
Richard was 72 when he was diagnosed and about two years ago, his symptoms worsened. In February, he underwent deep brain stimulation, a procedure that blocks electrical signals from targeted areas in the brain. According to the National Parkinson Foundation, it is only used for patients whose symptoms cannot be adequately controlled with medication.
Getting her act together
The turning point for Kathy, who had been an overweight, un-athletic child, came over the Christmas holidays in 2014, when Richard suffered a few falls.

“I need to get my act together,” she recalled thinking at the time.
Kathy’s first race was the Army Ten-Miler in Washington, DC, in October 2014. The event, with more than 30,000 runners, is a kind of rallying point for the military community and includes many wounded veterans, she said.
After the race she posted a photo on social media, detailing how she was running for her dad because he couldn’t. The outpouring of support and donations to the Parkinson’s Foundation in response to her photo inspired her to decide to run a race every weekend for a year.
Kathy participates in road races across the country, even looking for local races when she’s traveling for her work as a partner at a boutique public relations firms in DC that primarily consults with military men and women who want to transition to public office.  She mainly does 5Ks, but will do 10Ks and half marathons occasionally.
When asked how her father feels about her ambitious race plan, Kathy said it serves as a reminder that they’re in this together.
“I think, first of all, he’s so excited that his awkward, chubby daughter is finally getting in shape,” she said. “He knows when I post that photo, I carried him through that run.”
Finding the spiritual muscles
Kathy has chosen not to take any donations or fundraise for her races to ensure the focus isn’t on her, but on Parkinson’s and the military community.

“There are vets all across the country who don’t have resources,” she said. “Our Veterans Affairs system is terribly damaged and with my father and Parkinson’s disease, I want somebody to think about, when making donations, to keep thinking about that.”
For most of her races Kathy wears her West Point Fellowship of Christian Athletes (FCA) shirt, which garners attention from graduates and parents alike. She’s made it her goal to encourage a fellow runner in each race.
“Running is really a metaphor for life,” she said. “We need to dig down to find that spiritual well and that resource within ourselves to finish a race, sometimes having someone come alongside you and be that someone makes a difference.”
Her father and the cadets at West Point taught Kathy about spiritual muscles needed to get through a race— and life.
“Watching troops get decimated and they’re using that spiritual muscle they learned at West Point… it’s not about how strong you are, but what you have in that tank,” she said. “On some of those long runs I have to use what’s in that spiritual tank to get through.”
Every day for Richard is a challenge, but his wife of 58 years, Virjean, has kept him going. According to Kathy, many former cadets have reached out to offer their experience and support for his emotional health, as depression is a big hurdle with Parkinson’s.
“My father made his life supporting these men and women and there they are, turning around supporting him,” she said. “That’s how you know you made the right choices in life and it comes back to you like that.”

Premier Biomedical, Inc. Files Patent Application on Cockayne Syndrome Treatment

Which Could Potentially Lead to Major Breakthroughs Against Parkinson's Disease, Alzheimer's Disease and Aging

Cockayne Syndrome (CS) is a rare and devastating neurodegenerative disorder characterized by slow growth, premature aging (progeria), shortened lifespan, moderately to severely inhibited neurological development, hearing loss, eye abnormalities/blindness, and sensitivity to sunlight. Cockayne Syndrome is caused by an inherited gene mutation.
Mitchell S. Felder, M.D., the Chairman of Premier’s Scientific Advisory Board, and a board certified attending neurologist, stated, "The physiologic basis of Cockayne Syndrome is a dysfunction in autophagy, the intracellular "cleanup crew". Recent medical articles have shown autophagy to be a major cause of Parkinson's Disease, Alzheimer's Disease and aging. I deeply believe that by beating Cockayne Syndrome we will also make major therapeutic breakthroughs against Parkinson's Disease, Alzheimer's Disease, and even aging. This patent application will serve as a detailed and specific roadmap for achieving those major breakthroughs."
About Premier Biomedical, Inc.
Premier Biomedical, Inc. is a research-based company that intends to discover and develop medical treatments for a wide range of diseases in humans. Premier has licensed the technology behind multiple patents/patent applications in the United States and Europe in the areas of Cancer, Sepsis, and Multiple Sclerosis. Founded in 2010, Premier has partnered with the Department of Defense with Center of Expertise at the William Beaumont Army Medical Center and the University of Texas at El Paso (UTEP). The company's R&D efforts are centered in El Paso, TX and their business offices are in Western Pennsylvania. The Company's common stock trades on the fully reporting Over-The-Counter Bulletin Board under the ticker symbol "BIEI."

