Zambon Launches Xadago® (Safinamide) in the Netherlands for Patients with Mid- to Late-Stage Parkinson’s Disease

 July 6, 2016

Zambon S.p.A., an international pharmaceutical company strongly committed to the central nervous system (CNS) therapeutic area, and its partner Newron Pharmaceuticals S.p.A. (“Newron”) (SIX: NWRN), a biopharmaceutical company focused on the development of novel therapies for patients with diseases of the central nervous system (CNS) and pain, today announced the launch of Xadago® (safinamide) in the Netherlands for the treatment of mid- to late-stage Parkinson’s disease (PD).

Safinamide is now available in the Netherlands as an add-on therapy to a stable dose of levodopa (L-dopa) alone or in combination with other PD therapies for mid- to late-stage fluctuating patients providing a balanced control of motor symptoms and motor complications. 

Prof. Bas Bloem, from Radboud Universitair Medisch Centrum Nijmegen, medical advisor to Zambon, commented: “Despite optimal medical management, Parkinson’s disease remains a very debilitating disease. That is why I am excited to see the introduction of safinamide as a new treatment option for Parkinson in fluctuating patients. Safinamide has an interesting dual dopaminergic and non-dopaminergic mode of action, including the modulation of altered glutamatergic neurotransmission. As such, safinamide has the potential of becoming a long awaited treatment alternative as add on to L-dopa prolonging the window of L-dopa efficacy without worsening motor complications. I look forward to seeing which type of patients will benefit most in daily clinical practice.”

Elena Zambon, President of Zambon, said: “Zambon has a strong commitment to Parkinson’s disease, and we continue to look at ways to address unmet needs of patients that can benefit from new treatment options in the CNS therapeutic area.”

With the addition of the Netherlands, Xadago® is now available in ten countries: Germany, Switzerland, Spain, Italy, Belgium, Denmark, Sweden, UK and Luxembourg. 

About Xadago® (safinamide)

Safinamide is a new chemical entity with a unique mode of action, including selective and reversible MAO-B-inhibition and blocking of voltage dependent sodium channels, which leads to modulation of abnormal glutamate release. Clinical trials have established its efficacy in controlling motor symptoms and motor complications in the short term, maintaining this effect over 2 years. Results from 24 month double-blind controlled studies suggest that safinamide shows statistically significant effects on motor fluctuations (ON/OFF time) without increasing the risk of developing troublesome dyskinesia. This effect may be related to its dual mechanism acting on both the dopaminergic and the glutamatergic pathways. Safinamide is a once-daily dose and has no diet restrictions due to its high MAO-B/MAO-A selectivity. Zambon has the rights to develop and commercialize Xadago® globally, excluding Japan and other key territories where Meiji Seika has the rights to develop and commercialize the compound. The rights to develop and commercialize Xadago® in the USA have been granted to US WorldMeds, by Zambon. 

References:

Two-year, randomized, controlled study of safinamide as add-on to levodopa in mid to late Parkinson’s disease. Borgohain, Rupam; Szasz, Jozsef; Stanzione, Paolo; Meshram, Chandrashekhar; Bhatt, Mohit H et al. (2014)

Movement disorders : official journal of the Movement Disorder Society vol. 29 (10) p. 1273-80.

Anand R: Safinamide is associated with clinically important improvement in motor symptoms in fluctuating PD patients as add-on to levodopa (SETTLE). 17th International Congress of Parkinson’s Disease and Movement Disorders, Sydney, Australia, June 16-20, 2013. 

About Parkinson’s disease

PD is the second most common chronic progressive neurodegenerative disorder in the elderly after Alzheimer’s disease, affecting 1-2% of individuals aged ≥ 65 years worldwide. The prevalence of the PD market is expected to grow in the next years due to the increase in the global population and advancements in healthcare that contribute to an aging population at increased risk for PD. The diagnosis of PD is mainly based on observational criteria of muscular rigidity, resting tremor, or postural instability in combination with bradykinesia. As the disease progresses, symptoms become more severe. Early-stage patients are more easily managed on L-dopa. L-dopa remains as the most effective treatment for PD, and over 75% of the patients with PD receive L-dopa. However, long term treatment with L-dopa leads to seriously debilitating motor fluctuations, i.e. phases of normal functioning (ON-time) and decreased functioning (OFF-time). Furthermore, as a result of the use of high doses of L-dopa with increasing severity of the disease, many patients experience involuntary movements known as L-dopa-Induced Dyskinesia (LID). As the disease progresses, more drugs are used as an add-on to what the patient already takes, and the focus is to treat symptoms while managing LID and the “off-time” effects of L-dopa. Most current therapies target the dopaminergic system that is implicated in the pathogenesis of PD, and most current treatments act by increasing dopaminergic transmission that leads to amelioration of motor symptoms. 

