HEALTHY LIFESTLYES: Exercise key for those with Parkinson’s disease

• by  Angela Cowan - Peninsula News Review
• posted May 14, 2015 at 12:00 PM

ParkinGo Wellness Society’s exercise classes run three times a week at the Greenglade Community Centre in Sidney and are designed specifically for people with Parkinson’s Disease. 

— Image Credit: Angela Cowan

One of the biggest challenges for people with Parkinson’s disease, says former physiotherapist Jillian Carson, is the tendency to withdraw from the world because of the stigma associated with movement-based disabilities, but her exercise classes are aiming to help break that isolation.

“The biggest thing with people with Parkinson’s disease, is that we isolate ourselves,” she says.

Even their body language changes, she adds. Shoulders start to hunch in, feet drag on the ground, voices get muffled and quiet.

Carson, 55, was diagnosed with Parkinson’s in 2009 and experienced the changes firsthand, and when she heard about a Parkinson’s-specific exercise regime that an American neuroscientist was researching, it sparked a big interest.

She became entrenched in the Parkinson’s community, creating a video about her own journey that was shown at the opening ceremonies of the 2013 World Parkinson Coalition. Soon, Carson became a Parkinson’s Wellness Recovery Therapist, and founded the ParkinGo Society — which just recently gained registered charity status — and started up a class in 2012, with some tweaks of her own to include cognitive exercises as well.

The physical portion is high intensity, and Carson and the other instructors lob questions around like the rubber balls used in their warm-ups to build the relationship between muscle movement and brain activity.

The group counts down from 100 by sevens, or lists off what they had for breakfast yesterday as they keep their bodies moving, and the results are astounding.

“By the time they’re leaving, their writing is normal,” says Carson. “They’re smiling, and everyone is laughing and giggling. They’re doing more all of a sudden, and they’re living again.”

Several people have reduced their medications, like George Brown, a regular who’s had Parkinson’s for 20 years. Since starting the exercise class Brown has gone from nine meds to three, and no longer has to use either of his canes.

Another woman came in using walking sticks, and eight months later, she was running. Carson herself has halved her medication since beginning the regime.

“It is so remarkable what exercise can do for us,” says Carson. “I’ve got to share this with people.”

Caregivers and family or friends are more than welcome to join the classes as well, says Carson. The important thing is to get out and get moving.

“Our lives have changed from having the exercises,” she says. “It’s never too late. Never.”

The exercise classes run Mondays, Wednesdays and Fridays from 12:30 to 1:30 p.m. at Greenglade Community Centre, 2151 Lannon Way in Sidney.

For more information, visit parkingo.org, or crd.bc.ca/panorama/facilities/greenglade-community, or call Greenglade Community Centre at 250-656-7055.

http://www.peninsulanewsreview.com/lifestyles/303777421.html

The PD You Don't See: Cognitive and Non-motor Symptoms in Parkinson's

Accepting Parkinson's

Shocked by diagnosis, former educator decides to confront disease head-on

By WILLIAM D. DOWNS JR. Special to the Democrat-Gazette

Posted: May 18, 2015 at 1:53 a.m.

William Downs Jr. has found that exercise and support networks are vital components of living with Parkinson’s.By John Sykes Jr.
Credit: Arkansas Democrat-Gazette

Being the cockeyed optimist that I am, I never paid much attention to the occasional ribbing I received from good-natured colleagues at Ouachita Baptist University who accused me of shuffling when I walked down the hallways in our mass communications department.

Enlarge

William Downs and his wife, Vera, recently relocated to a retirement community in Bryant. (By: John Sykes Jr.)(Credit: Arkansas Democrat-Gazette)

About three years ago, however, I was trotting along on Feaster Trail in Arkadelphia when suddenly I was moving much faster than I intended and could not slow down. I also was about to faint.

A few yards ahead of me was an iron gate that I knew I had to reach before collapsing.

Moments later, gasping for breath, I crashed into it.

An OBU student who had been running a few steps behind me, yelled, "Way to go, Dr. Downs!" I suppose he mistook me for an out-of-control athlete.

I thanked him for helping me get back on my feet; we had a good laugh, and he drove away. Minutes later I made an appointment with my family physician, Dr. Noland Haygood. At that appointment, he referred me to a neurologist in Little Rock.

When I told the neurologist what had happened, he asked me to walk to the end of the hall outside his office and then to walk back toward him. When I returned, he said, almost triumphantly, "I know what your problem is. You have Parkinson's disease!"

"How did you know that so quickly?" I asked.

"Because you were shuffling," he replied.