Safe Harbor Notice
Certain statements contained herein are “forward-looking statements” (as defined in the Private Securities Litigation Reform Act of 1995). Premier Biomedical, Inc. cautions that statements, and assumptions made in this news release constitute forward-looking statements and makes no guarantee of future performance. Forward-looking statements are based on estimates and opinions of management at the time statements are made. These statements may address issues that involve significant risks, uncertainties, estimates made by management. Actual results could differ materially from current projections or implied results. Premier Biomedical, Inc. undertakes no obligation to revise these statements following the date of this news release.

Friday, August 21, 2015

Two proteins work together to help cells eliminate trash and Parkinson's may result when they don't

Friday 21 August 2015
Two proteins that share the ability to help cells deal with their trash appear to need each other to do their jobs and when they don't connect, it appears to contribute to development of Parkinson's disease, scientists report.
Much like a community's network for garbage handling, cells also have garbage sites called lysosomes, where proteins, which are functioning badly because of age or other reasons, go for degradation and potential recycling, said Dr. Wen-Cheng Xiong, developmental neurobiologist and Weiss Research Professor at the Medical College of Georgia at Georgia Regents University.
Inside lysosomes, other proteins, called proteases, help cut up proteins that can no longer do their job and enable salvaging of things like precious amino acids. It's a normal cell degradation process called autophagy that actually helps cells survive and is particularly important in cells such as neurons, which regenerate extremely slowly, said Xiong, corresponding author of the study in The Journal of Neuroscience
Key to the process - and as scientists have shown, to each other - are two more proteins, VPS35 and Lamp2a. VPS35 is essential for retrieving membrane proteins vital to cell function. Levels naturally decrease with age, and mutations in the VPS35 gene have been found in patients with a rare form of Parkinson's. VPS35 also is a critical part of a protein complex called a retromer, which has a major role in recycling inside cells. Lamp2a enables unfit proteins to be chewed up and degraded inside lysosomes.
If the two sound like a natural couple, scientists now have more evidence that they are. They have shown that without VPS35 to retrieve Lamp2a from the trash site for reuse, Lamp2a, or lysosomal-associated membrane protein 2, will be degraded and its vital function lost.
When the scientists generated VPS35-deficient mice, the mice exhibited Parkinson's-like deficits, including impaired motor control. When they looked further, they found the lysosomes inside dopamine neurons, which are targets in Parkinson's, didn't function properly in the mice. In fact, without VPS35, the degradation of Lamp2a itself is accelerated. Consequently, yet another protein, alpha-synuclein, which is normally destroyed by Lamp2a, is increased. Alpha-synuclein is a major component of abnormal protein clumps, called Lewy bodies, found in the brains of patients with Parkinson's.
"If alpha-synuclein is not degraded, it just accumulates. If VPS35 function is normal, we won't see its accumulation," Xiong said.
Conversely, when MCG scientists increased expression of Lamp2a in the dopamine neurons of the VPS35-deficient mice, alpha-synuclein levels were reduced, a finding that further supports the linkage of the three proteins in the essential ability of the neurons to deal with undesirables in their lysosomes.
Without lamp2a, dopamine neurons essentially start producing more garbage rather than eliminating it. Recycling of valuables such as amino acids basically stops, and alpha-synuclein is free to roam to other places in the cell or other brain regions where it can damage still viable proteins.
The bottom line is dopamine neurons are lost instead of preserved. Brain scans document the empty spaces where neurons used to be in patients with neurodegenerative diseases such as Parkinson's and Alzheimer's. One of the many problems with treatment of these diseases is that by the time the empty spaces and sometimes the associated symptoms are apparent, much damage has occurred, Xiong said.
Putting these pieces together provides several new, early targets for disease intervention. "Everything is linked," Xiong said.Dopamine is a brain chemical with many roles, including motor control, and patients with Parkinson's have a loss of the neurons that secrete this neurotransmitter. At least in mice, VPS35 is naturally expressed in dopamine neurons in areas of the brain affected by Parkinson's. 
Xiong and her colleagues reported in 2011 that reduced expression of VPS35 enables activity of the dormant-in-healthy-adults protein BACE1 to increase along with accumulation of the brain plaque that is a hallmark of Alzheimer's. Xiong said then that impaired VPS35 function likely also was a factor in Parkinson's.
In a definite vicious circle, trash starts overwhelming the brain cell's natural garbage disposal system. Proteins start getting misfolded and dysfunctional, potentially destructive proteins such as BACE1 and Lamp2a end up in the wrong place and get activated/inactivated, while good proteins get chopped up and/or bad proteins accumulate. 
Parkinson's disease is characterized by uncontrolled shaking, an unstable gait and cognitive loss. The research was funded by the National Institutes of Health and the Department of Veterans Affairs. Postdoctoral Fellow Dr. Fulei Tang is the study's first author.
Adapted by MNT from original media release

