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I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
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Monday, July 24, 2017

Price explains potential therapy for Parkinson’s

July 24, 2017   Rachel Adkins | The Daily Independent

Dr. Elmer Price, a professor of biological sciences at Marshall University, speaks at the Ashland Rotary Club on Monday. Rachel Adkins | The Daily Independent

ASHLAND Dr. Elmer Price of Marshall University shared with Ashland Rotarians on Monday a potential new therapy for Parkinson’s disease that he has developed.
Price, a professor of biological sciences, explained at the club’s meeting how the therapy works with the use of adult stem cells. He and his students have seen success with their research so far, with the use of lab rats who are given Parkinson’s disease.
Price’s method does not involve a stem cell transplant from another party, but instead uses someone’s own stem cells to help with Parkinson’s disease. This is done by redirecting stem cells from the patient’s olfactory bulb, a brain structure responsible for sense of smell, toward the other area of their brain that is damaged by the disease.
“A rats’ olfactory bulb gets replenished with about 10,000 neurons everyday. In humans it’s more like 1,000,” he said.
The cells are redirected through an implant in the shape of a cylinder that is 6 millimeters long with a diameter measuring 0.7 millimeters. The cylinder is made of a gel-like material that has components that are already commonly used by neurosurgeons.
The cylinder’s job is to create a new migratory path in the brain for the cells so they can travel to the damaged area. The implant is biodegradable and is gone after about eight weeks.
Price noted that out of the 70-80 animals that have received an implant, none have died from the surgery. He also added that the next day after receiving their implant, the rats go back to their normal lives.
He showed Rotarians a diagram of a rat’s brain eight weeks after the implant that revealed neurons following a new pathway to the designated area.
“Their Parkinson’s behavior is being basically reversed by this implant,” he explained.
In 2015 Price was awarded a three-year, $350,000 grant from the National Science Foundation for his research. In addition to Parkinson’s disease, his potential therapy could also be used for traumatic brain injuries.

Melbourne scientists discover brain iron may predict Alzheimer’s progression

July 24. 2017   Brigid O’Connell, Health reporter, Herald Sun

An specialised MRI scan, developed by the CSIRO, has been used to look for iron levels in the brain as a predictor Alzheimer’s disease.

MELBOURNE scientists have discovered scans for iron levels in the brain could identify people most at risk of Alzheimer’s.
In a major breakthrough in the fight against the devastating disease, scientists have found that those with significant brain plaque but low iron levels maintain cognitive performance over as much as six years.
But those with high iron levels — particularly in the hippocampus, the part of the brain involved in memory formation — progress faster to disease.
A team from the Florey ­Institute of Neuroscience and Mental Health and the CSIRO are behind the finding.
An iron chelator drug already on the market is showing promise at “mopping up” iron in the brains of Parkinson’s disease patients. The Florey team will now test if a twice-a-day dose taken over a year can slow Alzheimer’s progression.
If the trial is successful, Flor­ey Professor Ashley Bush said the 60-year-old GP health check could include a brain scan, followed by a PET scan if brain plaque is found, with medication to halt the disease before symptoms appear.

Flor­ey Professor Ashley Bush. Picture: Supplied

More than 413,000 Australians live with dementia symptoms, of which Alzheimer’s is the most common type.
Florey research fellow and lead author Dr Scott Ayton said: “For clinical trials to be effective, we want to treat people as early as possible.
“But until now we haven’t been able to identify who is going to decline.”
A third of adults aged over 65 have high levels of the plaque (beta-amyloid protein) in their brain, the equivalent to someone with advanced dementia. But many of these people are cognitively well and may never develop Alzheimer’s in their lifetime, showing there is more to the disease than just amyloid.
Hundreds of international clinical trials over the past 40 years focusing on these plaques have not resulted in any disease-modifying drug being approved for the clinic.
Prior studies by the Florey Institute of Neuroscience and Mental Health and others have suggested that iron levels in the brain — which have no connection to iron levels in the blood or iron consumed in the diet — could play a role in predicting who is at risk.
And working with the CSIRO, which developed a new method of measuring iron in the brain using a standard MRI machine, they recruited 117 participants and tested their cognitive function was tested every 18 months for six years.
The breakthrough findings were published today in the journal, Brain.
Prof Bush said: “For the first time, we will be able to assess someone’s risk of progressing into cognitive decline without needing to perform invasive or costly tests.”
The concept was first tested in a blinded experiment of 48 people published in 1991, which showed a first-generation iron chelator could half cognitive decline compared to placebo.
Dr Ayton said that study was never followed up as the international research world shifted its attention to the most logical target of beta-amyloid. But with more advanced scanning technology, he said they hoped to replicate the result.
If you are over 65 and have noticed your memory is declining, or you are newly diagnosed with dementia, register interest to be contacted when the study opens this year.

