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I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.

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Saturday, November 14, 2015

Brisk Walking May Help Curb Parkinson’s Symptoms


Nov. 14,2015
Parkinson’s disease who regularly walk for exercise may significantly improve their physical and mental function, a new study finds.
“The benefits of exercise that apply to a normal, healthy person are even greater in Parkinson’s disease because it also affects the symptoms of the disease. A person with Parkinson’s will get all the benefits that a normal, healthy person does, plus it will modify the symptoms of their disease,” said Dr. Daniel Corcos, a professor of physical therapy and human movement sciences at Northwestern University in Chicago. Corcos was not involved in the new study.Parkinson’s is a motor system disorder that impairs a person’s ability to control their muscle movements.
The new study, published online July 2 in the journal Neurology, involved 60 Parkinson’s disease patients between the ages of 50 and 80. All were in the early stages of the disease. They were living independently, had no signs of dementia or other serious health problems, and could walk without the aid of a cane or walker
while on their regular medications.
The researchers asked all the participants to walk three times a week, wearing a heart rate monitor to make sure they were striding at a moderately intense pace. They started with sessions of 15 minutes and gradually worked up to walking 45 minutes at a time.

The study defined moderate intensity as a heart rate that was at least 70 percent of the maximum heart rate for a person’s age. For most people, that meant they were working in the range of 104 to 111 beats per minute.
“This means that the participants were breaking a sweat but not working to the level of exhaustion,” explained study author Dr. Ergun Uc, a neurologist with the University of Iowa Hospitals and Clinics and the Veterans Affairs Medical Center in Iowa City.
Researchers tested the patients’ physical and mental function before the study began and then six months after people had started their walking programs.On the second round of testing, participants showed significant improvements in their aerobic fitness. They were also able to walk more quickly and with better balance. And, they experienced less stiffness than they had before the study started, the study authors noted.
In addition, some measures of brain function improved. The participants performed better on a test that gauges how well people can direct their attention. With regard to mood, the patients also reported less fatigue and depression, and a more positive outlook on life.
Because the study didn’t have a “control group” — a group of patients who took part in the study but didn’t walk — it’s hard to know whether the improvements seen were the result of the exercise alone. Sometimes, people can improve just because they’re getting better care from the doctors and nurses who are monitoring them for a study.
For that reason, Uc said his study results need to be repeated in a randomized, controlled trial, and he’s applied for a grant to do that.
But this study isn’t the first to find that exercise can yield important benefits for Parkinson’s patients.
Corcos led a study that showed weight training could result in similar benefits for Parkinson’s patients.
“This is a very important study. The reason the study is important is because it’s using an exercise that’s easy for people to do. And it got important results,” Corcos said.
The study authors agreed that walking is something most people can do to improve their health.
But, Uc said, “it has to be safe. It has to be according to their abilities, and it has to be prescribed by a trained person, like a physician.”
By Brenda Goodman
http://www.mymedclinic.info/2015/11/14/brisk-walking-may-help-curb-parkinsons-symptoms/

Health: New Device Being Used To Help People With Parkinson’s Disease « CBS Philly






Click on to watch video:

http://philadelphia.cbslocal.com/2015/11/12/health-new-device-parkinsons-disease/#.Vkd5VIb0xMI.link