Returning to Arkadelphia later that afternoon, I'll admit, I was asking myself, "Why me, Lord?" To my surprise, I immediately answered my own question: "Why not me?" Still, I was frightened by the unknowns that lay ahead. This was not a bad dream but a terrifyingly real illness to someone -- me -- who at 80 had never suffered a really serious illness.

Checking the Internet for a definition of Parkinson's disease, I found it described as "a progressive illness" (keeps getting worse) and incurable.

Rushing back to Haygood the next day, I asked him how I should handle what felt like life-shattering news. He quietly responded with one word -- "Acceptance."

He was right. From that moment on, whenever I begin to worry, I immediately recall his advice, and it always works to calm my fear.

WHAT'S AILING ME?

What is Parkinson's disease?

"Parkinson's disease is a progressive, neurodegenerative disorder that affects movement, muscle control, as well as numerous functions," according to the consumer-information website Medifocus (parkinsonsdisease-guidebook.com). "It is part of a group of conditions known as motor systems disorders. Parkinson's was named for James Parkinson, a general practitioner in London during the 19th century who first described the symptoms."

According to the Parkinson's disease pages on the National Institutes of Health's National Institute of Neurological Disorders and Stroke website, the hallmark symptoms are:

• Asymmetric tremors at rest, that is, tremors or trembling in hands, arms, legs, jaw or face on one side of the body but not the other;

• Rigidity, or stiffness of the limbs and trunk;

• Bradykinesia, or slowness of movement;

• Postural instability or impaired balance and coordination.

"There is currently no cure for PD; it is always chronic and progressive," the Medifocus website says, "meaning that the symptoms always exist and always worsen over time. The rate of progression varies from person to person, as does the intensity of the symptoms.

"Parkinson's disease itself is not a fatal disease, and many people live into their later years. Mortality of PD patients is usually related to secondary complications, such as pneumonia or falling-related injuries."

WHAT ARE THE CAUSES?

"PD is caused by a lack of the chemical messenger dopamine in the movement centers of the brain. The lack of dopamine -- a neurotransmitter acting within the brain to help regulate movement and emotion -- is a result of the death of dopaminergic neurons in these brain regions," said Chase Lambert of Bryant (full disclosure: my grandson), who is scheduled to earn his doctorate in neuroscience and pharmacology this summer from the University of South Florida in Tampa.

"I think it's important," he added, "to make the distinction that PD isn't just a result of not having enough dopamine. The underlying cause is that the neurons in the brain's movement centers that produce and use dopamine die, which leads to an overall decrease in the amount of dopamine being produced/used, and this leads to the motor dysfunction."

If the disease was simply due to a lack of dopamine, he said, it could be slowed or stopped using medications that increase dopamine levels (such as levodopa, aka L-DOPA). Levodopa does help people with their symptoms but it doesn't cure the underlying problem: the death of the neurons that use dopamine as a neurotransmitter in these brain motor regions.

"It will take a better understanding of what causes PD as well as a method by which to identify people with pre-PD symptoms to develop a therapy that can reverse or slow the death of dopaminergic neurons," Lambert said.

Besides a lack of dopamine, Parkinson's can be aggravated by exposure to pesticides or industrial toxins, a family's genetic history and the process of aging itself.

AGE AT ONSET

I am relatively old for a newly diagnosed Parkinson's patient, but the disease usually affects people older than 60, according to the national institute's website.

According to the Michael J. Fox Foundation for Parkinson's Research, the average age at onset of symptoms is 60, although some people have been diagnosed as young as age 18. The actor Michael J. Fox was in his 30s when he disclosed his condition to the public.

His foundation's website states that with no objective test for the condition, the rate of misdiagnosis could be high, and therefore estimates of how many Americans have Parkinson's "vary." The foundation estimates the disease affects about a million Americans.

So how is Parkinson's disease diagnosed? Because there are no specific laboratory tests, "doctors make the diagnosis based on the presence of typical signs and symptoms," according to an article on parkinsons.about.com written by neurology researcher Patrick McNamara of the Boston University School of Medicine.

He notes that the primary movement (or motor) symptoms can include slowness of movements, muscle rigidity (stiffness), resting tremor (shaking), impaired balance and posture, incontinence, difficulty in smelling or speech, loss of fine motor control (such as writing or buttoning a shirt), decreased arm swing, decreased facial expression or difficulties in speech, and, as previously noted, "a shuffling gait."

"If you have PD," McNamara writes, "you are probably aware that people ask you to repeat what you just said more than they used to. Speaking clearly and intelligibly becomes a little more difficult when you have PD. While 80 percent of people with PD experience some type of speech problems, fewer that 5 percent seek treatment for those problems.

"This is unfortunate since effective treatments are available for speech, voice and language problems."