Songs sung at Neuro Challenge stay at Neuro Challenge

July 24, 2017   BY RICHARD DYMOND

Care advisor Jennifer Williams speaks with Carol and Don Williams, Carol is challenged with Parkinson's. Neuro Challenge Foundation for Parkinson's opened a new office in Bradenton due to growing client numbers. Tiffany Tompkins

Although not approved by the American Medical Association, a Parkinson’s disease treatment a Bradenton woman endorses is called, “Singing Silly Girl Scout Songs in the Morning or Whenever.”
OK. We’re kidding. Peridia Golf and Country Club resident Carol Williams doesn’t really think singing Girl Scout camp songs will ever be a formal treatment for her Parkinson’s. But how can anyone discount the benefits of her intense laughter after belting out one of the old standards she recalls from her Girl Scout days?
“My mother cooked a chicken. She thought it was a duck,” Williams, 69, who has had Parkinson’s since 2013, sang out boldly in front of her care advisor from Neuro Challenge Foundation for Parkinson’s and her caregiver husband, Don.
“She put it on the table with the legs tied up!”

Read more here:
Carol Williams talks about Neuro Challenge Foundation for Parkinson’s~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Both Carol and Don Williams and their care adviser, Jennifer Williams, who is not related to them, all bent over with laughter.
This lighthearted and important moment surrounding Parkinson’s, which is a chronic and progressive neurological condition that impacts movement and thinking, occurred Wednesday in a small office opened on July 10 by Neuro Challenge at 3639 Cortez Road, Suite 104, Bradenton.
The office represents the organization’s first official expansion into Manatee County, an expansion that has occurred due to high demand, said Robyn Faucy, executive director of Neuro Challenge Foundation for Parkinson’s.
Neuro Challenge provides more than 30 monthly education, support and care advising programs for the Parkinson’s community in the area including nine monthly in Manatee County, all at no charge with no insurance billing, Faucy said.
A session of free one-on-one care advising, which the Williams were getting, is also free and by appointment, Faucy added.
“The care advisor sits down and walks a family through every aspect of the disease,” Faucy said. “They will be provided a resource guide and answer any questions they may have.”
In order to do these programs for free, the organization will raise roughly $500,000 this year, about half of that from an annual gala, Faucy added.
“Everything else is from individual contributions, foundation grants and a couple of other events,” Faucy said.
Carol Williams has no idea if it’s the Parkinson’s that is causing the old songs to spring to her lips or just happy memories. But she said she feels safe in sharing in this space.
“I try to stay happy most of the time and he’s right there with me,” Williams spoke about her caregiver husband, Don, to her counselor after the laughing subsided. “It’s always, ‘Whatever you want to do today we will do that.’ This poor guy. In the morning, after I am already up out of the bedroom and into the kitchen, I start singing my old Girl Scout songs, which are ridiculous. But at least he laughs, too.”

Read more here:

For the most part, Williams knows anything she says or sings in her Neuro Challenge private space stays there.

Meeting a Manatee demand

This expansion into Manatee happened because Neuro Challenge saw a need, Faucy said. 
People with Parkinson’s number an estimated 9,000 in Manatee, Sarasota and Charlotte counties, out of roughly 1 million who are afflicted nationwide, but the breakout of just Manatee sufferers is not known, Faucy said.
Neuro Challenge has made contact with roughly 2,000 of that 9,000 tri-county total and the number of those reaching out for its free services is growing rapidly, Faucy added.
“We saw the need because we had people from Manatee County coming to Sarasota to attend our various groups and activities,” Faucy added. “We saw an increase of the Manatee people we served from 2015 to 2016 of 38 percent. We realized, ‘There is a demand here. There is a need. We have to find a way to meet that need.’ ”
In 2016, Neuro Challenge started developing relationships with Manatee hospitals and neurologists to prepare for its expansion, Faucy said.
Right now, a bit more than halfway through 2017, Neuro Challenge, which will be celebrating its 10-year anniversary in 2018, has served the number of Manatee people it served in all of 2016, Faucy added.
Don Williams says the 7,000 who haven’t connected with Neuro Challenge are missing out on some important and free help.
“It has helped primarily by giving us a great deal of very helpful information to questions we might have,” Don Williams said. “But most of all it is support.” 
“They make sure I know I am not the only one with this disease and I am not alone,” Carol Williams said. “If I have to talk to someone I can pick up the phone at any time and call them. They will never shut you down. They will talk to you.”
Or sing with you.
To make an appointment for free care advising or for program information call Jennifer Williams at 941-266-5833 or
Richard Dymond: 941-745-7072@RichardDymond