By Stephanie Stahl
Nov.12, 2015
PHILADELPHIA (CBS) — New hope for people living with Parkinson’s disease.  One of the symptoms is difficulty talking, now there’s a device that’s helping them communicate and feel less isolated.
Parkinson’s disease is a progressive neurological disorder with a variety of symptoms like trembling. Patients say the inability to be understood when speaking can be devastating. Now there’s a fix for that.
Annie and Kevin Payton remember their wedding 22 years ago. His hand was shaking and it wasn’t because of nerves. At 26-years-old, Kevin was diagnosed with Parkinson’s disease.
“Kevin proposed and I said yes,” Annie said. “Then he got Parkinson’s and he thinks because he proposed he got it.”
Raising two sons has helped them keep their sense of humor.
As the disease progressed, Kevin had deep brain stimulation surgery, hoping that it would control some symptoms, and wrote about it.
But his slurred speech and mumbling, a symptom of Parkinson’s, continued to worsen.
“Kevin was feeling very isolated,” Annie stated.
Now a device that looks like a hearing aid is helping. It’s called Speech Easy.
Working with his speech pathologist, and wearing the device, Kevin reads passages. He is relearning enunciation.
“In those days not half a dozen men in the United States,” Kevin read.
“What it does is the person who’s wearing it hears themselves talking but at a slight delay,” said Kim Sabourin, Kevin’s speech pathologist. “It slows down the speaking rate of the person who’s using it.”
“Kevin fights it every day and I tell him as long as you fight I will fight with you,” Annie said. “It’s hard but I don’t talk about it much.”
While it can still be difficult to understand Kevin, he says Speech Easy has him feeling better about his life.
“It’s hard not to feel sorry for yourself,” Kevin said. “But for the most part how you choose to live your life is your choice.”
The Speech Easy device was originally used to treat people who stutter. The delayed feedback is now being used for Parkinson’s patients. The device does not work for everyone, it is unclear why.
http://philadelphia.cbslocal.com/2015/11/12/health-new-device-parkinsons-disease/

Sparks Mayor Martini announces he has Parkinson's disease; plans to stay in office

Mayor Geno Martini
11/13/2015 

SPARKS, Nev. (MyNews4.com & KRNV) -- "Everybody loves Geno," Sparks City Council member Ron Smith said. "When you think of Geno Martini and Sparks, they go together."


Many people in Sparks think Geno Martini is a one-in-a-million mayor, but he's also one of about a million people living with Parkinson's Disease in the United States. Mayor Martini received his diagnosis in 2012, but didn't announce it to the public until Friday.

"I didn't feel quite right, so I went to a neurologist," Martini said. "He took a look, did a few things, and 'you've got Parkinson's.'"

Parkinson's is a movement disease that affects a person's motor functions. "It's a progressive disease where you lose functions and things like that," Martini said. "I'm feeling pretty strong now and I'm still moving along and doing most stuff."

The 69-year-old is well aware of what his future likely holds. "It's a tough disease," he said. "My father died from Parkinson's, so I know how devastating it can be."

Sparks city staff just found out about their mayor's diagnosis a few days ago. "Geno is a tough guy," council member Ron Smith said. "If anybody can get through this, he'll get through it."

Smith said he and the other council members plan to support Martini however they can through his term. "We're there to support Geno with whatever he needs. We'll pick up the slack if he can't do it."

Mayor Martini said he plans to keep serving Sparks for the next three years. "Sooner or later, the Parkinson's will get to you," he said, "but I intend to keep pushing through and filling out my term until 2018."

He's still chipper," Smith said. The Sparks mayor's vibrant personality is reassuring his fellow staff. "He's still Geno. He's got a positive attitude and that's what it will take."

Martini said the disease isn't slowing him down too much yet.

"Parkinson's hasn't really stopped me from doing anything at all."

READ the full statement from Mayor Martini, below:

“I am one of more than a million Americans diagnosed with Parkinson’s disease. I was diagnosed with Parkinson’s in 2012. I have done my best to manage the matter privately, but have come to the realization that I now need to make this announcement. I feel great and remain strong and healthy and am continuing to receive great medical care from local physicians. While the disease has slowed me down a bit physically, I am committed to serving as Mayor through the end of my term (November 2018). I will remain engaged and involved in our community to enhance economic development and improve the quality of life for our residents. I am blessed to have a loving and supportive family, a first-rate dedicated staff at the City of Sparks, and to serve in the greatest job in the world. I love my hometown and its people, and I am grateful and overwhelmed for everyone’s love and support.”

http://health.einnews.com/article/296803581/r1l9W7WmkLTOb8PF

Shake Rattle and Rip: Let's Crunch Parkinson's


Nov 12, 2015 






BOISE, Idaho (KBOI) -- A Treasure Valley man could soon be a millionaire.
Richard Herdegen created a commercial for a Doritos competition and if he wins, he'll not only get the money but his ad will play during Super Bowl 50!
The commercial features a YMCA program called "Delay the Disease" that helps locals living with Parkinson's Disease and other neurological disorders.
Right now, Herdegen's video is one of the highest rated ads in the competition. Voting for the top 50 videos begins in January.
If the commercial wins Herdegen says the money will go to a nonprofit for Parkinson's. 