References:

BMC Oertel. European Handbook of Neurological Management, Vol1, Chapter 14 & 15, 2011.

NICE PD guideline, 2006. 

About Zambon

Zambon is a leading Italian pharmaceutical and fine-chemical multinational company that has earned a strong reputation over the years for high quality products and services. Zambon is well-established in 3 therapeutic areas: respiratory, pain and woman care, and is very strongly committed to its entry into the CNS space. Zambon SpA produces high quality products thanks to the management of the whole production chain which involves Zach (Zambon chemical), a privileged partner for API, custom synthesis and generic products. The Group is strongly working on the treatment of the chronic respiratory diseases as asthma and BPCO and on the CNS therapeutic area with Xadago® (safinamide) for the Parkinson treatment. Zambon is headquartered in Milan and was established in 1906 in Vicenza. Zambon is present in 19 countries with subsidiaries and almost 2,700 employees with manufacturing units in Italy, Switzerland, France, China and Brazil. Zambon products are commercialized in 84 countries.

For details on Zambon please see: www.zambongroup.com

About Newron Pharmaceuticals

Newron (SIX: NWRN) is a biopharmaceutical company focused on the development of novel therapies for patients with diseases of the central nervous system (CNS) and pain. The Company is headquartered in Bresso near Milan, Italy. In addition to Xadago® for Parkinson’s disease, Newron has a strong pipeline of promising treatments for rare disease patients at various stages of clinical development. For more information, please visit: www.newron.com

https://www.freshnews.com/zambon-launches-xadago-safinamide-in-the-netherlands-for-patients-with-mid-to-late-stage-parkinsons-disease/20160706

Single Dose of Old Drug Boosts Memory, Attention

July 6, 2016

A drug that for a century has been safely used as a stain and to treat medical disorders could boost activity in brain regions linked to short-term memory and attention, results of a placebo- controlled study demonstrate.

Using functional MRI (fMRI), researchers found that a single oral dose of methylene blue increased brain activity in the bilateral insular cortex, as well as the prefrontal cortex and parietal and occipital lobes, compared with placebo.

Timothy Q. Duong, PhD, from the University of Texas Health Science Center at San Antonio, pointed out that an advantage of methylene blue is that it has been proven to be nontoxic and is "very safe."

Dr Duong told Medscape Medical News that the drug has been available for about a century. It has been used on a long-term basis to treat methemoglobinemia and, in the emergency setting, cyanide and carbon monoxide poisoning.

He also pointed out that no other clinically approved drug is used to improve memory, making methylene blue "unique and novel in that sense."

"I'm sure there are a couple of supplements that can claim to have some memory effects," he said, adding that as far as he knows, these agents have not been tested in clinical trials, nor have they been approved by the US Food and Drug Administration.

The research was published online June 28 in Radiology.

Enhanced Performance

In the 1970s, studies in rodents demonstrated the memory-enhancing effects of methylene blue. However, the underlying neuronal mechanisms and the drug's impact on short-term memory and sustained attention have not been explored.

The researchers conducted a randomized, double-blinded, placebo-controlled clinical trial in which 26 healthy individuals aged 22 to 62 years were assigned to single-dose administration of methylene blue 280 mg or a blue food colorant as placebo.

The participants completed a psychomotor vigilance task to test sustained attention and a delayed match-to-sample task to measure short-term memory while undergoing fMRI, both before and 1 hour after administration of the study drug or placebo.

In addition, the impact of methylene blue on cerebrovascular reactivity was examined by determining cerebral blood flow during a carbon dioxide challenge before and after administration.

The results showed that during the psychomotor vigilance task, methylene blue was associated with significantly increased activity on fMRI in the bilateral anterior and posterior insular cortices during the attention phase (P = .01-.008).

In addition, methylene blue was associated with significantly increased fMRI activity during the short-term memory task in the bilateral occipital lobes, the basal ganglia, the thalami, the parietal lobules, the anterior cingulate gyrus, and the cerebellum (P = .03-.0003).

