Welcome to Our Parkinson's Place

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
updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. Please no advertisements.
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Thank you.

Saturday, September 5, 2015

Predicting Prognosis in Parkinson Disease

New Clinical Subtypes of Parkinson Disease and Their Longitudinal Progression: A Prospective Cohort Comparison With Other Phenotypes

Fereshtehnejad SM, Romenets SR, Anang JB, Latreille V, Gagnon JF, Postuma RB

JAMA Neurol. 2015;72:863-873

Study Summary

There is considerable heterogeneity in the clinical features and prognosis of patients with Parkinson disease (PD), but specific subtypes of the disease have not been well defined. Identification of distinct subtypes of PD may help clarify its underlying pathophysiology, determine prognosis, and ultimately design personalized treatment strategies. The goals of this prospective cohort study were to identify clinical phenotypes of PD and to compare prognosis and progression rates among these subtypes.In addition, the investigators compared the ability to predict prognosis for these phenotypes with previously identified clinical subtypes in the published literature.
From 2005 to 2013, the investigators enrolled 113 patients with idiopathic PD from two movement disorders clinics in Montreal, Canada. At baseline, they evaluated motor features of severity, motor complications, motor subtypes, and quantitative motor tests, as well as nonmotor features of autonomic dysfunction, psychiatric signs and symptoms, olfaction, color vision, sleep parameters, and neurocognition. There were 76 patients who returned after a mean of 4.5 years from baseline for follow-up assessment. At follow-up, the investigators also determined a global composite outcome by combining standardized scores for motor symptoms, motor signs, cognitive function, and other nonmotor features.
The specific features clustering together and best defining distinct subtypes were orthostatic hypotension, mild cognitive impairment, rapid eye movement sleep behavior disorder (RBD), depression, anxiety, and Unified Parkinson's Disease Rating Scale Part II and Part III scores at baseline. The three resulting subtypes identified were motor/slow progression, diffuse/malignant, and intermediate.
Even among patients of similar age and similar disease duration, those with the diffuse/malignant phenotype were more likely to have mild cognitive impairment, orthostatic hypotension, and RBD at baseline. In addition, these patients had increased odds of a rapid decline in cognition (odds ratio [OR], 8.7; 95% confidence interval [CI], 4.0-18.7; < .001), other nonmotor symptoms (OR, 10.0; 95% CI, 4.3-23.2; < .001), motor signs (OR, 4.1; 95% CI, 1.8-9.1; = .001), motor symptoms (OR, 2.9; 95% CI, 1.3-6.2; < .01), and the global composite outcome (OR, 8.0; 95% CI, 3.7-17.7; < .001), compared with patients without the diffuse/malignant phenotype.


The findings of this prospective cohort study suggest that patients with PD and mild cognitive impairment, orthostatic hypotension, and RBD at baseline have roughly nine times greater odds of rapid cognitive decline and 10 times greater odds of other nonmotor symptoms, in addition to having a worse prognosis for motor deterioration. There are, however, some limitations of this study, including a moderately small sample size, loss of more than 30% of patients to follow-up, and possible lack of generalizability to patients outside of Canadian movement disorder clinics.
On the basis of these results, it seems reasonable to screen patients with PD for mild cognitive impairment, orthostatic hypotension, and RBD, even at baseline visits. These nonmotor characteristics appear to define a diffuse/malignant phenotype likely to have the most rapid rate of deterioration.

Drug successfully reverses effects of Alzheimer's in rats

The study authors were able to prevent and repair damage to the brains of rats caused by Alzheimer's disease using IRL-1620.