Thursday, August 20, 2015

Phase III Study of Xeomin® (Incobotulinumtoxina) for Spasticity to Be Published in “Muscle & Nerve”

Clinical Data From Merz Neurosciences’ Phase III Study of Xeomin® (Incobotulinumtoxina) for Spasticity to Be Published in “Muscle & Nerve”

RALEIGH, NC, USA (August 17, 2015)
Merz Neurosciences, a division of Merz North America (U.S. affiliate of the global Merz Pharma Group), today announced that data from its Phase 3 PURE: Post-stroke Spasticity UppeLimb Study to Investigate Efficacy and Safety of NT 201 clinical trial for incobotulinumtoxinA has been accepted for publication by the medical journal “Muscle & Nerve” (John Wiley & Sons). Merz has submitted an sBLA to the FDA to seek approval for the use of incobotulinumtoxinA in the treatment of post-stroke upper limb spasticity and anticipates FDA action prior to the end of this calendar year.
“We are pleased to announce ‘Muscle & Nerve’s’ acceptance of data from our pivotal Phase 3 clinical trial in spasticity,“ said Glenn Block, Vice President and Head – US Neurosciences for Merz North America. “At Merz Neurosciences, everything we do centers on the needs of the patients and physicians in our areas of focus, and we are proud to be working toward a better experience for movement disorder and spasticity patients via ongoing research and development programs.”
The PURE trial, an FDA registration trial of incobotulinumtoxinA for spasticity of the upper limb, met both co-primary endpoints. In the primary analysis, the co-primary variables were improvements in muscle tone defined as ‘change in Ashworth Scale score from baseline to Week 4’ and improvements in functional outcomes, defined as ‘investigator's Global Impression of Change at the Week 4 visit’. Both showed statistical significance, with p < 0.001 and p = 0.003 respectively. The trial also met a key secondary outcome measure, in which subjects with an improvement ≥1 on the Ashworth Scale at Week 4 were classified as responders and showed significant improvements in disability associated with spasticity (p<0.001). Treatment related adverse events were reported for 3.8% and 1.9% of subjects treated with incobotulinumtoxinA and placebo, respectively.
“Targeted, robust research programs are needed in order to continue to deliver meaningful treatment options for individuals living with movement disorders such as upper limb spasticity. Clinical studies such as the PURE trial are essential in helping us to better understand and meet the unique needs of these patients,“ said Dr. Christina Marciniak, MD, co-investigator and Associate Professor in the Department of Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine. Dr. Marciniak is also an Attending Physician with the Rehabilitation Institute of Chicago, the world’s leading hospital and research enterprise in physical medicine and rehabilitation.
preview of this manuscript is now available online in the Accepted Articles section of “Muscle & Nerve.”
About PURE
The Phase 3 PURE trial was a prospective, multicenter, randomized, double-blind, placebo-controlled main period (12-week duration) with a single incobotulinumtoxinA 400 U treatment or placebo, followed by a 36-week open-label extension in which subjects (n=259) could receive up to three additional treatment cycles. The main period randomization rate of incobotulinumtoxinA to placebo was 2:1.
The study was conducted at 46 sites in North America and Europe. A Primary Target Clinical Pattern (PTCP) for each patient was determined by the investigators and had to be treated with a fixed dose (flexed elbow: 200 U; flexed wrist: 150 U; clenched fist: 100 U). The primary outcome measure was change from baseline in Ashworth Scale Score (AS) score of the PTCP at Week 4. For the responder analysis (a secondary outcome measure), subjects with an improvement ≥1 were classified as responders. The Co-primary outcome was Investigator’s Global Impression of Change in spasticity at Week 4, based on clinical experience and using a 7-point Likert scale ranging from -3 = very much worse to +3 = very much improved. For more information on this trial, please visit using the identifier NCT 01392300.
About Merz Neurosciences
Merz Neurosciences is a division of Merz North America, a specialty healthcare company that develops and commercializes treatment solutions in aesthetics, dermatology and neurosciences in the U.S. and Canada. Merz Neurosciences is committed to providing high-quality products and outstanding service to physicians in the fields of neurology, physiatry and otolaryngology. By developing products that improve patients’ health and help them to live better, feel better and look better, Merz will continue to make significant contributions to the well-being of individuals around the world. Merz Neurosciences is an important contributor to the U.S. neurosciences space, offering a well-balanced product portfolio that includes the neurotoxin Xeomin® (incobotulinumtoxinA), the anticholinergic Cuvposa™ (glycopyrrolate) Oral Solution and the Prolaryn™ family of products.