After administration of methylene blue, there was also an approximately 7% increase in the number of correct behavioral responses (P < .01). No change was observed in the participants who were given placebo. There were no significant changes in cerebral blood flow.

"The results support the notion that methylene blue enhances memory performance and functional MR imaging activity in brain regions associated with a visuospatial short-term memory task," the investigators write. They note that their findings are "consistent with behavioral measurements in the same subjects."

Highlighting the fact that the current study did not examine the impact of methylene blue on long-term memory, Dr Duong said that he and his colleagues are currently conducting a clinical trial of the drug in patients with mild cognitive impairment and Alzheimer's disease. They will report the results early next year.

The study was supported by the National Center for Advancing Translational Sciences and the Julio C. Palmaz, MD, Endowment for Excellence in Radiology Research. The authors have disclosed no relevant financial relationships.

http://www.medscape.com/viewarticle/865748

Parkinson’s A daily battle with a degenerative disease

• By Tabitha Goodling 

• July 6, 2016

• LIVERPOOL - Dean Stephens is not ignoring the fact that he has a progressive disease. Day by day he can feel differently. Today may be a very good day, and he may not need his walker at all.
  Tomorrow, his brain might not be able to tell his feet to move in order to take a step.
  Stephens, 70, has Parkinson’s disease, a movementrelated illness that took the life of boxer Muhammad Ali a few weeks ago.
  Stephens is a retired engineer and farmer from Liverpool who has owned several businesses over the years and considered himself an active person. Five years ago, he said, he felt like he was “dragging weights around.” His wife Gail agreed something wasn’t right.
  After six months of tests and unanswered questions, the diagnosis of Parkinson’s was given.
  Parkinson's is due to the abnormal protein, lewy body, explained Dr. Glen Finney, a neurology specialist at Geisenger’s campus in Wilkes-Barre. The proteins regulate body movement.
  In cases where the body needs to respond to normal movements that are fast and smooth, the brain fails to give that signal in a quick manner.
  Dopamine is a chemical in the brain that helps with movement, and medications help increase this chemical.
  Some key symptoms in patients include a decrease in facial expressions, shuffling of feet when walking and some shaking.
  At times, a person can be suspected of having Parkinson’s, Finney said, but they may just have the symptoms and in fact have a different disorder.
  “The strongest sign that it is Parkinson’s,” Finney said, “is if the patient responds well to the increase in dopamine in the brain.
  Stephens said medication has certainly helped. He has begun seeing a specialist at Penn State Hershey Medical Center who increased his medications. The shaking he had had in his left hand is not as bad, Stephens said.
  “The medicine certainly lessens the symptoms. You gain some better movement,” he said. Currently Stephens does not need to use his walker as much. While these are all good indicators, he knows there will come a day when even the best medicines will not help him.
  “Parkinson’s is a progressive disease. That’s just how it is. I can’t paint it any differently,” Stephens said of the reality.
  He said he wears a neck brace so that his neck can stay straight when sitting.
  “And I was shuffling like Tim Conway,” he said with a laugh referring to the comedian who was known for being a character who walked with short steps on “The Carol Burnett Show.”
  As the person progresses with the illness, symptoms increase. Swallowing and speaking become difficult. And one third of all Parkinson’s patients also experience dementia, Finney said.
  Even these more difficult symptoms can be treated with therapy, he said.
  There’s no real known cause of the disease, but Finney said there is some research pointing to exposure to pesticides and lack of activity early in life.
  It is very common in older adults, Finney said, and the biggest misconception is that the disease is rare.
  “People like Muhammad Ali and Michael J. Fox have done an incredible job at bringing about awareness.”
  The doctor also said that family members should not assume that memory loss is normal in older people nor that slow movements are normal. An exam by a neurologist is highly encouraged when patients experience these changes
  http://www.dailyitem.com/news/lifestyles/health/parkinson-s-a-daily-battle-with-a-degenerative-disease/article_aab8990a-4396-11e6-88b2-b3a0aa734897.html

Study of Mutations in Key Protein in Fruit Flies May Have Implications for Parkinson’s Disease

Ines Martins
JULY 6, 2016

Studies of the fruit fly, or Drosophila melanogaster, have shown that a protein called clueless, or clu, is associated with the mitochondrial defects observed in Parkinson’s disease patients.

The study showing that clu mutations lead to muscle degeneration, “Drosophila clueless is involved in Parkin-dependent mitophagy by promoting VCP-mediated Marf degradation,” was published in Human Molecular Genetics.