Carol Williams meets with care advisor Jennifer Williams. Neuro Challenge Foundation for Parkinson's opened a new office in Bradenton due to growing client numbers. Tiffany Tompkins
Read more here: here:

Read more here:
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FoxFeed Blog: Did You Watch Our Facebook LIVE Chat with Jimmy Choi and Akbar Gbajabiamila?

By Cheryl Blowers  
Today The Michael J. Fox Foundation (MJFF) hosted a special Facebook LIVE event featuring an interactive conversation with Team Fox all-star Jimmy Choi and Akbar Gbajabiamila, host of NBC's Emmy-nominated American Ninja Warrior. On an episode that aired July 3, Jimmy inspired audiences worldwide when he ran the obstacle course and discussed his journey after being diagnosed with Parkinson's disease (PD) at age 27.  
During their live broadcast, Jimmy and Akbar discussed how exercise can be a critical part of living well with Parkinson's, the role family plays as symptoms change and taking a first step toward involvement with the PD community.   
If you're looking for more on the topics discussed, check out these resources:
Ask the MD: Parkinson's and Exercise: In this blog and video, Rachel Dolhun, MD, shares the benefits of physical activity for people with Parkinson's, how to stick with an exercise regimen and what the latest research says about exercise and PD.
Team Fox Athletics: The grassroots fundraising arm of the Foundation offers opportunities to set a fitness goal of any type and join a community of people dedicated to accelerating Parkinson's research. Take part in any of the athletic events listed or create your own challenge to help raise critical funds -- 100 percent of all Team Fox proceeds go directly to MJFF's mission to speed a cure.
Parkinson's 360: If you or a loved one have recently received a diagnosis of Parkinson's or have been living with PD for many years, this multimedia toolkit offers honest and relatable guidance on navigating the disease and its motor and non-motor symptoms. A downloadable book, online resources on topics such as diet and medication, and short, personal films (including one featuring Jimmy) can help patients and families chart their best course. 

And if you missed the conversation, you can watch it by going to:

Prana and Takeda Will Investigate PBT434 as Treatment for Gastrointestinal Damage in Parkinson’s


Prana Biotechnology and Takeda Pharmaceuticals International are teaming up to investigate whether Prana’s PBT434 can improve gastrointestinal damage associated with Parkinson’s disease.
PBT434 showed promise as a treatment for neuronal loss and movement problems in mice with Parkinson’s, according to a preclinical-trial study.
The collaboration will deal with whether PBT434 can improve non-motor symptoms, such as constipation, colon motility — or abnormal intestinal contractions — and inflammation.
“This early research is important because our major therapeutic objective is to treat these disabling symptoms and provide an early therapeutic intervention for both motor and non-motor Parkinsonian symptoms,” which may significantly impact quality of life, David Finkelstein, Prana’s senior scientific consultant, said in a news release.
The hallmark of Parkinson’s is loss of neurons, or nerve cells, which results in movement problems. Neuron loss also underlies non-motor symptoms of the disease, such as damage to the gastrointestinal system.
Researchers do not know how this happens. But they seem to believe that the clumping of the alpha-synuclein protein that is involved in Parkinson’s movement problems is involved in non-movement problems as well.
Earlier this month, a study that Prana sponsored showed that PBT434 prevented neuron loss in mice with Parkinson’s. The research, “The novel compound PBT434 prevents iron-mediated neurodegeneration and alpha-synuclein toxicity in multiple models of Parkinson’s disease,” was published in the journal Acta Neuropathologica Communications.
It showed that the drug improved brain levels of iron and prevented alpha-synuclein clumping. PBT434 also eliminated the clumped protein’s toxic effects. This included oxidative stress, which damages other cell molecules, leading to neuron loss.
PBT434 protected dopamine-producing neurons in mice’s substantia nigra brain region, which play a key role in movement coordination, researchers said. Neuron loss in that region is a feature of Parkinson’s. PBT434 also improved movement problems in mice with the disease.
Dopamine is a neurotransmitter, or chemical that conveys signals between neurons and other parts of the body. Loss of substantia nigra neurons affects the normal functioning of another region, the basal ganglia, which governs voluntary movements.