For more information about Merz Neurosciences and their U.S. product portfolio, please visit
About Xeomin® (incobotulinumtoxinA)
XEOMIN® is a prescription medicine that is injected into muscles and used:
  • to treat the abnormal head position and neck pain that happens with cervical dystonia (CD) in adults.
  • to treat abnormal spasm of the eyelids (blepharospasm) in adults who have had prior treatment with onabotulinumtoxinA (Botox®).
XEOMIN® may cause serious side effects that can be life threatening. Call your doctor or get medical help right away if you have any of these problems any time (hours to weeks) after treatment with XEOMIN:
  • Problems with swallowing, speaking, or breathing can happen after an injection of XEOMIN if the muscles that you use to breathe and swallow become weak. If these problems are severe, you could die. People with certain breathing problems may need to use muscles in their neck to help them breathe and may be at greater risk for serious breathing problems with XEOMIN.
  • Swallowing problems may last for several months, and during that time you may need a feeding tube to receive food and water. If swallowing problems are severe, food or liquids may go into your lungs. People who already have swallowing or breathing problems before receiving XEOMIN have the highest risk of getting these problems.
  • Spread of toxin effects. In some cases, the effect of botulinum toxin may affect areas of the body away from the injection site and cause symptoms of a serious condition called botulism. The symptoms of botulism include: loss of strength and muscle weakness all over the body, double vision, blurred vision and drooping eyelids, hoarseness or change or loss of voice, trouble saying words clearly, loss of bladder control, trouble breathing, trouble swallowing.
Do not take XEOMIN if you: are allergic to XEOMIN or any of the ingredients in XEOMIN; had an allergic reaction to any other botulinum toxin product such as rimabotulinumtoxinB (Myobloc®), onabotulinumtoxinA (Botox®, Botox® Cosmetic), or abobotulinumtoxinA (Dysport®); have a skin infection at the planned injection site.
Before you take XEOMIN, tell your doctor about all your medical conditions, including if you have a disease that affects your muscles and nerves (such as amyotrophic lateral sclerosis [ALS or Lou Gehrig's disease], myasthenia gravis or Lambert-Eaton syndrome), as you may be at increased risk of serious side effects including difficulty swallowing or breathing. Tell your doctor if you have: had any side effect from any other botulinum toxin in the past; breathing problems such as asthma or emphysema; a history of swallowing problems or inhaling food or fluid into your lungs (aspiration); bleeding problems; drooping eyelids; plans to have surgery; had surgery on your face. Also tell your doctor if you are pregnant or plan to become pregnant (it is not known if XEOMIN can harm your unborn baby); are breastfeeding or plan to breastfeed (it is not known if XEOMIN passes into breast milk).
Tell your doctor about all the medicines you take, including prescription and nonprescription medicines, vitamins and herbal products. Using XEOMIN with certain other medicines may cause serious side effects. Do not start any new medicines until you have told your doctor that you have received XEOMIN in the past.
Especially tell your doctor if you have received any other botulinum toxin product in the last four months or in the past. Be sure your doctor knows exactly which product you received. The dose of XEOMIN may be different from other botulinum toxin products that you have received. Tell your doctor if you: have recently received an antibiotic by injection; take muscle relaxants; take an allergy or cold medicine; take a sleep medicine; take a blood thinner medicine.
XEOMIN may cause loss of strength or general muscle weakness, blurred vision, or drooping eyelids within hours to weeks of taking XEOMINIf this happens, do not drive a car, operate machinery, or do other dangerous activities.
XEOMIN may cause other serious side effects including allergic reactions. Symptoms of an allergic reaction to XEOMIN may include: itching, rash, redness, swelling, wheezing, asthma symptoms, or dizziness or feeling faint. Tell your doctor or get medical help right away if you get wheezing or asthma symptoms, or if you get dizzy or faint.
Other side effects of XEOMIN include: dry mouth, discomfort or pain at the injection site, tiredness, headache, neck pain, muscle weakness, and eye problems, including double vision, blurred vision, drooping eyelids, swelling of your eyelids, and dry eyes. Reduced blinking can also occur. Tell your doctor or get medical help right away if you have eye pain or irritation following treatment.