Older students in the Berean Sunday School class I taught for 25 years at First Baptist Church in Arkadelphia began to complain that they could not hear or understand me, and so I contacted the speech therapy department at OBU where I received excellent vocal training. It worked.

WILL IT BE CURED?

My grandson assures me there are some very promising treatments, including levodopa drug therapy, other drug therapies, physical therapy and surgery. I can read about the latest research developments at parkinson.org/whatshot.

For instance, in March, Dr. Michael Okun, national medical director of the National Parkinson Foundation, posted "Everything a Parkinson's Disease Patient Needs to Know About the New Dopamine Pump."

"One of the common dreams shared by Parkinson's disease patients around the globe," Okun begins, "is the possibility of living a pill-free existence. One year ago we shared the news of a therapy coming to the United States with the possibility to make this a reality for a select group of patients. The therapy has received a full FDA approval and will be sold under the name Duopa (AbbVie, USA).

"One cannot blame the Parkinson's disease patient or caregiver for dreaming big," Okun continues. "A single day living in Parkinson's disease shoes is not uncommonly accompanied by the need for dozens of pills. In many cases, pills are taken as frequently as every hour or two. If you ask Parkinson's disease patients to place an entire pill regimen for the day into the palms of their hands, there is a very good chance that they will not be able to hold all of the tablets and capsules."

Okun cautions that in two decades of once-promising research, deep brain stimulation failed to replace medications. But the dopamine pump looks like a comer. Okun writes, "Entering the market in the coming weeks is a new dopamine pump. The pump strategy offers the possibility for constant stimulation of the brain's dopamine receptors through the use of a continuous dopamine infusion pump technology."

LIFE GOES ON

"It is possible to live an active life with PD," McNamara writes. "If you take advantage of the best treatment options for you, maintain an exercise regimen as best you can, and create and use a support network, you will increase your ability to remain independent and to live a pretty normal life. Learn as much as you can about PD and allow yourself to accept help from others when you need it. It's also a must to make your family and friends aware of this new term in your life."

Echoing Haygood's advice, McNamara writes, "For most people with Parkinson's disease, acceptance is an emotional necessity. Acceptance allows them to be more available emotionally to their family and friends, to more easily plan for the future and helps patients to stay on track with respect to the treatment plan their doctor recommends."

Acceptance opens the gate and helps me move forward.

Bill Downs is professor emeritus of mass communications at Ouachita Baptist University, where he taught for more than 40 years. He is also the author of two books, The Fighting Tigers and Stories of Survival: Arkansas Farmers During the Great Depression.

http://health.einnews.com/article/265982428/jbjaiIC5-SBPDvKt

Scientists awarded £90,000 to unlock the secrets behind Parkinson's

STV 

18 May 2015 10:11 BST

TO SEE VIDEO:

 http://news.stv.tv/tayside/1320799-scientists-get-90000-to-unlock-secrets-behind-parkinsons-at-dundee/

The team from Dundee University will use state-of-the-art technology to study how a gene linked to Parkinson's affects cells in the brain.The money has been awarded by Parkinson's UK, the country's leading charity supporting those with the condition

One in 500 people in the UK have the degenerative neurological condition, which can leave them struggling to walk, speak and sleep.It affects around 10,000 Scots, including comedian Billy Connolly, but as yet there is no known cure.

Parkinson's occurs when nerve cells in the brain start to die, however the original cause of the disease remains unknown. Many believe that if the cause can be found, a cure will soon follow.

The three-year project at Dundee University will focus on a gene known as PINK1, which has been linked to Parkinson's, in a bid to see if it causes the disease.

PINK1 is vital for protecting mitochondria, the power-houses of cells. The scientists will investigate what happens when brain cells no longer respond to PINK1, and if this can lead to Parkinson's.

Dr Miratul Muqit, the lead researcher on the project, said: "In a cell you will see thousands of pathways, but we want to find the crucial ones.

"PINK1 is a gene that causes changes in the cells and we want to know if these changes disturb an essential pathway.

"We hope to create a road map of the pathways vital for the survival of brain cells. This way we can better understand how to diagnose and treat the condition."

Dr Arthur Roach, director of research and development at Parkinson's UK, said: "Understanding the role of genes in Parkinson's could be the key to discovering what causes some people to develop Parkinson's, something that has remained unknown for so long.

"Funding projects like this in Dundee is crucial if we are to progress in our research and one day find a cure."

http://health.einnews.com/article/265997130/cZfJQPg3I4B0wg5h

Scientists to use iPS cells to develop method to treat Parkinson's disease

The Asahi Shimbun

Toggle

By AKIYOSHI ABE/ Starff Writer

Researchers at Kyoto University are set to begin clinical studies, possibly as early as next year, to verify a cell replacement therapy that uses human induced pluripotent stem (iPS) cells to treat Parkinson’s disease.