Study Identifies New Brain Death Pathway in Alzheimer’s Disease

Article ID: 678259
Released: 24-Jul-2017 11:00 AM EDT

First of its kind study may lead to new era of Alzheimer’s drug discovery and therapeutic targets

Credit: Deanna Dent, Arizona State University

Credit: Michelle Saldana, Biodesign Institute
In a new study published today, Arizona State University-Banner Health neuroscientist Salvatore Oddo and his colleagues from Phoenix’s Translational Genomics Research Institute (TGen) — as well as the University of California, Irvine, and Mount Sinai in New York — have identified a new way for brain cells to become fated to die during Alzheimer’s diseases.

Alzheimer’s disease tragically ravages the brains, memories and ultimately, personalities of its victims. Now affecting 5 million Americans, Alzheimer’s disease is the sixth leading cause of death in the U.S., and a cure for Alzheimer’s remains elusive, as the exact biological events that trigger it are still unknown.
In a new study published today, Arizona State University-Banner Health neuroscientist Salvatore Oddo and his colleagues from Phoenix’s Translational Genomics Research Institute (TGen) — as well as the University of California, Irvine, and Mount Sinai in New York — have identified a new way for brain cells to become fated to die during Alzheimer’s diseases.
The research team has found the first evidence that the activation of a biological pathway called necroptosis, which causes neuronal loss, is closely linked with Alzheimer’s severity, cognitive decline and extreme loss of tissue and brain weight that are all advanced hallmarks of the disease.
“We anticipate that our findings will spur a new area of Alzheimer’s disease research focused on further detailing the role of necroptosis and developing new therapeutic strategies aimed at blocking it,” said Oddo, the lead author of this study, and scientist at the ASU-Banner Neurodegenerative Disease Research Center at the Biodesign Institute and associate professor in the School of Life Sciences.
The findings appear in the advanced online edition of Nature Neuroscience
Necroptosis, which causes cells to burst from the inside out and die, is triggered by a triad of proteins. It has been shown to play a central role in multiple sclerosis and Lou Gehrig’ disease (amyotrophic lateral sclerosis, or ALS), and now for the first time, also in Alzheimer’s disease.
“There is no doubt that the brains of people with Alzheimer’s disease have fewer neurons,” said Oddo. “The brain is much smaller and weighs less; it shrinks because neurons are dying. That has been known for 100 years, but until now, the mechanism wasn’t understood.”
Links with Alzheimer’s
Necroptosis was first identified as a result of inflammation, a common malady in Alzheimer’s.
Three critical proteins are involved in the initiation of necroptosis, known as RIPK1, RIPK3 and MLKL. The study describes a key event in the process of necroptosis when RIPK1 and RIPK3 form a filamentous structure known as the necrosome.
The formation of the necrosome appears to jump-start the process of necroptosis. It activates MLKL, which affects the cell’s mitochondria, eventually leading to cell death.
Winnie Liang, TGen assistant professor, director of TGen Scientific Operations and director of TGen's Collaborative Sequencing Center, said MLKL executes necroptosis to ultimately cause cell death.
“In this study, we show for the first time that necroptosis is activated in Alzheimer’s disease, providing a plausible mechanism underlying neuronal loss in this disorder,” said Liang, who contributed to the study’s gene expression analyses.
To explore necroptosis, the research team utilized multiple cohorts of human samples obtained from the Brain and Body Donation Program at the Banner Sun Health Research Institute and Mount Sinai VA Medical Center Brain Bank.
First, they measured RIPK1, RIPK3 and MLKL in a specific region of the brain that is typically ravaged by cell loss during the advance of Alzheimer’s disease—the temporal gyrus. Results showed that during necroptosis, these markers were increased in the brains of people with Alzheimer’s disease.
Next, they identified the molecular cascade of necroptosis activation, with RIPK1 activating RIPK3 by binding with it. This protein complex then binds to and activates MLKL. Analysis of mRNA and protein revealed elevated levels of both RIPK1 and MLKL in the postmortem brain tissues of patients with Alzheimer’s when compared with normal postmortem brains.  
Furthermore, they also demonstrated that necroptosis activation correlated with the protein tau. Intriguingly, necroptosis did not appear to be linked with the other chief physiological characteristic of Alzheimer’s pathology, beta-amyloid plaque.
Engines of decline
To assess the relationship between necroptotic protein levels and cognitive health, the study revisited the scores of patients whose postmortem brain tissue was evaluated for necroptosis. Results showed a significant association between RIPK1, MLKL and diminished scores on the Mini-Mental State Examination (MMSE), a widely used test measuring cognitive health.
Given the established relationship between necroptosis and Alzheimer’s pathology, including cell loss and attendant cognitive deficit, the study sought to inhibit the process to study the dynamic effects on cell death and memory loss.
With such experiments not possible in people, the team demonstrated in a mouse model of the disease that lowering the activation of the necroptosis pathway reduces cell loss and improves performance in memory-related tasks, offering new hope for human therapeutics to halt or reverse the effects of Alzheimer’s.
The results reveal that the inhibition of necroptosis activation through the blockage of RIPK1 prevents cell loss in mice. Compellingly, mice with inhibited activation of necroptosis pathways performed significantly better in tests of spatial memory involving navigation through a water maze. 
New understanding, new hope
The study opens a new window on Alzheimer’s research and offers hope for therapies targeting cell loss in the brain, an inevitable and devastating outcome of Alzheimer’s progression.
Oddo stresses that RIPK1, RIPK3 and MLKL are among many potential drug targets, and others will likely follow as the links between necroptosis and Alzheimer’s become clearer. While multiple causes of the disease are likely, understanding more clearly all targets that trigger disease will offer the best hope since neuronal loss has been found in people more than a decade before any symptoms of dementia.
“One may not agree as to which molecules trigger Alzheimer’s disease, ” said Oddo, “but everybody agrees that the end result is the neuronal loss. If you can prevent that you may have a beneficial effect.” 
Media Contacts:
Joe Caspermeyer
Managing Editor
Biodesign Institute
Arizona State University