http://health.einnews.com/article/296694900/CJcKJfpByqNxDlAF

Friday, November 13, 2015

Discovery: Molecular mechanism at root of familial amyloidosis and other diseases


Friday 13 November 2015
A team of local researchers has proposed a molecular mechanism that may be responsible for the development of life-threatening diseases called amyloidoses. The best known of such diseases is Alzheimer's disease (AD), but there are many others that are receiving increased scrutiny, in part because of mounting evidence linking them to atherosclerosis and aging.
The findings, which appear in the Journal of Molecular Biology, may ultimately lead to the development of therapeutic targets for one of these diseases.
A group of disorders, called amyloid diseases, occurs due to proteins that form abnormal clumps and deposit in different organs, causing damage to the brain (AD, Parkinson's disease), heart (cardiac amyloidosis), kidney, liver and other vital organs. One such protein called apolipoprotein A-1 (apoA-1) forms the scaffold of the so-called "good cholesterol," or high-density lipoprotein (HDL). Normally, apoA-1/HDL removes excess cholesterol and other fats from the body and is protective against cardiovascular disease. However, when mutations or other errors occur within this protein, apoA-1 has the potential to aggregate and manifest as familial form of amyloidosis, which is a life-threatening incurable disease. ApoA-I can also deposit in arteries, thereby contributing to atherosclerosis. While the medical community has known for some time that abnormal proteins can cause disease due to exposed vulnerable "hot spots" that clump together, there has been a lack of understanding about how a "good" protein can become so "bad," especially at a molecular level.
Using cutting-edge technology to study the dynamic behavior and molecular shape of apoA-1 and its various mutant forms, researchers at Boston University School of Medicine (BUSM) and Northeastern University were surprised to discover that exposed "hot spots" in apoA-I do not always cause amyloid disease. Some mutations led to decreased protection in other vulnerable parts, which helped the body to get rid of the protein before it clumps. These mutations in apoA-I did not cause amyloid disease in humans. The researchers suggest that this finding is not limited to apoA-I but possibly applies to other amyloid-forming proteins. Surprisingly, some mutations occurring at one end of the protein acted like "molecular remote-controls" and changed the structure and activity of the other end.
According to the researchers, solving the puzzle of the molecular changes that cause amyloid diseases has important implications for potential treatments. "If one could predict what makes any given protein to form amyloid, one could begin to design tools to decelerate or even block this pathogenic process before it starts," explained corresponding author Olga Gursky, PhD, professor of Physiology and Biophysics at BUSM.
http://www.medicalnewstoday.com/releases/302606.php?tw

Parkinson's disease: A new tool for healthcare professionals aims to improve diagnosis and advance treatment

McGill University



November 13, 2015


A group of experts working under the umbrella of the International Parkinson and Movement Disorder Society (MDS), have developed a new tool for healthcare professionals that they hope will mark a significant advancement in the diagnosis and treatment of Parkinson's disease, especially in its early stages. The results of their study, published in the journal Movement Disorders, could also have a major impact on the quality of research on Parkinson's disease.
Parkinson's disease (PD) is a neurological condition related to the death of specific brain cells, including cells that control movement, mood, sleep and cognition. The symptoms, which include tremors, slowness of movement, stiffness or rigidity, sleep disorders, loss of the sense of smell, depression, and cognitive dysfunction, can appear in people as young as their thirties, but more commonly appear around the age of 60. It is estimated that the disease touches more than one in 50 people in this age group.
Currently, diagnosis of PD can only be established through an analysis of medical history and a neurological examination by a clinician with expertise in movement disorders -- no objective test for the disease exists. As the symptoms of PD often resemble those of other neurological disorders, the rate of misdiagnosis can be as high as 25 per cent, which causes distress in patients. It also creates a challenge for researchers as the data collected in clinical studies can become compromised by misdiagnosis in their pool of subjects.
The new criteria gathered knowledge and data from movement disorder experts around the world to create the most comprehensive diagnostic criteria ever developed for the disease, with the aim of improving and broadening diagnosis and treatment of the disease, especially in the early stages.
"In light of the latest scientific insights and technological advances, we were able to establish a new list of criteria based on expert clinical diagnosis," says Dr. Ron Postuma, co-Chair of the MDS task force, who is also a researcher in neurosciences at the Research Institute of the McGill University Health Centre and at The Neuro, and associate professor in the Department of Neurology and Neurosurgery at McGill University. "Our aim was to create a benchmark that will systematize the diagnostic process, make it reproducible across centers and that will enable a wider range of non PD-specialized clinicians to provide patients with an accurate diagnosis."
"These criteria accent how Parkinson's disease is much more than a simple motor disorder, now incorporating motor and non-motor symptoms as well as the genetic component in some forms of PD," adds Dr. Daniela Berg, Chair of the MDS task force and Associate Professor at the University of Tübingen, Germany.
The research team is proposing a new stage classification of the disorder with the aim of focusing attention on the early stages of PD. "With this new classification our goal is to set up a research agenda that will help identify the features that signal the presence of the disease early on," explains Dr. Postuma. "Our hope is that, as research advances, our understanding of the mechanisms at play in the disorder will enable us to develop therapies and treatments that can be administered early in this process, eventually slowing or stopping the progression of PD altogether."
An estimated 100,000 Canadians live with PD. Although some drugs and clinical treatments can help control or minimize symptoms there is currently no cure.
http://www.sciencedaily.com/releases/2015/11/151113112436.htm