At present, the US Food and Drug Administration (FDA) have approved five medications to treat Alzheimer's disease. However, while these only mask the symptoms of Alzheimer's, the researchers were able to treat the disease itself in rats using a chemical called IRL-1620.
They found that the drug improved memory, prevented oxidative stress and enhanced neurovascular modeling in rats that had demonstrated impaired learning and increased oxidative stress caused by the disease.
"We used the novel approach of stimulating the endothelin B receptors by intravenous injection of IRL-1620 to prevent and repair the damage to the brain caused by Alzheimer's disease," reports study co-author Seema Briyal, a senior scientist and adjunct assistant professor at Midwestern University in Downers Grove, IL.
Endothelin B (ETB) receptors have previously been identified by researchers as important in brain development, and stimulation of these receptors has been shown to provide protection to the nervous system.
Alzheimer's disease is the most common cause of progressive dementia, a group of symptoms that impair brain function. An estimated 5.3 million Americans currently have Alzheimer's. According to the Alzheimer's Association, every 67 seconds, someone in the US develops the disease.
The condition is also one of the leading causes of death in the US, with the Alzheimer's Association estimating that 700,000 people will die with the disease over the course of 2015.

Memory deficit improved and oxidative stress reduced in rats with Alzheimer's

For the study, the researchers injected rats with Alzheimer's disease with IRL-1620, a drug known to bind to ETB receptors and observed its effects on spatial memory, oxidative stress and the expression of certain proteins in the brain.
debilitating condition.
The new research is being presented at the 14th International Conference on Endothelin: Physiology, Pathophysiology and Therapeutics, held in Savannah, GA.
Recently, Medical News Today reported on a study published in the journal Cell Stem Cell revealing that an abnormal build-up of fat droplets in the brain may cause or speed up the progression of Alzheimer's disease.
Written by 
Copyright: Medical News Today

Researchers Explore Memory Problems Related to Parkinson's

FRIDAY Sept. 4, 2015, 2015 -- Many people with Parkinson's disease have memory problems, researchers report.

The study included 40 people with early stage Parkinson's disease and 40 healthy older adults. While the disease is generally viewed as a movement disorder, about half of the Parkinson's patients had difficulty with some aspect of memory, such as learning and retaining information, or recalling spoken information, the investigators found.
"And then half of those participants, or nearly one-quarter of all participants with Parkinson's, were really having a difficult time consistently with their memory, enough that it would be noticeable to other people," said study author Jared Tanner. Tanner is an assistant research professor in the department of clinical and health psychology at the University of Florida at Gainesville.
Still, there was good news: Most of the Parkinson's patients did not have significant memory problems, according to the authors of the study published online recently in the journal PLoS One.
Because of the study's design, the researchers could only show an association between Parkinson's disease and memory problems; they couldn't prove a cause-and-effect relationship.
"While a large proportion of people with Parkinson's will experience slower thinking speed, which may make them less quick to speak or have difficulty doing two things at once, we now know that there are a subset of individuals with Parkinson's disease who have memory problems," senior study author Catherine Price, an associate professor in the clinical and health psychology department, said in a university news release.
"It is important to recognize which people have issues with learning and memory so we can improve diagnostic accuracy and determine if they would benefit from certain pharmaceutical or behavioral interventions," she said.
Parkinson's disease-related movement problems are caused by low levels of a brain chemical called dopamine. Some experts have suggested that thinking and memory problems in patients are also due to a shortage of dopamine.
But brain scans of the Parkinson's patients in this study revealed changes in the brain's gray and white matter that appear unrelated to dopamine loss. Also, these changes were only present in those with memory problems.
Tanner explained that it's not only gray matter that's important for memory. "In Parkinson's disease, white matter connections between the temporal lobe and a region in the posterior portion of the brain called the retrosplenial cortex were particularly important in the recall of verbal information," he said in the news release.
"People with Parkinson's disease who had stronger connections between these areas of the brain did better at remembering information," he said.

Dean Jones dead at 84 from Parkinson's

Dean Jones, who’s all-American manner and boyish good-looks made him one of Disney’s favorite stars during the 1960’s and ‘70’s has passed away from Parkinson’s Disease at the age of 84.
Born in Decatur, Alabama on January 25, 1931, Dean Carroll Jones first caught the eye of Walt Disney while starring in the TV show “Ensign O’Toole,” which preceded Disney’s own Sunday night program on NBC in 1962. Two years later Disney offered him a role in “That Darn Cat,” opposite Hayley Millls, released in 1965. It was the first of 10 films he did for the studio between 1965-1977, including the “Herbie the Love Bug” series about a VW Beetle with a “human” personality. He was later honored by being inducted into the Disney Legends Hall of Fame.