Steve Yozwiak
TGen Senior Science Writer

This work was supported by grants from the Arizona Alzheimer’s Consortium and the National Institutes of Health (R01 AG037637) to Salvatore Oddo, and R01 NS083801 and P50 AG016573 to Kim Green.
Data for the RIPK1 causal regulatory gene network were generated from postmortem brain tissue collected through the Mount Sinai VA Medical Center Brain Bank and were provided by Dr. Eric Schadt from Mount Sinai School of Medicine. The computational resources and staff expertise provided by the Department of Scientific Computing at the Icahn School of Medicine at Mount Sinai also contributed to the performance of this research.
Paper Title: Evidence for necroptosis activation in Alzheimer’s disease

Scientists capture first image of major brain receptor in action

July 24, 2017

Structures of the ion channel of the glutamate receptor in the closed (left, blue) and open (right, orange) states viewed parallel (top) or perpendicular (bottom) to the membrane, from the extracellular (synaptic) side. Credit: Sobolevsky lab/Columbia University Medical Center

Columbia University Medical Center (CUMC) researchers have captured the first three-dimensional snapshots of the AMPA-subtype glutamate receptor in action. The receptor, which regulates most electrical signaling in the brain, is involved in several important brain activities, including memory and learning.
The findings were published today in Nature.
"With our new findings, we can now, for the first time, visualize how the  opens  ion channels," said Alexander Sobolevsky, PhD, associate professor of biochemistry and  at Columbia and senior author of the paper. "This is the fundamental process that directly affects learning and memory, and finding its structural determinants has been the primary goal of molecular neuroscience since the '90s."
Most signaling in the brain is triggered by , a neurotransmitter that activates proteins on the surface of neurons called glutamate receptors. Glutamate receptors underlie a variety of high cognitive functions, including learning and memory. AMPA receptors are glutamate receptors that open and close very quickly—in less than a millisecond—and are involved in fast processes in the brain, such as the rapid perception and reaction of an organism to its surrounding environment.
Previously, the Sobolevsky lab deciphered the structures of the AMPA receptor alone and in complex with other proteins that regulate the speed and strength of synaptic connections. In the current study, the researchers captured the AMPA receptor in action, as glutamate activates the receptor to allow ions to flow through its channel and initiate signaling in the brain. This provides the first precise insights into how receptors mediate brain function.