Mitochondrial dysfunction is known to affect cells with high energy demands, such as neurons and muscle cells, and seems to be associated with the development and progression of Parkinson’s disease. Now, researchers at Kansas State University have investigated the role of clueless in mitochondrial function in fruit fly muscle cells.

“If you think about a tissue in the body that uses more energy than anything else, of course it’s your muscle tissue,” senior author Erika Geisbrecht, Kansas State University associate professor of biochemistry and molecular biophysics, said in a press release. “Proper mitochondrial function is essential to having healthy, developed muscles. It’s an important connection.”

Although humans are very distinct from fruit flies, they share similar muscle structures and most of the proteins known to be involved in Parkinson’s, which allowed researchers to address the role of clu.

Fruit flies have short life cycles — they need only 10 days to become adults — so their muscle development and maintenance can be studied in shorter time periods.

“We are trying to understand how muscles develop and how healthy muscles are maintained throughout the entire life of a fruit fly in the hopes of applying this knowledge to the human body,” Geisbrecht said.

The researchers found that a mutation in the clueless gene resulted in defects in mitochondrial localization and in the elimination of defective mitochondria, which are toxic to the cells. In fact, mitochondria that are damaged or senescent accumulate toxic reactive oxygen species (ROS) and fuse and contaminate healthy mitochondria. A buildup of these toxic mitochondria ultimately impairs the muscle and nerve cells from properly functioning.

Clueless was found to interact with parkin, a protein that is also involved in the mitochondria quality control process and whose mutations result in Parkinson’s disease development later in life.

Both parkin- and clueless-mutated flies die as they reached an adult phase due to neuron and muscle degeneration.

Geisbrecht’s work with Drosophila will offer better understanding of how these and other Parkinson’s-causing genes are involved in muscle function. In the future, it may lead to better treatment options that target such proteins.

Also, muscle tissue function is often impaired in other non-neurodegenerative diseases, such as diabetes or cancer. The researchers now want to understand the molecular mechanisms involved in muscle degeneration in those diseases.

“Muscle wasting for people with end-stage diabetes or cancer is often a bigger problem than the cancer or diabetes itself because it causes people to become immobile and lose the ability to make their muscles function well again,” Geisbrecht said. “We want to understand what happens at the cellular level — what these genes or proteins are doing.”

http://parkinsonsnewstoday.com/2016/07/06/scientists-study-clueless-protein-to-understand-parkinsons-disease/

Depression in Parkinson's Strongest Predictor of Anxiety

Daniel M. Keller, PhD

July 06, 2016

BERLIN — Anxiety may affect up to 50% of all patients with Parkinson's disease (PD) at some point in their illness, but investigators have identified several predictors that may allow physicians to intervene and reduce the prevalence of this disabling condition.

Investigators, led by author Kangdi Zhu, MD, MSc, from the Department of Neurology at Leiden University Medical Center in the Netherlands, found that depression was the strongest predictor of anxiety in this patient population.

"Anxiety is a common feature in PD, that in all likelihood partly shares a common pathophysiological mechanism with depression," said Dr Zhu.

Dr Zhu reported the findings here at the 20th International Congress of Parkinson's Disease and Movement Disorders.

Dr Zhu noted that most studies of anxiety in PD have been cross-sectional, but this study was based on the Dutch PROfiling PARKinson's Disease (PROPARK) longitudinal cohort study of 414 patients with PD who were examined annually for 5 years. The study has documented a range of motor and nonmotor features.

The aim of the study was to "examine which factors are associated with longitudinal changes in anxiety levels" among patients with PD.

Of 409 patients with Hospital Anxiety and Depression Scale–Anxiety (HADS-A) subscale scores available at baseline, 67 (16%) had anxiety at baseline (score of 11 or greater on HADS-A). These patients were more often female, but age, disease duration, and age at PD onset were not associated with anxiety at baseline. The investigators noted that "patients with anxiety were more severely affected on several motor and nonmotor domains."

Of the 409, another 316 who did not have anxiety at baseline (HADS-A scores less than 11) were available for follow-up; 252 remained free from anxiety, and 64 developed anxiety during follow up.

In a linear mixed models analysis with depression as a covariate, depression was the factor most strongly associated with higher HADS-A scores. Without depression as a covariate, higher HADS-A scores over time were associated with female sex, greater cognitive impairment, more insomnia at baseline, and gastrointestinal and cardiovascular autonomic dysfunction.