In Parkinson’s, There’s Growing Recognition of Cognitive Problems

Nov. 12, 2015
When most people think about Parkinson’s disease (PD), they focus on movement problems almost exclusively. But mild cognitive impairment is among other potential disease symptoms, although medical professionals and researchers currently disagree on the extent and exact nature of this problem in Parkinson’s patients.
Progressive tremors and rigidity occur in PD largely due to the degeneration of the substantia nigra dopamine-producing neurons, and loss of dopamine. For this reason, most treatments for PD focus on restoring lost dopamine and helping with impaired movement. Recognition of cognitive impairment in PD is increasing, though, with a recent article in the journal Neurodegenerative Disease Management devoted to exploring controversies in mild cognitive impairment in Parkinson’s disease (PD-MCI).
Mild cognitive impairment is a risk factor for dementia in PD, one that needs to be better recognized and understood, the researchers explain. The article explores signs of PD-MCI, as well as biomarkers, disease progression, and how PD-MCI factors into clinical trial design.
Jennifer Goldman, MD, MS, article co-authored with Neelum T. Aggarwal, MD, and Cynthia D. Schroeder, MHScolleagues from Rush University Medical Center Department of Neurological Sciences. In a press release, Dr. Goldman noted, “Recent research on mild cognitive impairment in Parkinson’s disease (PD-MCI) has sought to define its characteristics and risk factors as well as possible precursors of Parkinson’s dementia.”
“Precursors under investigation include serum, cerebrospinal fluid, and neuroimaging biomarkers, some of which may be similar in concept or in scientific findings to those found in Alzheimer’s disease,” she added. “Lessons learned from the Alzheimer’s disease field may help Parkinson’s disease clinicians and researchers further the development of good screening and accurate diagnostic algorithms, which may predict future cognitive decline, and ultimately assist in making treatment decisions.”
Goldman and colleagues explored how PD-MCI definitions have evolved over the years, and how prevention may be incorporated into PD treatment. In addition, monitoring PD-MCI is now being incorporated as a measurement for PD clinical trials. The group reviews the most effective biomarkers and other assessments for PD-MCI and discusses how the field of Alzheimer’s disease research has informed studies of PD-MCI.
“The authors elegantly synthesize advances and challenges in PD-MCI, a complex field which currently lacks consensus, and make comparisons with the more advanced field of AD-MCI,” stated Daphne Boulicault, commissioning editor. “We are pleased to offer this thoughtful review in both our MEDLINE-indexed journal, and free of charge on our industry portal, Neurology Central.”
http://parkinsonsnewstoday.com/2015/11/12/parkinsons-theres-growing-recognition-cognitive-problems/

Thursday, November 12, 2015

MJFF Conference Highlights Progress in Parkinson’s Research






The Michael J. Fox Foundation’s ninth annual scientific meeting — The Parkinson’s Disease Therapeutics Conference — took place on November 3 in New York City. Nearly 300 scientists and business professionals came together to hear the latest in Parkinson’s disease (PD) research. Here are a few of the exciting updates that were shared.
Disease-Modifying Therapies

The topic of glial derived neurotrophic factor (GDNF) — a protein that may prevent the loss of dopamine cells (and even regenerate those that are lost) — was first on the agenda. GDNF can’t be taken orally, so cells that continuously produce GDNF need to be implanted into the area of the brain where most dopamine cells are missing in Parkinson’s. Lars Wahlberg, MD, PhD, of biotech NsGene, Inc., explained how encapsulated cell therapy might make this possible. A Phase Ib safety study is planned for 2016. 