In addition to starring in over 46 films, such as “Somebody Up There Likes Me (1956), “Jailhouse Rock” with Elvis Presley (1957) Imitation General (also 1957) with Glenn Ford and “Never So Few (1959) with Frank Sinatra, Jones also starred in 5 Broadway shows. In fact, he made his Broadway debut (along with Jane Fonda) in the 1960 play There Was a Little Girl.” He also played Dave Manning in the Broadway comedy “Under the Yum-Yum Tree, a role which he repeated in the 1963 movie version starring Jack Lemmon, and originated the role of Bobby in Stephen Sondheim's “Company.” He also appeared on a number of other TV shows, and recorded a singing album, Introducing Dean Jones, for Valiant Records.
Dean Jones became a devout born-again Christian in 1973–1974, before his father's death in 1979, and wrote a book, Under Running Laughter (1982) about his experience of Christianity. He had had a history of suffering from depression. His wife Lory Patrick stated, “One night he got down on his knees and prayed that God would free him from the miserable moods that he had always suffered. He told me that in an instant it was gone and he felt peace and joy flood into his heart."[2] Jones appeared in several Christian films, and in 1998, founded the Christian Rescue Committee (CRC), an organization that helps provide a "way of escape to Jews, Christians, and others persecuted for their faith.
In addition to Lory, he is survived by 2 children from his first wife Mae Inez Entwistle, as well as 8 grandchildren, and 3 great-grandchildren.

Thursday, September 3, 2015

Top 5 Causes, Symptoms and Treatment of Dystonia Disease

Dystonia is a movement disorder in which a person’s muscles contract uncontrollably. The contraction causes the affected body part to twist involuntarily, resulting in repetitive movements or abnormal postures. Dystonia can affect one muscle, a muscle group, or the entire body. Dystonia affects about 1% of the population, and women are more prone to it than men.

What Are the Symptoms of Dystonia?

Symptoms of dystonia can range from very mild to severe. Dystonia can affect different body parts, and often the symptoms of dystonia progress through stages. Some early symptoms include:
  • A “dragging leg”
  • Cramping of the foot
  • Involuntary pulling of the neck
  • Uncontrollable blinking
  • Speech difficulties
Stress or fatigue may bring on the symptoms or cause them to worsen. People with dystonia often complain of pain and exhaustion because of the constant muscle contractions.
If dystonia symptoms occur in childhood, they generally appear first in the foot or hand. But then they quickly progress to the rest of the body. After adolescence, though, the progression rate tends to slow down.
When dystonia appears in early adulthood, it typically begins in the upper body. Then there is a slow progression of symptoms. Dystonias that start in early adulthood remain focal or segmental: They affect either one part of the body or two or more adjacent body parts.

What Causes Dystonia?

Most cases of dystonia do not have a specific cause. Dystonia seems to be related to a problem in the basal ganglia. That’s the area of the brainthat is responsible for initiating muscle contractions. The problem involves the way the nerve cells communicate.
Acquired dystonia is caused by damage to the basal ganglia. The damage could be the result of:
  • Brain trauma
  • Stroke
  • Tumor
  • Oxygen deprivation
  • Infection
  • Drug reactions
  • Poisoning caused by lead or carbon monoxide
Idiopathic or primary dystonia is often inherited from a parent. Some carriers of the disorder may never develop a dystonia themselves. And the symptoms may vary widely among members of the same family.