The brain grown in a LAB: Researchers say breakthrough could help test drugs and shed new light on Alzheimer's

  • Brain 'organoid' was created from reprogrammed skin cells 
  • Pencil eraser sized organ comparable with that of a five-week-old foetus
  • Has 99% of the genes present in foetal brain, rudimentary spinal cord, and even the beginnings of an 'eye'
  • Will be used to test new drugs and treatments for brain disorders 

A near-complete human brain comparable with that of a five-week-old foetus has been grown in a laboratory dish.
The brain 'organoid' was created from reprogrammed skin cells and is about the size of a pencil eraser.
Scientists hope the lumpy mass of functioning nerve cells and fibres will prove to be a valuable research tool for non-animal testing of new drugs and investigating brain disorders such as Alzheimer's.
This image of the lab-grown brain is labelled to show identifiable structures: the cerebral hemisphere, the optic stalk and the cephalic flexure, a bend in the mid-brain region, all characteristic of the human fetal brain.
This image of the lab-grown brain is labelled to show identifiable structures: the cerebral hemisphere, the optic stalk and the cephalic flexure, a bend in the mid-brain region, all characteristic of the human fetal brain.


Already the scientists have gone on to create brain organoid models of Alzheimer's and Parkinson's disease, and autism, in a dish.
With the addition of a blood circulation, which is currently lacking, they also hope to use the model to study stroke therapies.
Military applications include research on Gulf War syndrome, traumatic brain injury, and post-traumatic stress disorder. 
As well as neurons and their signal-carrying projections - axons and dendrites - the 'brain' also contains support and immune cells. 
It has 99% of the genes present in the foetal brain, a rudimentary spinal cord, and even the beginnings of an 'eye'.
Lead researcher Professor Rene Anand, from Ohio State University in the US, said: 'It not only looks like the developing brain, its diverse cell types express nearly all genes like a brain.
'We've struggled for a long time trying to solve complex brain disease problems that cause tremendous pain and suffering. 
'The power of this brain model bodes very well for human health because it gives us better and more relevant options to test and develop therapeutics other than rodents.'

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To build the replica brain, the team transformed adult skin cells into induced pluripotent stem (iPS) cells by altering their genes. 
'The artificially created stem cells were then coaxed into developing the different cell types and signalling circuitry of the brain.
Full details of the brain growing process are being kept confidential by the scientists but involved causing the stem cells to differentiate into the full range of brain tissues.
The organoid was allowed to grow to the equivalent of 12 weeks in the womb, almost matching the maturity of a five-week-old foetal brain.
Already the scientists have gone on to create brain organoid models of Alzheimer's and Parkinson's disease, and autism, in a dish.
Already the scientists have gone on to create brain organoid models of Alzheimer's and Parkinson's disease, and autism, in a dish.
'If we let it go to 16 or 20 weeks that might complete it, filling in that 1% of missing genes,' said Prof Anand. 'We don't know yet.'
He spoke about the work at the 2015 military health system research symposium, run by the US department of defence, in Fort Lauderdale, Florida, US.
Already the scientists have gone on to create brain organoid models of Alzheimer's and Parkinson's disease, and autism, in a dish.
With the addition of a blood circulation, which is currently lacking, they also hope to use the model to study stroke therapies.
Military applications include research on Gulf War syndrome, traumatic brain injury, and post-traumatic stress disorder. 

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CSF biomarkers predict dementia risk in PD patients

Published on August 19, 2015 at 5:15 PM 
By Lucy Piper, Senior medwireNews Reporter