For patients who did not have anxiety at baseline, a Cox proportional hazards model revealed that depressive symptoms, more cognitive impairment, insomnia, and gastrointestinal and cardiovascular autonomic dysfunction were independent predictors of the future development of anxiety.

The investigators proposed that insomnia and dysautonomia could contribute to anxiety in PD, and vice versa. Because of the association of cognitive dysfunction and the development of anxiety, they suggested monitoring patients with cognitive dysfunction more closely for symptoms of anxiety.

The authors noted that anxiety in PD may be episodic or nonepisodic and may vary with motor fluctuations. Motor deficits may induce anxiety, for example, because of a fear of falling from freezing.

Peter Schmidt, PhD, senior vice president and chief mission officer of the National Parkinson Foundation, Miami, Florida, told Medscape Medical News that anxiety is prevalent in PD, as shown in this study, and can be very disabling.

Dr Schmidt said one often hears about anxiety among patients with PD, "but it's not a paramount feature that people will talk about in terms of behavioral health in Parkinson's." More often people will talk about depression or later disease psychosis, "but anxiety is kind of left off the list as an important factor although it can be very disabling…. So it's good to have studies highlighting anxiety," he said.

There was no commercial support for the study. Dr Zhu and Dr Schmidt have disclosed no relevant financial relationships.

20th International Congress of Parkinson's Disease and Movement Disorders. Abstract 347. Presented June 20, 2016.

http://www.medscape.com/viewarticle/865758

‘Be like Ali': The widow of the late boxer and humanitarian announces plan to commemorate his life

By Vickie Elmer
July 6, 2016

Muhammad Ali poses during the World Economic Forum in Davos, Switzerland, in January 2006. (Reuters/Andreas Meier)

Muhammad Ali was a humanitarian who supported the Special Olympics and advocated for the poor, for peace and for research into Parkinson’s disease. Now a month after the world famous boxer’s death, his widow is calling on members of the public to “be like Ali”  and take part in a public service campaign she’s creating in her husband’s honor.

People would be asked to volunteer for a total of 75 hours, starting on Muhammad Ali’s 75th birthday on Jan. 17, 2017, and lasting throughout the year.

The campaign will officially kick off in mid-July with a series of events, including one in Muhammad Ali’s hometown of Louisville, Ky. Last week, Lonnie Ali shared a few details at the annual Points of Light volunteer conference in Detroit.

“He often said ‘service is the rent you pay for your room here on earth,'” she said. “The time has come for all of us to pick up the torch from Mohammad and shine our own lights on the places and people who have been in the shadows for too long.”

Ali said the idea for the campaign came to her while preparing to attend the conference, which brought together 3,000 nonprofit leaders, corporate social responsibility staff and active volunteers.  But the seeds were planted, she said, by a conversation she had with her husband.

“A few years ago, he said when it was time for him to go, to  use his life and his death as a teaching moment for the country. That was what he wanted,” Lonnie Ali said. He wanted the world to know that adversity “cannot rob you of your power to achieve your dreams” and that service to others is part of what makes America great.

The campaign will be led by a street team of college interns, who signed up charity and civic leaders in Detroit last week. Up next is Forecastle, a music festival in Louisville that attracts thousands of young people, said Donald Lassere, president and CEO of the Muhammad Ali Center, a museum and cultural center headquartered in downtown Louisville that promotes education, gender equality and global citizenship.

The effort dovetails with the center’s annual humanitarian awards, given in September to activists and change agents ages 14 to 30, and its Generation Ali initiative, which focuses on helping young people realize “they can be great by helping humanity,” Lassere said.  The museum also will debut new exhibits in September that will ask questions and encourage people to “seek greatness doing service,” he said.

Ali, a heavyweight champion in the 1960s, died June 3 at a Scottsdale, Ariz., hospital, after suffering from Parkinson’s disease and respiratory problems. His death triggered an outpouring of sympathy and reminiscence of his showy boxing style and the thousands who greeted him as he toured the world preaching unity and peace and visiting prisoners, hospital patients and others in need of help.

President George Bush in 2005 awarded Ali the Presidential Medal of Freedom, calling him “a fierce fighter and a man of peace” who possessed a “beautiful soul.”

Ali’s last public event occurred in April at a Celebrity Fight Night dinner in Phoenix to raise money for Parkinson’s.

It’s unclear whether the campaign will continue after next year.  Organizers aim to attract at least 1 million participants initially but hope the campaign will take off internationally and include millions more, Lassere said.