Are There Different Types of Dystonia?
Dystonias are classified by the body part they affect:
  • Generalized dystonia affects most of or all of the body.
  • Focal dystonia affects just a specific body part.
  • Multifocal dystonia affects more than one unrelated body part.
  • Segmental dystonia involves adjacent body parts.
  • Hemidystonia affects the arm and leg on the same side of the body.
Dystonias can also be classified as syndromes based on their patterns:
  • Blepharospasm is a type of dystonia that affects the eyes. It usually begins with uncontrollable blinking. At first, typically, it affects just one eye. Eventually, though, both eyes are affected. The spasms cause the eyelids to involuntarily close. Sometimes they even cause them to remain closed. The person may have normal vision. But this permanent closing of the eyelids makes the person functionally blind.
  • Cervical dystonia, or torticollis, is the most common type. Cervical dystonia typically occurs in middle-aged individuals. It has, though, been reported in people of all ages. Cervical dystonia affects the neck muscles, causing the head to twist and turn or be pulled backward or forward.
  • Cranial dystonia affects the head, face, and neck muscles.
  • Oromandibular dystonia causes spasms of the jaw, lips, and tonguemuscles. This dystonia can cause problems with speech and swallowing.
  • Spasmodic dystonia affects the throat muscles that are responsible for speech.
  • Tardive dystonia is caused by a reaction to a drug. The symptoms are typically only temporary and treatable with medication.
  • Paroxysmal dystonia is episodic. The symptoms occur only during attacks. The rest of the time, the person is normal.
  • Torsion dystonia is a very rare disorder. It affects the entire body and seriously disables the person who has it. Symptoms generally appear in childhood and get worse as the person ages. Researchers have found that torsion dystonia is possibly inherited, caused by a mutation in the gene DYT1.
  • Writer’s cramp is a type of dystonia that only occurs while writing. It affects the hand and/or forearm muscles.

How Is Dystonia Treated?

There are several options for treating dystonia. The doctor will determine the course of treatment based on the type of dystonia and its severity.
A recently introduced treatment isbotulinum toxin, also called Botox or Xeomin. The toxin is injected into the affected muscle. There it blocks the effect of the chemical acetylcholine that produces muscle contractions. The injection needs to be repeated about every three months.
When dystonia causes someone to become disabled, deep brainstimulation is an option. With deep brain stimulation, an electrode is implanted into a particular area in the brain. It is then connected to a battery powered stimulator implanted in the chest. The electrode transmits electrical pulses created by the stimulator to the brain region to reduce the muscular contractions. The person’s doctor regulates the frequency and intensity of the electrical pulses.
Medications can help reduce the “overdrive” messages that cause muscles to contract excessively in dystonia. Drugs used include:
  • Levodopa
  • Procyclidine hydrochloride
  • Diazepam
  • Lorazepam
  • Clonazepam
  • Baclofen
Sensory trick is another option. With sensory trick, stimulation applied to the affected or nearby body part may reduce the muscular contractions. By simply touching this area, people can control their own contractions.
Speech therapy, physical therapy, and stress management may also be used to treat the symptoms of dystonia.

Clinical Trial may Restore Quality of Life for Parkinson's Patients

Sept. 3, 2015

For years focused ultrasound has been used to treat cancers, but for the first time in the U.S. it is being used it in a clinical trial to treat symptoms of Parkinson's Disease.
The most visible sign of the disease is the uncontrollable shaking or tremors, it is  a reality Parkinson's patients deal with. Currently there is no cure for the disease, only treatments. 
A clinical trial is under weigh at the University of Virginia Medical center that may  change the face of treatment options for patients of the disease. 
Dr. Neil Kassell is the chairman of the Focused Ultrasound Foundation in Charlotteville, he is also a professor of Neurology at U.Va. he says
Parkinson's is a chronic degenerative disease where some brain cells die causing symptoms like the tremors and slowness of movements. Kassell says current treatments aren't easy.
"It's treated either with drugs or if the drugs don't work in certain instances deep brain stimulations," said Kassell, "an incisions in the scalp a hole in the head and electrode put into the brain connected to a pacemaker."
However, thanks in part to a grant from the Michael J. Fox foundation,Kassell says they have been able to conduct research leading to the trial.
Unlike other treatments, focused ultrasound is totally non-invasive. Kassell says right now, all eyes are on the brain.
"Where each of the individual beams of ultrasound go into the tissue it has no effect," said Kassell, "but the point they converge, it heats up and kills the abnormal cells (in the brain)."Kassell says if the trial works, he envisions a real change.
"Focused ultrasound will provide an alternative for large numbers of patients,"said Kassell, "an alternative to surgery."