Early analysis of cerebrospinal fluid (CSF) could help diagnose parkinsonian disorders and enhance the prediction of dementia in Parkinson’s disease (PD) patients, study results indicate.
Specifically, the presence of high CSF levels of neurofilament light chain protein (NFL) and heart fatty acid-binding protein (HFABP) and low levels of β-amyloid (Aβ)1-42 predicted the likelihood of dementia accurately enough “to be clinically useful”, say the study researchers.
“Changes in these biomarkers, even at the time of the diagnosis of PD, may alert physicians to a patient’s risk of developing dementia”, they add.
As published in JAMA Neurology, David Bäckström (Umeå University, Sweden) and colleagues quantified the cerebrospinal fluid concentrations of a panel of biomarkers in 128 patients with new-onset PD or related parkinsonian disorders.
At baseline, the results showed distinct CSF patterns in 104 of the participants with PD compared with 13 with progressive supranuclear palsy and 30 healthy control individuals, but not relative to 11 patients with multiple system atrophy.
In PD patients, NFL levels were significantly increased compared with controls, while Aβ1-42 levels were slightly lower and the ratio of these biomarkers distinguished PD patients from controls with a diagnostic accuracy of 69%.
These CSF biomarkers also distinguished patients with progressive supranuclear palsy from those with PD. A baseline CSF NFL level above 2020 ng/L diagnosed progressive supranuclear palsy with an accuracy of 82%, a sensitivity of 75% and a specificity of 83%, while the ratio of NFL to Aβ1-42 improved diagnostic accuracy to 87%. At values exceeding 2.3, the ratio distinguished progressive supranuclear palsy from PD with 100% sensitivity and 68% specificity.
These results remained stable when CSF was analysed a year later following dopaminergic treatment.
“Marked elevation in NFL might reflect a more aggressive, accumulating subcortical axonal degeneration in [progressive supranuclear palsy] compared with PD”, the researchers suggest.
“If validated, this difference could serve as a supportive diagnostic criterion for [progressive supranuclear palsy] in early disease”, they say, adding that NFL may also serve as a biomarker for neurodegeneration in patients with the condition.
As well as diagnosing parkinsonian disorders, an early CSF pattern of high NFL and low Aβ1-42, along with high HFABP levels, predicted the risk of dementia in PD patients.
Baseline levels of these three CSF biomarkers correlated with the development of dementia in 35 of 99 PD patients over a follow-up of 5 to 9 years.
Patients with PD who, at baseline, had NFL levels exceeding 1100 ng/L, Aβ1-42 levels below 626 ng/L and HFABP levels above 500 ng/L were a respective 2.6, 2.8 and 2.8 times more likely to develop dementia than other patients.
A combination of the ratio of NFL and HFABP to Aβ1-42 provided the greatest diagnostic accuracy, at 83%, with a baseline ratio exceeding 2.1 associated with a hazard ratio for dementia of 11.8, giving a sensitivity of 90% and a specificity of 71%.
The researchers note that only two of the 25 PD patients with ratio values of 1.0 or below went on to develop dementia.
They also confirm that the predictive ability of the three CSF biomarkers remained after taking into account age, and was only slightly lowered after adjustment for baseline mild cognitive impairment.

Licensed from medwireNews with permission from Springer Healthcare Ltd. ©Springer Healthcare Ltd. All rights reserved. Neither of these parties endorse or recommend any commercial products, services, or equipment.

Safinamide in Parkinson disease: No hint of added benefit


Relevant study data were not considered / analyses in the dossier were incomplete regarding serious side effects in the comparator therapy, long-term data and other aspects
Safinamide (trade name: Xadago) has been available since February 2015 as add-on therapy for the treatment of mid- to late-stage Parkinson disease in adults. In combination with levodopa alone or together with other Parkinson disease medicinal products, this monoamine oxidase (MAO-B) inhibitor is used to help restore dopamine levels in the brain. The German Institute for Quality and Efficiency in Health Care (IQWiG) examined in a dossier assessment whether this drug offers an added benefit over the appropriate comparator therapy.
Such an added benefit cannot be derived from the dossier, however, because relevant study data were not considered and the analyses were therefore incomplete.
Indirect comparison with limited study pool
Due to a lack of studies of direct comparisons, the drug manufacturer conducted an adjusted indirect comparison with studies that tested either safinamide or the COMT inhibitor entacapone as appropriate comparator therapy against placebo. All six studies included provided data on a 24-week treatment: Two studies provided data on safinamide and four studies on entacapone.
One of the safinamide studies (016) was followed by an extension phase (018), in which the patients were treated for another 78 weeks (total duration 016/018: 102 weeks). The manufacturer did not include this extension phase in the benefit assessment because it did not identify an entacapone study with the same duration. It had limited study selection to the exact duration (24 and 102 weeks). The additionally relevant and more current entacapone study BIA-91067-301 with a treatment duration of 52 weeks was therefore not included in the study pool.
Analyses incomplete because relevant study data were lacking
The limitation of the study pool is methodologically inadequate and resulted in an important loss of information. The analyses in the dossier are therefore incomplete and cannot be used for the assessment of the added benefit: It would be possible to conduct a comparison with the long-term data from the safinamide study 016/018 in connection with the missing entacapone study.
Furthermore, only the BIA-91067-301 study provided information on serious side effects (SAEs) on the entacapone side of the indirect comparison. Moreover, treatment of adults with Parkinson disease has probably changed in the last 5 to 15 years so that the missing study results may be more similar to the safinamide studies from about the same period of time than the four entacapone studies included, all of which were approximately ten years older.
G-BA decides on the extent of added benefit
This dossier assessment is part of the early benefit assessment according to the Act on the Reform of the Market for Medicinal Products (AMNOG) supervised by the Federal Joint Committee (G-BA). After publication of the dossier assessment, the G-BA conducts a commenting procedure and makes a final decision on the extent of the added benefit.