It would be the first time for nerve cells developed from iPS cells to be transplanted into the human brain.

The team at the university’s Center for iPS Cell Research and Application (CiRA), headed by stem cell pioneer Shinya Yamanaka, will apply for the project's approval in June from a review committee to be created within the university.

If the cell replacement therapy is proven to be effective, it could lead to the discovery of a cure for the degenerative disorder of the central nervous system. There currently are about 150,000 patients with Parkinson’s disease in Japan.

Parkinson’s disease damages dopamine-producing nerve cells, or neurons, in the brain. Although symptoms of the disease can be treated with conventional medicine, there is no cure for Parkinson’s.

Scientists are investigating how cell replacement therapy could be used to treat the disease. Clinical trials to transplant healthy nerve cells taken from deceased infants into patients’ brains have been performed overseas.

But the efficacy of such treatment has not been authenticated because of the difficulty of obtaining a sufficient amount of healthy nerve cells. Also, donated cells contain a variety of cells that are not dopamine-producing neurons.

According to a project developed by Jun Takahashi, a professor of neurosurgery at CiRA, the team will produce dopamine-producing nerve cells from iPS cells that are created from a patient’s own cells.

The synthetic neurons will then be injected into the central area of the patient’s brain at a precise location.

The main purpose of the project is to determine if such cell replacement treatment can be damaging to a patient’s health. But if the transplanted neurons function effectively, they could halt progress of the disease’s symptoms.

Because unwanted neurons can be produced in the process of formulating synthetic cells, the team has already developed a method to sort out useful neurons from a large amount of nerve cells. Animal tests have already proven the effectiveness of the neuron-screening method.

Transplanted iPS cells can also multiply prolifically in the human body and cause cancer and other tumors when they are transplanted before they develop into specific types of cells.

To confirm the safety of the transplantation of iPS-originated cells, a team of researchers at the Riken Center for Developmental Biology is currently conducting the world’s first clinical study to transplant retina cells produced from iPS cells into patients’ eyes.

Unlike retina cell transplantation, the transplantation of neurons in human brains will require image diagnostic methods, including magnetic resonance imaging (MRI), to observe the effectiveness of the treatment.

Kyoto University’s review committee will take six months or longer to discuss safety measures for the observation methods and other issues before approving the clinical trial for Parkinson’s disease treatment.

After it obtains the committee’s approval, the research team will begin preparation for producing iPS-originated nerve cells to be used in clinical tests. If the clinical trials deliver the expected results, the team plans to apply for further clinical trials based on the pharmaceutical and medical device law so that the treatment will be applicable to insurance.

http://health.einnews.com/article/265757930/DPMY8cLhvbBrlR9w

Parkinson's disease increasing, but so are better treatments

Friday, May 15, 2015

JON-MICHAEL SULLIVAN/STAFF

Dr. David Standaert, professor and chair of neurology at the University of Alabama at Birmingham, gives a presentation during the "Know More; Live More: Parkinson's 101" event presented by the Georgia Regents Neuroscience Center held at the Kroc Center in Augusta.

There is a “tsunami” of new Parkinson’s disease cases that will hit the U.S. in coming years as the population ages overall, an expert told the audience at a Georgia Regents Health System forum on Friday.But better treatments and new insights into the way damage may spread in the brain could help stem that tide.

Dr. David Standaert, director of the Center for Neurodegeneration and Experimental Therapeutics at the University of Alabama at Birmingham, spoke to a forum for patients and caregivers hosted by Georgia Regents Neuroscience Center.

Risk for Parkinson’s increases with aging, with an average of one case per 100 at age 65 but two or three per 100 at age 85, he said. With the Baby Boomer population just now hitting their 60s, the number of people with Parkinson’s is expected to increase from 1.5 million now to 4 million within the next 25 years, Standaert said.

“We’re going to see a tsunami of Parkinson’s disease as a result of the aging of the population,” he said. “We need to have better treatments for this or we’re going to have a very serious problem.”

Parkinson’s patients have long had treatments that can really help them, notably the drug levadopa and carbidopa, and more recently electrical deep brain stimulation, which makes it different from many other neurodegenerative diseases, Standaert said.

In the last year, it has seen three new treatments, including a gel form for levadopa and carbidopa delivered by an infusion pump directly into the gastrointestinal tract that can provide a “leveling out” of drug relief for patients, Standaert said.