Cryo-electron micrograph (left) and 3-D structural reconstruction (right) of the activated glutamate receptor synaptic complex with stargazin (STZ). Credit: Sobolevsky lab/Columbia University Medical Center

To freeze the AMPA receptor in an active state, the researchers fused it with stargazin, a regulatory protein that prompts the channel to open. The images they captured show that when signaling molecules such as glutamate are present, the entrance to the AMPA receptor, which consists of four units, opens up like a camera's iris, or aperture, to reveal its pore. To shepherd the ions through, the receptor widens the diameter of its channel, and a specialized channel pore lining ushers the ions into the cell.
"These new fundamental discoveries have implications for our understanding of neurotransmission by glutamate, our brain's major neurotransmitter" says Edward C. Twomey, a PhD candidate at CUMC and first author of the paper. "Understanding these processes will impact future studies on glutamate receptor signaling in neurodegenerative diseases as well as drug design."
To study the receptor, Sobolevksy's team used cryo-electron microscopy, a technique that captures an array of two-dimensional images of a molecule and combines them into a three-dimensional structural image. The method was pioneered by co-author Joachim Frank, PhD, professor of biochemistry and molecular biophysics and of biological sciences at CUMC.
Defects in glutamate , or the processes they mediate, are implicated in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis and glaucoma; psychiatric disorders such as anxiety, depression, schizophrenia, and drug use disorders; as well as in acute disorders such as  trauma and stroke. The new structure of an active AMPA receptor and understanding of the activating mechanism create a solid platform for developing therapeutics to treat neurological disorders that are associated with glutamate receptor dysfunction.
More information: Edward C. Twomey et al. Channel opening and gating mechanism in AMPA-subtype glutamate receptors, Nature (2017). DOI: 10.1038/nature23479 
Journal reference: Nature

Mitsubishi Tanabe bags NeuroDerm and its PhIII Parkinson’s program for $1.1B

July 24, 2017 By John Caroll

Masayuki Mitsuka —President Mitsubishi Tanabe

Mitsubishi Tanabe is gobbling up the Israeli biotech NeuroDerm $NDRM, offering an early morning taste of the M&A activity that has been woefully short in the industry so far this year.
The Japanese pharma company agreed to pay $1.1 billion for the biotech, which has been developing a lead program for continued dosing of levodopa/carbidopa for Parkinson’s patients. That’s $39 a share, or a 79% premium over the unaffected early June price.
NeuroDerm’s biggest accomplishment has been developing a liquid formulation of levodopa/carbidopa that could be continuously delivered via a wearable pump. The Japanese buyer thinks this will fit well with Radicava, its newly approved ALS drug that is being launched next month in the US. NeuroDerm is also developing apomorphine, a mid-stage program for Parkinson’s, and a transdermal patch for CNS diseases and cognitive disorders.
Peter Wellford at Jefferies has been a keen advocate of the company’s prospects, projecting peak sales of its late-stage ND0612 at $1.7 billion – provided it gained an approval.
Wellford noted today:
Both ‘0612L/H are liquid formulations of the current Parkinson’s disease (PD) standard-of-care L-dopa/carbidopa as NeuroDerm has circumvented challenging chemistry to overcome the short half-life and poor bioavailability that has plagued L-dopa oral use. A convenient, continuous infusion of L-dopa could offer substantial clinical benefits for more advanced PD patients, avoiding the fluctuations of peak-dose dyskinesias and wearing-off, plus the potential for improved quality of sleep and delayed morning “on” given night-time dosing. We forecast $1.7bn WW peak sales, including $900m in the US. Assuming 50% probability of success, arguably overly cautious given the products’ profile, and late-2019E launches we derive a $37/share NPV.
Just a few weeks ago investigators outlined data indicating that the new dosing approach was effective in reducing “off” times for patients.
Most analysts started the year looking for a boost in the level of M&A deals in biopharma this year. But aside from the Ariad and Actelion buyouts along with a short string of smaller deals like this, the big buyers have not been eager to pay large premiums for new experimental products.