LRRK2 kinase inhibitors — drugs that work against the LRRK2 genetic mutation that causes Parkinson’s in some — were next. MJFF’s Marco Baptista, PhD, discussed that these medications might help everyone with PD, not just those with the mutation. He shared the results of an MJFF-led consortium of three competingdrug makers who cooperated (pooling their data and compounds) to determine that mild lung changes seen in pre-clinical testing did not cause breathing problems and were reversible. “There is a path forward for LRRK2 kinase inhibitors and this consortium is a collaborative model we can use to move ahead across Parkinson’s research,” said Dr. Baptista.
Symptomatic Treatments

Talk of symptomatic therapies was on optogenetics — combining light (“optics”) and genetics to treat Parkinson’s motor symptoms. Christopher Moore, PhD, Brown University, reminded us how cells communicate with each other — through electrical signals created by the opening and closing of ion (calcium, sodium, etc.) channels. Optogenetics allows scientists to place a light-sensitive channel inside nerve cells and then open or close that channel with light. Optogenetics is currently being studied in pre-clinical models and shows potential for lessening motor symptoms.

Research Tools

The presentation on research tools focused on finding imaging biomarkers (disease indicators) for cognitive (memory and thinking) problems in Parkinson’s. Kathleen Poston, MD, MS, Stanford University, spoke about how today’s clinical trials call for multiple tests (which can be costly and time-consuming) to look for patterns of cognitive problems. She and her colleagues wanted to see if a single test — a “resting state functional MRI,” which examines the brain while a person is relaxed — could replace all of them and accurately diagnose cognitive difficulties in PD. Their study results are currently being analyzed.

Parkinson’s Progression Markers Initiative “Super Session” 

Five years into The Parkinson’s Progression Markers Initiative (PPMI) — MJFF’s landmark observational study to find PD biomarkers — the Principal Investigator, Ken Marek, MD, gave an update on how the number and types of participants has expanded, and the categories of valuable data these volunteers are contributing. Researchers reviewed what they’ve concluded thus far from PPMI imaging and genetics information. John Seibyl, MD, The Institute for Neurodegenerative Disorders, talked about why measuring PD with a brain scan is hard — the disease course is slow and variable — and why imaging might therefore not be the only biomarker for Parkinson’s. Andrew Singleton, PhD, agreed, saying, “We’re having a maturing view of Parkinson’s disease that it’s more than one disease, so we may need more than one biomarker to track it.” Dr. Singleton went on to discuss how analysis of PPMI data led to the identification of five potential predictive factors for PD — smell loss, age, gender, family history of PD and a genetic risk score.

Dr. Marek finished by telling the researcher attendees that all of the PPMI data is available to them —we hope they’ll take advantage of it to help us move closer to a biomarker and nearer to a cure.
Hot Topics in Parkinson’s Disease Research 

Novel ways to deliver levodopa and innovative methods of tracking symptoms and disease progression rounded out the day. C. Warren Olanow, MD, Mount Sinai, brought us up to speed on dyskinesias(abnormal involuntary movements) and how continuous levodopa delivery might prevent them. He discussed Rytary and Duopa — the latest levodopa preparations to reach market in early 2015 — and then delved into formulations in development — the Accordion pill (designed to slowly release levodopa from the stomach) and continuous under the skin and oral administrations. The first two are in Phase III studies; the oral therapy is in Phase II trials. 