Adapted by MNT from original media release

'I wish my mum could die like my beloved dog

'I wish my mum could die like my beloved dog': LINDA KELSEY argues that we put pets out of their misery - yet leave the elderly to suffer and deteriorate 

  • Linda Kelsey's mother has Parkinson's disease, anxiety and depression
  • The 87-year-old continually asked to die before becoming too weak to talk 
  • Linda doesn't want to deny her ailing mother a peaceful and gentle death 
My beloved 12-year-old Labrador, Cuba, was put peacefully to sleep two weeks ago.
I did not expect the grieving process to be easy, but in the long days following Cuba's death, I have found my memories of my sweet dog constantly, and disturbingly, interrupted by thoughts of my ailing, 87-year-old mother and her own deteriorating condition.
I have come to the conclusion, which I am well aware many may find abhorrent, that my poor mum deserves the dignified death that was granted to my dog. But as she's a human being - a superior creature altogether - she must be denied a gentle goodbye and continue to exist in her ghastly state of living death.
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A living death: Linda Kelsey, right, with her mother, left. Linda's 87-year-old mother has Parkinson's disease

The old idiom 'to die like a dog' was, in former times, used to express the idea of dying in degrading circumstances, or dying in a cowardly way, begging for mercy. How ironic, in the age of pampered and cosseted pets, that we do not allow our dogs to die like dogs; only people.
Here is what is wrong with my once beautiful and kind mother. For 25 years, since she was diagnosed, at the age of 62, with Parkinson's disease, accompanied by extreme anxiety and deep depression, she has been in gradual retreat from the world. Today, she lives (if you can call it that) in a state-of-the-art care home. Her teeny body, which weighs just over 5 stone, is covered in huge purple bruises and sores from blood vessels that rupture at the slightest touch, and even spontaneously.
She cannot walk, or dress, or do anything for herself, other than just about feed herself her soft-food diet, which goes everywhere, and drink a cup of tea with her trembling hand. She doesn't read or watch television. Her voice is barely audible (a symptom of Parkinson's). She is confused, with a degree of dementia.
On the upside, she recognises me and my sister, exchanges a few half-sentences here and there, and, miraculously, with major prompting from me, can still conjure up some of the answers to the Daily Mail crossword.
It breaks my heart to see her suffering, and her total dependence on the kindness of her carers.
Right from her diagnosis, it was as though my mother had given up the will to live - or at least to enjoy her life. The Parkinson's, in fact, was relatively mild compared to many others with her condition, but her anxiety and depression were incapacitating.
Linda with  Cuba before he was put down after being diagnosed with suspected cancer
Linda with Cuba before he was put down after being diagnosed with suspected cancer

At least she had her dedicated and ever-supportive husband - my father Sam - to care for her and cajole her into the world.
And so for many years, albeit with increasing reluctance on her part, they continued to go to their holiday home in Spain four times a year, and my mother still took enjoyment in regular visits from me and my sister, and from her four grandchildren.
Then she fell, breaking her pelvis and her hip, and this, alongside the impaired gait caused by the Parkinson's, made walking more and more difficult.
Eight years ago, my dad - who was 13 years older than my mum, and by then 92 - became ill himself.
 Linda, left, with her mother in her mid fifties, right, before she was diagnosed with Parkinson's disease at 62
 Linda, left, with her mother in her mid fifties, right, before she was diagnosed with Parkinson's disease at 62