Still, 75 hours is a huge commitment, when the average American donated a median of 52 volunteer hours in the year ending September 2015.  Younger people, ages 16 to 34, donated a median of 36 hours in 2015, according to the Bureau of Labor Statistics data.  Those 65 and older were most likely to donate 100 hours or more a year.

The Ali campaign will target families to volunteer together and young people ages 13 to 24. But Leslie Lenkowsky, a professor of practice at the Lilly Family School of Philanthropy at Indiana University and a former CEO of the Corporation for National and Community Service, said it will be difficult to increase volunteer hours by so much and bring more into the fold.

“That’s a big lift,” Lenkowsky said. The share of Americans who volunteer time has stayed between 25 and 26 percent for several years now, even as individual campaigns like the Ice Bucket Challenge, drew a lot of attention.

The launch date of Jan. 17 also falls near the annual Martin Luther King Jr. Day of Service scheduled for Jan. 16 next year, perhaps pushing the limits of volunteerism further.

However, Samantha Jo Warfield, press secretary at the Corporation for National and Community Service, the federal agency that administers MLK Day, pointed out that Ali shared some of King’s beliefs in nonviolence and community, and suggested that the two efforts might work well in tandem.

A campaign by Lonnie and Muhammad Ali could “light a spark” and invite in people who have never before been asked to volunteer, she said.

Ali married Yolanda ‘Lonnie ‘ Ali in 1986, shortly after he was diagnosed with Parkinson’s.  His fourth wife, she had met him when she was 6 and he was a rising boxing star whose parents lived in her neighborhood. After they wed, she managed his business affairs and his health as his caregiver, and helped to open the Muhammad Ali Center.

Lonnie Ali has been advocate for caregivers and for youth education and served for three years on the Presidential Commission for the Study of Bioethical Issues.  At  the Detroit conference, she spoke of her husband’s legacy as a beautiful beacon to young people, folding her hands, as if in prayer, as she talked.

“Even though he was slowed by Parkinson’s Disease, Muhammad was compelled to use his gifts to support the victims of poverty and strife,” she remarked. He loved the idea of inspiring service by others, as the best gift anyone could give him, she said. Lonnie Ali received a standing ovation when her 8 1/2-minute speech ended with these words:

“My husband believed that the soul of a nation could be measured in the goodness of its people. And I see that goodness here in this room. So I ask you to pick up that torch. In honor of my husband’s memory, I ask you to prove that there is Ali in all of us, and your own greatness in the love and service you provide to each other and to the world.”

See Video:

https://www.washingtonpost.com/news/inspired-life/wp/2016/07/06/be-like-ali-the-widow-of-the-late-great-boxer-and-humanitarian-announces-plan-to-commemorate-his-life/

EC approves Bial’s Parkinson’s disease therapy

July 6, 2016

Ongentys will be given a phase roll-out in 2016 and 2017

The European Commission has approved a novel, once-daily treatment for people who suffer from the neurodegenerative, progressive motor disorder Parkinson´s disease.

Manufactured by Bial, Ongentys (opicapone) is indicated as adjunctive therapy to preparations of levodopa/DOPA decarboxylase inhibitors (DDCIs) in adults with Parkinson's and end-of-dose motor fluctuations who cannot be stabilised on those combinations.

Bial says its drug will be available for patients in Europe in 2016 and 2017 following the EC's approval of Ongentys, which was supported by two pivotal phase III studies, BIPARK-I and BIPARK II.

These demonstrated that Ongentys achieved an absolute reduction in OFF-time of 2 hours without increasing ON-time with troublesome dyskinesia, statistically significant reductions in absolute OFF-time compared to placebo and increases in ON-time without troublesome dyskinesia.

Awareness of the condition has been raised by high-profile sufferers such as US actor Michael J Fox and the late Muhammad Ali.

Caused by the loss of dopamine-producing neurons in the brain, Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's, and is estimated to affect 7 to 10 million people worldwide.

More prevalent in men, signs of Parkinson's tend to become apparent after the age of 50 with the average age for diagnosis approximately 60 years old. As with Alzheimer's, there is currently no cure.

Levodopa has been used to treat Parkinson's since the 1960s, but is associated with long-term motor complications such as motor fluctuations and dyskinesias.

Within four to six years of treatment with levodopa, the effects of the drug in many patients begin to last for shorter periods of time after a dose - which means they may choose to increase their dosage or frequency, although this leads to an increased risk of dyskinesia.