But future treatments could come from a better understanding of not only what causes Parkinson’s disease but what really causes the damage and makes the disease progress from year to year. An excess of a particular 

protein called alpha-synuclein is known to accumulate in the brains of Parkinson’s patients and is thought to misfold and clump together, similar to what is thought to happen in the brains of Alzheimer’s patients with another type of protein.

Standaert and others believe these clumped, misfolded proteins can travel through the brain and cause an inflammatory reaction there.

“Synuclein is the upstream culprit of the thing that actually is killing neurons and producing the damage,” he said. While there are other causes, from genetics to the environment, of why people start to develop Parkinson’s, “I think once you trigger that, then that’s where inflammation becomes important,” Standaert said. “The cause is upstream but inflammation is what makes it worse from year to year.”

There are other diseases where there are drugs to fight an improper immune response in the brain, such as lupus or multiple sclerosis, so even if the cause is different some of the treatments might eventually be beneficial, he said.

“I think there could be a convergence in treatments, absolutely,” Standaert said.

His own lab has used a mouse model to knock out a key immune protein that found where synuclein was not toxic to those animals. While that is not possible in humans, Standaert’s lab has targeted the gene that controls that protein and has a grant from the Michael J. Fox Foundation for Parkinson’s Research to explore whether that could be a target for interventions.

But part of the problem will also be just getting the correct diagnosis in the first place.

Marilyn Sullivan, of Aiken, noticed years before her husband, Robert, was diagnosed with Parkinson’s that he was shuffling his feet and she was having trouble hearing him. She bought him new shoes and took him around to different specialists before he was finally diagnosed two years ago.

“No one ever mentioned Parkinson’s,” she said. Dr. Kapil Sethi, director of the Georgia Regents Movement Disorders Program, told her she shouldn’t feel bad it took so long.

“You did your job,” he said. “It’s a common problem” with the diagnosis.

http://health.einnews.com/article/265709286/cDuNcheGGHypvWKC

A LITTLE TIDBIT OF INFORMATION

OUGH & GAG: Oh, that pesky phlegm!

Sherryl Klingelhofer

September 17, 2012 at 11:10am

Dad had so much trouble with it, and I know others who do, too...

Here’s an idea if you are already dealing with this common Parkinson’s problem! 

We had a Physical Therapist show us an exercise to help the body "remember" how to swallow that helped Dad clear his throat a bit.  Doesn't get RID of the phlegm, but made it easier to deal with.

• SIT UPRIGHT---make sure the head is over the torso and the torso is not leaning back or in a concave shape that would curve the esophagus or compromise the entry in the throat.  If needed, put a small pillow or rolled towel behind the spine against the back of the chair to assist upright posture!

• Cough.  Drink a SIP of water.  Cough. (you may need to swallow---do so with or without the sip of water)

• Wait and repeat about half a dozen times.  Do this a couple times daily in between meals, but also try it BEFORE eating to jump start the brain...

That laying back in a bed or lounge chair is a real booger (we might just as well stay in icky-mode)!  It lets the phlegm sit right on the "swallower", so positioning is really important!  Next time you start the choking, shove your hips back into the chair and lean slightly forward to cough/swallow.

…………………………
You can practice opening and closing the throat if swallowing is being compromised!  And since you never think about keeping the muscles in the throat active, until after the fact, begin these now to avoid future issues!

• Say “X” then “R” several times (yes, out loud so it can be heard!)---do it slowly and pretend you telling someone how to enunciate and say them correctly!

• Say “QUICK-QUACK-QUIRK” several times as above

• Make a fire engine noise by saying (loudly!)  “rrr-RRR-rrr-RRR-rrr-RRR” and make it go up and down as they do:  you will feel your throat at work!

Nerve cells in the fast lane

Last updated: Friday 15 May 2015 at 12am PST 

Dopamine-producing neurons  important function in the brain

Nerve cells that produce dopamine for the purpose of transmitting signals to other cells affect numerous crucial brain functions. This becomes evident in diseases such as Parkinson's and schizophrenia, where dopamine transmission in the brain is impaired. In collaboration with researchers from Bonn, RUB scientists at the Mercator Research Group "Structure of Memory" have now identified in what way a specific form of this important cell is generated and which networks it forms in the course of brain development. In the process, the researchers discovered a data highway of sorts: the nerve cells use not only dopamine for signal transmission, but also the much-faster glutamate. The results have now been published in the trade magazine Nature Neuroscience.

Crucial role in signal transmission

Dopamine-producing neurons fulfil a crucial role in signal transmission: as the brain develops, they mature into several specialised subtypes, which, acting as a kind of networkers, generate synapses to other important brain regions. Their name derives from the fact that they utilise dopamine as a messenger. This neurotransmitter is very important: it affects, for example, motor control, reward behaviour, motivation and impulse control. Symptoms of diseases such as Parkinson's and schizophrenia include dying of dopamine neurons resp. disruption of dopamine signal transmission.