The system of carers we had in place broke down, and we had to sell their home to fund nursing home facilities for them both. A few months later my dad was dead.
For almost eight years now, my mum has lived in a care home. For the first five years, without fail on my twice-weekly visits, my mother told me she wanted to die.
My mother told me she wanted to die. 'Put me out of my misery,' she begged
'Put me out of my misery,' she begged.
'Oh Mum, I can't do that, you know I can't,' I'd reply.
The platitudes I uttered about the quality of the care home felt hollow. I repeated over and over how fortunate it was that my sister and I lived so nearby that we could visit regularly, as could the grandchildren.
But all I heard was 'I want to die', 'I want to die'. I heard it so often that I began to concede - to myself but not to her - that she was right to want to die. And, for her sake, I wished that she would.
These past three years she has stopped pleading with me, but I know it's only because she no longer has the strength to muster up the words.
But back to my dog Cuba's final days. She had been slowing down for months. If, 
when she was a puppy, I'd found it impossible to keep up with her, no drag her round the block.Three weeks ago, this greediest of dogs, who'd hoover up the remains of discarded chicken vindaloo containers in the park, swallow cup-cake wrappings from the gutter, and once gobbled an entire Pavlova intended for my guests, gave up eating.
I put it down to exhaustion after taking her for a longer than usual walk on a hot day, but 48 hours later she could barely walk at all and I took her to the vet, where they admitted her immediately.
Around 10pm that night, I rang to see if the results of tests had come through. She appeared to have a disease, called Immune-Mediated Hemolytic Anaemia, in which the red blood cells start self-destructing. She needed a blood transfusion.
They told me they couldn't rule out cancer. And there'd be a long course of steroids, and a big possibility of relapse. The vet said it was up to me, but euthanasia was an option I might want to consider.
The decision needed to be quick as the transfusion would have to be done within hours. I said I needed to discuss matters with my son Thomas, now 27. He no longer lives at home, but Cuba was a member of his family, and I knew he'd expect to be involved.
With a heavy heart, Thomas agreed that putting Cuba to sleep was the kindest option and insisted on coming to the vets with me.
My partner Ronny was at home with me at the time. Ronny only got to know Cuba when we met after my divorce, but he had grown incredibly fond of her and always took on the duty of the last walk at night. He wasn't going to miss out on saying goodbye to a dear companion.
No sooner had I put down the phone to my son than Thomas rang his dad (my ex), who had lived with Cuba in the early years. He, too, insisted on being there.
It was almost midnight when the four of us gathered at Cuba's bedside, where she was hooked up to a drip. Her heart was racing. Each of us stroked, kissed and talked to her in turn. She even managed to wag her tail and raise her head to look at us. Then each of us placed a hand on her, nodded to the vet, and the syringe went in. Within seconds she was gone. Not a shudder, not a yelp or a moan, just a gentle drift into the good night.
Linda at her father Sam's 90th birthday party. He took care of his wife until he died at the age of 92
Linda at her father Sam's 90th birthday party. He took care of his wife until he died at the age of 92

Parkinson's: If you understood would you act differently?
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We all wept. But there was nothing ugly or horrible about it. What a great way to go we all agreed. A good life and a good death.
One of the hot topics amongst my 60-something friends is that of 'living wills'. We're all planning to write them - sooner rather than later. So many of us have seen our parents go through years of needless suffering, and we are terrified of the same thing happening to us.
Even so, we know that living wills may not be enough to ease our final journey. We talk about Dignitas, too. We crack dark jokes about booking club class flights to Switzerland with the last of our savings - but that's only because we don't know how else to deal with the even darker prospects of the future.
The euthanasia debate is difficult and contentious and deeply personal. There are those who argue that loosening the laws on euthanasia would greatly increase the risk of people who want to live being killed.
Linda's parents at their wedding, 1947. Her mother was 20, her father 32. They were married for over 60 years
Linda's parents at their wedding, 1947. Her mother was 20, her father 32. They were married for over 60 years

They would also argue that the danger of violating the right to life is so great that we should ensure euthanasia remains illegal at all costs.
I know only this: that I wish my mum - as I would wish for myself in similar circumstances - could die exactly as Cuba did. With a doctor at her side to send her peacefully away, and my sister and me there to smile and hold her and kiss her farewell.
If it were legal, I'd do it in a heartbeat. I would grant her the request she made when she had the words to express it. I would not recoil in horror. I would not feel guilty. It would be a sad blessing.
Soon, I will receive Cuba's ashes following her cremation. There are plans for a family picnic on Hampstead Heath, Cuba's favourite playground, where she'd run for hours, swim in the pond, roll for joy in the mud.
We will scatter her ashes and talk about all the pleasure she gave us and know that we gave her the death she deserved.
If only I could do the same for my darling mum.