Opicapone is a third-generation catechol-O-methyltransferase (COMT) inhibitor which increases the bioavailability of levodopa by up to 55% versus placebo, which means a dose-dependent reduction in OFF time.

The approval of Ongentys should help patients' quality of life in an area which has some appeal for companies keen to tap into unmet need: various firms are attempting to develop their own treatments, with gene therapy seen as one possible route to better treatments.

Last year the Google-backed genetic testing company 23andMe signed a $60m research deal with Roche subsidiary Genentech to generate whole genome sequencing data for about 3,000 people with Parkinson's disease

http://www.pmlive.com/pharma_news/ec_approves_bials_parkinsons_disease_therapy_1059625

Alzheimer's and Parkinson's not contagious: Study

July 6, 2016

UNITED STATES - Despite concerns that faulty brain proteins could be transferred from person to person by treatments involving human fluids and tissues, a new study finds no signs of increased risk for two major degenerative brain diseases among recipients.

"I think it's reassuring to people who had transplants, blood transfusions, morticians and researchers who work on these diseases," said the study's senior author, Dr. John Trojanowski, from the University of Pennsylvania Perelman School of Medicine in Philadelphia.Reviewing the records of children who were injected as long as 50 years ago with human growth hormones derived from cadavers showed that the recipients did not go on to develop Alzheimer's or Parkinson's disease with any greater frequency than the rest of the population - which suggests the two conditions are not contagious.

Trojanowski and his colleagues, who published their findings in JAMA Neurology, in fact found no cases of Alzheimer's or Parkinson's disease in about 800 individuals who were injected with growth hormones that came from the bodies of people who may have had one of those two illnesses.

Doctors switched to synthetic hormones in the 1980s when they realised some children had received contaminated cadaver growth hormones that later led to their developing Creutzfeldt-Jakob disease (CJD), the human version of "mad cow" disease, which causes a fast decline in mental functioning and generally death within a year. (See Reuters Health story of August 19, 2011 here:).

Because CJD is caused by a rogue protein called a prion, which causes other proteins in the brain to fold in strange ways and lose their function, there was concern that abnormal proteins involved in Parkinson's and Alzheimer's diseases could transmit those illnesses in the same way.

"There's been concern recently because a lot of the proteins involved in neurogenic diseases are similar to these prions," said Karen Duff, who studies Alzheimer's and Parkinson's at Columbia University Medical Center in New York.

Based animal studies, some researchers feared that receiving cornea or organ transplants, blood transfusions, or working with the brains of people who had Alzheimer's and Parkinson's may put people at an increased risk for those diseases, according to Trojanowski.

For the new study, his team looked at data on 6,190 people who had a growth problem as children and were injected with human growth hormones taken from cadavers between 1963 and 1985.

The researchers also determined how likely it was that the hormones injected into the children came from cadavers with any of a variety of brain diseases.

Examining brain tissue from 34 cadaver donors, the researchers found 10 had no diseases, 9 had Alzheimer's, 3 had Parkinson's, 4 had both and the rest had other types of brain diseases.

Turning to the group of growth hormone recipients, the researchers then examined the death certificates of the 796 who died before 2008.

Overall, none of the hormone recipients' death records mentioned Parkinson's or Alzheimer's, even though the researchers determined that it's very likely they were injected with hormones from people who had those diseases.

Duff, who was not involved in the new study, agreed that the results allay fears about the diseases being contagious, especially for people involved in simply handling brain tissues and fluids.

She added that while this study can't confirm there's no risk, any chance of "catching" Alzheimer's or Parkinson's disease from even a contaminated piece of medical equipment would be much less than from having the hormones directly injected, so the study should be reassuring.

http://health.einnews.com/article/334157619/hwysN1KVsOe0vc8i

EU clears Bial’s new Parkinson’s drug

By Selina McKee

July 6, 2016

Over the next year certain patients with Parkinson's disease could get access to a new treatment option in Europe after regulators green-lighted Bial's Ongentys.

The European Commission has approved the drug as adjunctive therapy to preparations of levodopa/DOPA decarboxylase inhibitors in adult patients with the disease and end-of-dose motor fluctuations who cannot be stabilised on those combinations.

The decision came after regulatory advisors recommended Ongentys' (opicapone) clearance earlier this year, highlighting its ability to decrease off-time (time when patients are severely restricted by their symptoms) and increase on-time without troublesome dyskinesia.