Ray Dorsey, MD, MBA, University of Rochester, wrapped up with a potential research tool most of us have in our pockets — the smartphone. He spoke about how smartphone sensors could monitor PD symptoms and disease course, detect treatment response (as in measuring an improvement in balance after medication is administered), even differentiate people who have PD from those who don’t. He also discussed how smartphone apps that log symptoms (voice, dexterity and balance changes) could help find a biomarker, change the way research is done (reach more volunteers and decrease costs and time of clinical trials) and improve care for people with Parkinson’s disease.
It was a full day and a whirlwind tour of the latest research!  We left, though, with a renewed energy and excitement about the progress that’s been made and what we hope to accomplish for people with Parkinson’s.
https://www.michaeljfox.org/foundation/news-detail.php?mjff-conference-highlights-progress-in-parkinson-research&et_cid=403402&et_rid=61620490&et_lid=read+more

Pharnext's pleodrug PXT-864 demonstrates positive effects in Parkinson's disease

Published: Thursday 12 November 2015
acamprosate

baclofen

 SAS has announced the publication of positive preclinical results in Nature's Scientific Reports for its pleodrug PXT-864 in Parkinson's disease. After promising Phase 2 clinical data in Charcot-Marie-Tooth with PXT-3003 and preliminary positive clinical data in Alzheimer's disease with PXT-864, the data provide further validation of the company's pleotherapy R&D approach. It is based on a proprietary network pharmacology platform that allows the development of pleodrugs, synergistic low dose combinations of repositioned drugs with established safety profiles.
In the article titled, "Combination of acamprosate and baclofen as a promising therapeutic approach for Parkinson's disease," authors Rodolphe Hajj, et al., report that PXT-864, a combination of baclofen and acamprosate, improved multiple endpoints associated with the development and progression of Parkinson's disease. In cellular and in rodent relevant models of Parkinson's disease, the authors specifically found that PXT-864:
  • Synergistically protected neuronal cells against oxidative stress in vitro, a hallmark of Parkinson's disease pathology
  • Synergistically protected dopaminergic neurons in vitro in an induced toxicity model
  • Protected motor function from 6-OHDA lesions in rats
  • Protected substantia nigra pars compacta (SNc) dopaminergic neuronal cell bodies and striatal nerve terminals in vivo
  • Restored symptomatically motor function in 6-OHDA pre-lesioned rats
  • Did not negatively interact with L-Dopa
PXT-864 may represent an efficient and valuable strategy to slow or stop the progression of Parkinson's disease. In addition, PXT-864 could also improve symptoms of patients without inconvenience related to L-Dopa treatment.
Anthony Schapira, M.D., FMedSci., Head of the Department of Clinical Neuroscience at the UCL Institute of Neurology , London, said, "The data presented provide compelling evidence of PXT-864's potential in the treatment of Parkinson's disease. Today there are no treatments capable of altering the progressive course of the disease by slowing the destruction of dopaminergic neurons. I look forward to the clinical development of PXT-864 to see if these effects can be translated to patients with Parkinson's disease."
Ilya Chumakov, Ph.D., D.Sc., co-founder of Pharnext and scientific advisory board chairman, said, "These data validate and demonstrate the potential of Pharnext's pleotherapy approach. It builds upon the recently published positive results of PXT-864 in Alzheimer's disease and Phase 2 clinical data of lead pleodrug, PXT-3003, in Charcot-Marie-Tooth disease Type 1A (CMT 1A)."
Daniel Cohen, M.D., Ph.D., chairman, chief executive officer and co-founder of Pharnext, said, "The diseases we are targeting such as Alzheimer's, Parkinson's and CMT 1A with our lead pleodrugs are exceedingly difficult for patients in that they are all progressive in nature with worsening symptoms over time. Patients have little to no acceptable treatment options and medical unmet needs remain high. As such, the published results of this multitarget approach are very encouraging for the future."
http://www.medicalnewstoday.com/releases/302538.php?tw

Minister authorises Phase IIb Parkinson’s study





12 November 2015 – Sydney, Australia & Auckland, New Zealand – 

Living Cell Technologies Limited’s application to conduct a Phase IIb study of NTCELL® in Parkinson’s disease has been authorised, subject to the usual conditions, by New Zealand’s Minister of Health, Hon Dr Jonathan Coleman
.
The study protocol will now be submitted to the ethics committee for approval. Once the committee has approved the study design, patient recruitment can commence.
The study will involve up to 18 patients under the age of 65 who have had Parkinson’s disease for at least 5 years. Patients will be treated in three groups. Each group will receive bilateral implants of NTCELL at a range of doses. In each group, two patients will receive a placebo dose.
At the end of the 26-week follow up period the study will be unblinded, at which point the patients who received the placebo will receive an implant of NTCELL at the dose determined to be most effective.