Glutamate facilitates rapid signal transmission

In collaboration with colleagues from the German Center for Neurodegenerative Diseases (DZNE), the Life & Brain Center Bonn and the Mercator Research Group "Structure of Memory", scientists at Bonn University discovered a data highway of sorts in the animal model. While dopamine-aided signal transmission between neurons is relatively slow, the analysed dopamine-producing neurons have additionally used glutamate as a messenger.

Researchers excited single nerve cells with light stimuli

Using genetic-engineering methods, the researchers coupled the dopamine-producing neurons of mice with light-sensitive proteins. Thus, they were able to excite individual dopamine-neurons with light stimuli and track the signalling pathways. With the aid of glutamate, locally inhibiting neurons were activated in the prefrontal cortex, a control centre in the brain. These, in turn, are responsible for the regulation of signal transmission in the prefrontal cortex: they are involved, for example, in deciding if a signal should be forwarded. In order to identify in what way different subtypes of dopamine-producing neurons are generated, the researchers muted one gene in mice. Thus, the formation of dopamine-neurons in the prefrontal cortex was suppressed.

Mice had to nudge a blinking light

What were the consequences of the lack of dopamine-producing cells? Together with the team headed by Prof Dr Magdalena Sauvage from Ruhr-Universität Bochum, the researchers from Bonn tested this in attention experiments. Mice were rewarded with food if they nudged a rapidly blinking light as quickly as possible. "The results have shown that animals in which the dopamine-producing cells had been genetically switched off didn't demonstrate any apparent changes to their attention and impulse control, but they pursued acquired behaviour patterns much more persistently," says Prof Sauvage. A pathological clinging to certain notions or repeating words and movements in an unsuitable context does also occur in mental disorders such as obsessive-compulsive disorder or schizophrenia, where the function of the prefrontal cortex is disturbed. Accordingly, the results of the research cooperation contribute to an improved understanding of the development and function of dopamine-producing neurons and possibly the diseases related thereto.

http://www.medicalnewstoday.com/releases/293853.php?tw

Amarantus Announces Successful Delivery and Distribution of MANF in Preclinical Model to Brain Areas Involved in Parkinson's Disease

SAN FRANCISCO and GENEVA, May 15, 2015 (GLOBE NEWSWIRE) 

-- Amarantus BioScience Holdings, Inc. (OTCQB:AMBS), a biotechnology company focused on developing therapeutic and diagnostic products for neurological disorders and orphan indications, announced that it has completed a study of mesencephalic-astrocyte-derived neurotrophic factor (MANF) administration to the putamen and the substantia nigra of pigs by convection-enhanced delivery. This study generated MANF brain delivery and distribution data, further supporting the rationale for MANF's development in the treatment of Parkinson's disease (PD). The study was conducted in the United Kingdom in collaboration with Renishaw plc's (LON:RSW) Neurological Applications Department and its leading academic partner, Functional Neurosurgery Research Group at the University of Bristol.

In previously reported studies, MANF has been demonstrated by multiple laboratories to be neuroprotective and neurorestorative in rat models of Parkinson's disease. The current study demonstrated that: (i) MANF can be delivered to the porcine putamen and substantia nigra, brain areas centrally involved in PD, and (ii) that pharmacologically efficacious levels are achieved using Renishaw's convection-enhanced delivery device currently in human clinical development. The porcine brain is considered a good model to evaluate the feasibility of delivering therapeutic agents to the human brain, as it has a significantly larger brain volume than that of a rat or non human primate (NHP). These data demonstrating accurate surgical targeting and distribution of MANF mark an important step in the development of MANF for the treatment of PD.

"We are very encouraged by this important set of data demonstrating that MANF can be delivered to the brain with great accuracy," said Gerald E. Commissiong, President & CEO of Amarantus. "MANF was precisely delivered to sites of the brain affected by Parkinson's disease and the volume of distribution was thought to be sufficient to elicit a treatment effect. This data further positions Amarantus in the Parkinson's disease space, as we are preparing to initiate our Phase 2b small molecule program of our lead product candidate, eltoprazine, in Parkinson's disease levodopa-induced dyskinesia and continue with the development of MANF as a potential disease-modifying treatment for PD."