This was evidenced by data from two pivotal Phase III studies, BIPARK-I and BIPARK II, which demonstrated that the drug achieved an absolute reduction in OFF-time of two hours without increasing ON-time with troublesome dyskinesia, while a one-year extension study also showed that this effect was sustained.

"Motor complications in Parkinson's disease remain an unmet medical need for a significant number of patients," noted Professor Joaquim Ferreira, ‎Professor of Neurology and Clinical Pharmacology at the University of Lisbon. "Opicapone is a new treatment option and fulfils the need for a more potent COMT inhibitor, offering an important alternative to the currently available armamentarium for the treatment of motor fluctuations."

"It may become the treatment of choice when levodopa-treated patients need additional help to improve motor symptoms such as wearing off in Parkinson's disease," added Professor Heinz Reichmann, Professor and Chair Department of Neurology and Dean of Medical Faculty at the University of Dresden.

The European Parkinson's disease Association estimates that 1.2 million people have Parkinson's disease in the European Union. Bial said it plans to start launching its new drug across the region in 2016 and 2017.

http://www.pharmatimes.com/news/eu_clears_bials_new_parkinsons_drug_1059623

Butter IS bad for you (today's study claims) Eating a diet high in saturated fats 'raises the risk of death from heart disease, cancer and dementia'

• By SOPHIE BORLAND HEALTH EDITOR FOR THE DAILY MAIL
  5 July 2016B
• 
  

Harvard researchers found saturated fat diet increased chances by 8%
But slashing intake by 5% reduced overall risk of mortality by a quarter
Follows study saying one tablespoon of butter had no impact on death 
Scientific Advisory on Nutrition is reviewing guidelines on saturated fat

Confusion over the safety of butter has intensified after a major study claimed it does raise the risk of dying from heart disease.

Harvard research involving 120,000 adults found that those who ate the most saturated fat were up to 8 per cent more likely to die.

The findings come less than a week after another study found that one tablespoon of butter had no impact on death, heart disease or strokes.

And one leading cardiologist claims that eating butter and other saturated fats are not harmful and may actually help you lose weight.

But this latest study found that slashing the intake of saturated fats by just 5 per cent reduced the overall risk of mortality by more than a quarter.

People who eat a diet high in saturated fat, which is found in foods like butter, were found were up to eight per cent more likely to die, researchers at Harvard found

This would yield ‘substantial health benefits and should continue to be a key message in dietary recommendations’, the study published in the journal JAMA Internal Medicine concluded.

Saturated fat is has also been linked to dementia, by blocking the blood flow to the brain, and cancer as it contains oestrogen which fuels tumour growth.

Other experts broadly agreed with the findings including Dr Ian Johnson, emeritus fellow at the Institute of Food Research, in Norwich, who said: ‘There is nothing in these results consistent with the notion that ‘butter is back’.”

Dr Gunter Kuhnle, Associate Professor in Nutrition and Health, University of Reading, said: ‘The results of the study broadly confirm current dietary recommendation and in particular show that total saturated fat intake is associated with a higher, unsaturated fat with a lower risk for all-cause mortality.’

Eating foods high in saturated fats, such as mince, were found to be more prone to die from diseases including cancer, heart disease and Alzheimer’s and Parkinson’s

The study looked at the records of 126,233 men and women in the US over a 32 year period.

Those whose diets were highest in saturated fat were 8 per cent more likely to die over that time – including from cancer, heart disease or degenerative illnesses such as Alzheimer’s and Parkinson’s.

But closer analysis revealed that switching 5 per cent of saturated fats with polyunsaturated fats cut the risk of death by 27 per cent.

Saturated fats have been demonised since the 1970s after a major study linked them to high levels of cholesterol.

Recently however these findings have been disputed by experts including Dr Aseem Malhotra, a cardiologist at Frimley Park Hospital in Surrey and founder of the campaign group Action On Sugar.

Dr Malhotra claims that saturated fat does not necessarily increase the risk of heart disease and may even protect against it.

He also argues that cutting saturated fat from our diets has led to us replacing it with sugar and carbohydrates, which are fuelling obesity.

The Government’s expert group, the Scientific Advisory on Nutrition, is now reviewing their guidelines on saturated fat over concerns it has been unfairly demonised. 

http://www.dailymail.co.uk/health/article-3675261/Butter-bad-today-s-study-claims-Eating-diet-high-saturated-fats-raises-risk-death-heart-disease-cancer-dementia.html