LCT intends to begin patient recruitment in December 2015. LCT expects the first patient to be implanted in February 2016 and the study will be completed in 2017.
CEO of Living Cell Technologies, Dr Ken Taylor, says the study is the next step in the company’s development of NTCELL as a disease-altering treatment for Parkinson’s disease.
“We’re looking to confirm the ability of NTCELL to halt disease progression and restore quality of life for people with Parkinson’s disease,” says Dr Taylor.

The minister also authorised an amendment to the protocol of the Phase I/IIa study to enable ongoing monitoring of the four patients in that study. Evaluation of the patients at 42 weeks post-implant showed a clinically and statistically significant improvement in their neurological scores from their pre-implant baseline. That improvement is equivalent to approximately 5 years of Parkinson’s disease remission. 

http://www.otcmarkets.com/otciq/ajax/showNewsReleaseDocumentById.pdf?id=17708

NEURODERM ANNOUNCES STREAMLINED U.S. DEVELOPMENT PLAN FOLLOWING FDA FEEDBACK ON ND0612H AND ND0612L FOR THE TREATMENT OF PARKINSON'S DISEASE

Based on FDA input, NeuroDerm is not required to conduct its largest Phase III pivotal trial of 360 patients
Company to host conference call today at 8:30 a.m. ET
/EIN News/ -- REHOVOT, Israel, Nov. 11, 2015 (GLOBE NEWSWIRE) -- NeuroDerm Ltd. (Nasdaq:NDRM), a clinical-stage pharmaceutical company developing drugs for central nervous system (CNS) diseases, today announced that it has modified its U.S. development plan for ND0612H and ND0612L, the company's continuous, subcutaneously delivered levodopa/carbidopa product candidates for the treatment of Parkinson's disease. The updated and abbreviated plan incorporates written feedback that the company recently received from the U.S. Food and Drug Administration (FDA) within the framework of an ongoing Type C meeting communication that was initiated by the company. NeuroDerm asked the agency to provide strategic and operational guidance related to the U.S. clinical and regulatory development of ND0612H and ND0612L.
NeuroDerm's new development plan for ND0612H and ND0612L consists of the following:
ND0612H:
Clinical development of ND0612H for the U.S. will proceed as planned with one Phase II trial and one Phase III trial of essentially the same design, treatment duration and patient numbers as originally planned.  The Phase II trial will include centers in Israel and the EU in addition to U.S. centers, however essentially preserving the original design, number of centers, number of patients and treatment duration.
ND0612L:
Clinical development of ND0612L for the U.S. and the EU will be based on only one and not two pivotal efficacy trials of essentially the same design, treatment duration and patient numbers (200-240) as originally planned.  The second pivotal efficacy trial of 360 patients that was originally planned for this product candidate is not required by the FDA.
ND0612 Safety Follow-up:
A safety follow up study for both ND0612H and ND0612L will include at least 100 patients treated for one year of whom at least half will receive the maximum dose.  The safety follow-up studies that were originally planned included 50-150 patients treated for 6-12 months for each of the product candidates.
Timelines:
The supplier of the delivery devices used in the clinical trials of both ND0612L and ND0612H has been requested by the FDA to provide additional documentation pertaining to good manufacturing practices of the Quality System regulation.  Until documentation is provided to the satisfaction of the FDA, this supplier may not import devices into the U.S.  This does not preclude the sale or use of devices currently in the U.S. nor the importation of devices for investigational purposes if approved as part of an investigational study.  Nevertheless, NeuroDerm has decided to request additional documentation from the device manufacturer before proceeding with enrollment at U.S. investigator sites.  Patient enrollment in its upcoming clinical trials will thus begin at non-U.S. investigator sites. NeuroDerm expects that the requested documents will be provided by the supplier in the first quarter of 2016 enabling the company to start enrolling U.S. patients in the second quarter of 2016.
In the EU, the pharmacokinetic pilot dose finding study of ND0612H is ongoing and topline results are now expected in the second quarter of 2016. NeuroDerm does not foresee any changes to previously disclosed timelines related to anticipated EU submission.
The currently anticipated timelines for the ongoing and upcoming clinical trials are as follows:
ND0612H