In the study single bilateral catheters were implanted into the putamen and the substantia nigra, respectively. High accuracy to within 0.5 mm of the planned target was demonstrated by post-operative magnetic resonance imaging (MRI) while infusing Gadolinium-DTPA (Gd) during real-time scanning. MANF was administered to the porcine brain target sites 14 days later by convection-enhanced delivery. No evidence of reflux was detected. Immuno-staining on serial axial and coronal sections combined with volumetric analysis demonstrated MANF distribution volumes of 307 mm³ and 105 mm³ for the putamen and the substantia nigra, respectively. The observed distribution in porcine putamen was comparable to the one required to elicit neuroprotection in the rat PD model. Moreover, MANF and Gd distribution volumes correlated well and Gd did not appear to alter MANF's pattern of distribution. The Company believes these data provide a firm basis for studies in NHPs as well as subsequent human clinical trials.

The Company expects to publish further data from this study in peer-reviewed journals and at scientific congresses over the course of 2015.

About Parkinson's Disease

Parkinson's disease is a chronic, progressive neurological disorder that causes motor symptoms such as tremors, rigidity and slowed movements as well as non-motor symptoms including cognitive impairment and autonomic dysfunction. The Parkinson's Disease Foundation estimates that there are approximately one million people living with PD in the United States and seven to ten million PD patients worldwide. The most commonly prescribed treatments for PD are levodopa-based therapies. There is currently no cure available for Parkinson's disease.

About Mesencephalic-Astrocyte-derived Neurotrophic Factor (MANF)

MANF (mesencephalic-astrocyte-derived neurotrophic factor) is believed to have broad potential because it is a naturally-occurring protein produced by the body for the purpose of reducing and preventing apoptosis (cell death) in response to injury or disease, via the unfolded protein response. By manufacturing MANF and administering it to the body, Amarantus is seeking to use a regenerative medicine approach to assist the body with higher quantities of MANF when needed. Amarantus is the front-runner and primary holder of intellectual property around MANF, and is initially focusing on the development of MANF-based protein therapeutics. MANF, a naturally-occurring protein that reduces and prevents apoptosis (programmed cell death) in response to injury or disease, was discovered utilizing Amarantus' proprietary PhenoGuard^™ Protein Discovery Engine.

MANF's lead indication is retinitis pigmentosa, and additional indications including Parkinson's disease, diabetes and Wolfram's syndrome are currently being pursued. Further applications for MANF may include Alzheimer's disease, traumatic brain injury, myocardial infarction, antibiotic-induced ototoxicity and certain other rare orphan diseases currently under evaluation.

About Amarantus BioScience Holdings, Inc.

Amarantus BioScience Holdings (AMBS) is a biotechnology company developing treatments and diagnostics for diseases in the areas of neurology, psychiatry, ophthalmology and regenerative medicine. AMBS' Therapeutics division has development rights to eltoprazine, a Phase 2b ready small molecule indicated for Parkinson's disease levodopa-induced dyskinesia, adult ADHD and Alzheimer's aggression, and owns the intellectual property rights to a therapeutic protein known as mesencephalic-astrocyte-derived neurotrophic factor (MANF) and is developing MANF-based products as treatments for brain and ophthalmic disorders. AMBS' Diagnostics division owns the rights to MSPrecise^®, a proprietary next-generation DNA sequencing (NGS) assay for the identification of patients with relapsing-remitting multiple sclerosis (RRMS) at first clinical presentation, has an exclusive worldwide license to the Lymphocyte Proliferation test (LymPro Test^®) for Alzheimer's disease, which was developed by Prof. Thomas Arendt, Ph.D., from the University of Leipzig, and owns intellectual property for the diagnosis of Parkinson's disease (NuroPro). AMBS also owns the discovery of neurotrophic factors (PhenoGuard^™) that led to MANF's discovery.

For further information please visit www.Amarantus.com, or connect with the Company on Facebook, LinkedIn, Twitter and Google+.

Forward-Looking Statements

Certain statements, other than purely historical information, including estimates, projections, statements relating to our business plans, objectives, and expected operating results, and the assumptions upon which those statements are based, are forward-looking statements. These forward-looking statements generally are identified by the words "believes," "project," "expects," "anticipates," "estimates," "intends," "strategy," "plan," "may," "will," "would," "will be," "will continue," "will likely result," and similar expressions. Forward-looking statements are based on current expectations and assumptions that are subject to risks and uncertainties which may cause actual results to differ materially from the forward-looking statements. Our ability to predict results or the actual effect of future plans or strategies is inherently uncertain. Factors which could have a material adverse effect on our operations and future prospects on a consolidated basis include, but are not limited to: changes in economic conditions, legislative/regulatory changes, availability of capital, interest rates, competition, and generally accepted accounting principles. These risks and uncertainties should also be considered in evaluating forward-looking statements and undue reliance should not be placed on such statements.