  • Pharmacokinetic (PK) pilot dose finding study (EU trial): ongoing; topline results expected in the second quarter of 2016
  • Initiation of Phase II efficacy trial and long-term safety follow-up (Israel-EU-U.S.): end of 2015 – beginning of 2016
ND0612L
  • Initiation of Phase III efficacy trial and long-term safety follow-up (Israel-EU-U.S.): first half of 2016
"We are pleased that based on feedback from the FDA the largest clinical trial in our development program will not be required, resulting in a streamlined clinical development plan," said Oded S. Lieberman, PhD, NeuroDerm's CEO. "We believe our product candidates have the potential to revolutionize the treatment of Parkinson's disease and we are committed to provide a new treatment option to both advanced and moderate Parkinson's patients."
Conference Call Details 
NeuroDerm will host a conference call at 8:30 a.m. ET today to discuss the Company's updated development strategy and review third quarter 2015 financial results. Individuals can access the webcast in the Events and Presentations section of the Company's website, by clicking here, or by dialing 888-389-5988 (U.S.) or 719-325-2428 (outside of the U.S.). The passcode is 5664132. A webcast will be archived on the website.
ND0612H and ND0612L
ND0612H and ND0612L are designed to significantly reduce motor complications in Parkinson's disease patients through continuous, subcutaneous delivery of LD/CD. Previously completed Phase II trials demonstrated that ND0612L maintained steady, therapeutic levodopa plasma concentrations that were associated with major changes in several clinical parameters including "off time" reductions when added to optimized oral standard of care. ND0612H, intended for severe Parkinson's disease patients, was shown to reach even higher levodopa steady plasma levels, indicating that it may provide an effective therapy alternative to current treatments requiring surgery such as deep brain stimulation and LD/CD Intestinal Gel.
About Parkinson's disease
Parkinson's disease is a progressive neurodegenerative illness characterized by reduced dopamine in the brain, resulting in a debilitating decrease in the patient's motor and non-motor functions. Its symptoms, such as trembling in the extremities and face, slowness of movement and impaired balance and coordination, worsen over time and gravely impact the patient's quality of life. As the disease progresses, these symptoms become more severe, resulting in debilitating periods of decreased motor and non-motor functions, also referred to as "off" time. In addition, mainly as a result of excessive/intermittent oral doses of levodopa aimed at treating the "off" time, some patients experience involuntary movements, or dyskinesia. The "off" time and dyskinesia affect the majority of Parkinson's disease patients and interfere with day-to-day functions, causing patients to become severely disabled. Continuous administration of levodopa has been shown to effectively treat motor fluctuations in Parkinson's disease patients, however, a convenient route of continuous administration has not been introduced to date.
About NeuroDerm
NeuroDerm is a clinical-stage pharmaceutical company developing central nervous system (CNS) product candidates that are designed to overcome major deficiencies of current treatments and achieve enhanced clinical efficacy through continuous, controlled administration. In Parkinson's disease, the company has four product candidates in different stages of development which offer a solution for almost every Parkinson's disease patient from the moderate to the very severe stage of the disease. The company has developed a line of LD/CD product candidates administered through small belt pumps that deliver a continuous, controlled dose of LD/CD. The LD/CD line of product candidates includes: ND0612L and ND0612H, delivered subcutaneously, for moderate and for advanced Parkinson's disease patients, respectively. In addition, NeuroDerm is developing ND0701, a novel subcutaneously delivered apomorphine formulation for patients who suffer from severe Parkinson's disease and who do not respond well to LD/CD. NeuroDerm is headquartered in the Weizmann Science Park in Rehovot, Israel.
CONTACT: NeuroDerm Contact:
Oded S. Lieberman, PhD, MBA, CEO
oded@neuroderm.com
29
 Cell: +1-617-517 6
Tel.: +972-8-946 27077
U.S. Investor and Media Contact:
dcarey@lazarpartne
David Carey
Lazar Partners Ltd. rs.com
+212-867-1762
http://health.einnews.com/pr_news/296357184/neuroderm-announces-streamlined-u-s-development-plan-following-fda-feedback-on-nd0612h-and-nd0612l-for-the-treatment-of-parkinson-s-disease?n=2&code=lAb0qDE0aV13cmUw