Investor and Media Contact:
Jenene Thomas
Jenene Thomas Communications, LLC
Investor Relations and Corporate Communications Advisor
T: (US) 908.938.1475E:

- See more at: http://globenewswire.com/news-release/2015/05/15/736287/10134645/en/Amarantus-Announces-Successful-Delivery-and-Distribution-of-MANF-in-Preclinical-Model-to-Brain-Areas-Involved-in-Parkinson-s-Disease.html?f=22&fvtc=3&fvtv=4000#sthash.vEQmLOOU.dpuf

http://health.einnews.com/article/265601829/AfTvGVLtyHuOc4df

Genentech Brain Trust Leaves With $217 Million For New Startup To Fight Alzheimer's And Parkinson's

Marc Tessier-Lavigne

Three former top researchers at Genentech , the legendary biotech that is now part of Roche Holding , have raised $217 million in venture capital to start a new company, Denali Therapeutics, focused on treating and curing neurodegenerative diseases like Alzheimer’s, ALS, and Parkinson’s.

The news is another sign of both the large amounts of money available to all biotechnology startups and for a financial turnaround for research efforts against brain diseases that have been tough to beat. NeuroPerspective, a newsletter that tracks neurological treatments, says in the past five years the number of drugs being developed by large drugmakers for brain and nervous system disorders fell 50% to 129 – but that last year, investors poured $3.3 billion into the field, more than in any of the last ten years. The raise for Denali is a series A, the very first round of getting funding for a new company. It is the largest such round in biotech history.

One reason for the overstuffed purse: One co-founder, Denali’s chairman of the board of directors, is Marc Tessier-Lavigne, a well-known neuroscientist and president of Rockefeller University in New York. He served as Genentech’s head of drug research during its legendary run in the late 2000s, before the company was bought by Roche in 2009. He’s also giving up a board seat at pharma giant Pfizer PFE +1.18% in order to make time for his new company.

“The science in the field has been breaking open and this has been accelerating over the past decade,” says Tessier-Lavigne. “Denali is based on the idea that the time is right to tackle these diseases systematically and deeply.”

Denali CEO Ryan Watts

Leading day-to-day operations as chief executive will be Ryan Watts, until now director of neuroscience at Roche’s Genentech division. Alex Schuth, who headed technology innovation and diagnostics business development at Genentech, is the third co-founder. The company will be based in San Francisco.

The company is named after the tallest mountain in North America. “For me it means an inspiring challenge,” says Watts. “We wanted a name that was recognizable that represents a huge unmet need.”To climb this particular mountain, Watts says that Denali will be avoiding already crowded areas in the development of drugs for diseases like Alzheimer’s. For instance, companies including Biogen, Eli Lilly , Merck, and Genentech are all trying to slow the progression of Alzheimer’s with drugs that block a substance called beta amyloid, which is present in tangles in the brains of Alzheimer’s patients. Watts says Denali won’t pile in.

Instead, Watts sees a new generation of drug targets emerging from human genetics. He says that just as oncogenes – cancer genes – have lead to a flood of cancer drugs, newly discovered genes linked to degenerative brain disease (the Denali guys called them degenogenes) will provide a basis for a new generation of brain medicines.

Denali co-founder Alex Schuth

Denali will also focus on how inflammation drives brain disease; how the trafficking of substances between cells is involved in Parkinson’s and Alzheimer’s; and on factors that influence how brain cells die that are common to all brain diseases. Already, the company is looking at least 12 different drug targets in these areas, though it will not disclose more about them yet.

Investors include Fidelity Biosciences, ARCH Venture Partners, Flagship Ventures and the Alaska Permanent Fund (represented by Crestline Investors). Additional investors include sovereign wealth funds, public mutual funds and private family offices, with significant reserves for additional future financing.

Robert Nelsen, co-founder of  ARCH Ventures and an investor in other hot biotech startups like JUNO Therapeutics and Agios, both of which now sport $4 billion market capitalizations, says that combining forces in a big effort is already drawing attention among researchers even before the company officially launches.

“The best scientists in the world are now calling us, “ Nelsen says. The next step, he says, is engaging the Food and Drug Administration about how to develop brain drugs more quickly, as has happened in HIV, hepatitis C, and cancer. “ You can’t wait 10 or 20 years for the perfect study in Alzheimer’s when it’s going to cost us a trillion dollars in today’s dollars by 2050. The societal cost of these diseases is mind-blowing.”

http://www.forbes.com/sites/matthewherper/2015/05/14/former-genentech-researchers-raise-217-million-for-company-to-fight-alzheimers-and-parkinsons/?ss=pharma-healthcareAlso on Forbes:

The Top 10 Biotech Companies In The U.S.