Scientists identify mechanism behind statin-induced muscle weakness

Sept. 2, 2015

New research suggests that muscle weakness and related side effects that can arise from statin use is likely due to the drug's effect on the energy production centers, or mitochondria, of muscle cells.
The researchers, from Radboud University Nijmegen Medical Center in the Netherlands, report their findings in the journal Cell Metabolism.
Statins are a commonly prescribed medication for lowering cholesterol; they work by blocking cholesterol production in the liver. Cholesterol is a major risk factor for heart disease and stroke, which cause nearly 1 in 3 deaths among Americans.
According to the Centers for Disease Control and Prevention (CDC), more than a quarter of American adults aged 40 and over use a prescription cholesterol-lowering medication, the vast majority of these being statins.
However, for around 25% of patients, statins can give rise to unpleasant side effects in the form of muscle weakness, pain and cramps, without any sign of damage to the tissue. These side effects can impair quality of life and often cause patients to stop taking the drugs.
Frans Russel, co-senior author of the new study and professor in molecular pharmacology and toxicology, says previous studies have linked side effects of statins and other drugs to mitochondria, but the underlying mechanisms are often unknown.

Lactone form of statin interferes with mitochondrial function

In the human body, statins exist in two forms: acid and lactone. Most statin drugs are of the acid form and target cholesterol production in the liver. The lactone form has no therapeutic effect - however, the acid form can convert to this type.
This would not normally be a problem except that the study shows the lactone form can interfere with the function of mitochondria - the powerhouses inside cells that produce ATP, the cellular "currency" of energy.
Using muscle cells from mice, the team showed that statins of the lactone form are around three times more powerful at disrupting mitochondria than those of the acid form.
They confirmed this finding in cells taken from muscle biopsies of patients experiencing statin-induced side effects.
They showed that the cells of the patients had reduced ATP production compared with cells from healthy controls. The lactone form of statins appears to reduce activity in a protein structure known as "complex III."
Prof. Russel says further independent studies are needed to look at the effects of different statins on mitochondrial function, and to confirm whether the mechanism they have identified could be a useful marker to predict which patients are likely to experience side effects from statin use. He also notes that:
"Interindividual differences in the enzymatic conversion of the acid into the lactone form could be an explanation for the differences between patients in susceptibility for statin-induced muscle pain."
He and his colleagues believe their findings will lead to new classes of cholesterol-lowering drugs without the unwanted muscle effects. 
In their study, the team also found they could reduce lactone's ability to interfere with mitochondrial function, suggesting there are ways to prevent or reverse the side effects of statins.
The team is currently pursuing both opportunities.
Meanwhile,  Medical News Today recently learned about new research that suggests  statins are being used by very elderly Americans "without any evidence from testing."
Writing in JAMA Internal Medicine, the researchers note that despite a lack of clear recommendation for statin use in the very elderly, over the last decade or so there has been a large increase in the use of the cholesterol-lowering drugs among the over-80s.
Copyright: Medical News Today

How I Turned a Clerk’s Insult About My Neck Into Dystonia Awareness

Sept. 2, 2015

When my dystonia was severe, my neck was turned and locked towards my right shoulder. Most people would look and not say anything. Then there were some who looked and asked questions, and then there were a few who were downright rude. Those were the tough ones to handle early on because I was already angry for having dystonia and I didn’t need someone to put fuel on that fire. However, one incident made me realize I can turn an insult into awareness when I respond appropriately.
I walked into a convenience store when I was having a particularly tough day. As soon as I went in, the girl behind the counter turned her neck to mimic how mine looked. At first I was taken aback and wanted to lash out at her for being mean. Instead, I stopped myself and realized that although it was rude, she didn’t mean any harm. She thought I was doing it on purpose. Instead of getting upset, I smiled and told her what was wrong. She apologized profusely for mocking me, and we had a nice conversation about dystonia. Instead of creating a scene, I appealed to her sensitive side and it became an education…for both of us! She learned about dystonia, and I learned that every encounter is an opportunity to raise awareness.
Not only did this encounter help me realize every situation gives me the opportunity to teach others about dystonia, it also made me realize everyone responds to us differently and what matters most is how we respond to them. I could have gotten angry, but I looked at it as an opportunity to talk to her. It also made me more comfortable, gave me confidence and better prepared me for future interactions.
Taking advantage of these opportunities helps us educate others, and at the same time, reduce our anxiety about dystonia. Give people a chance to show their compassion by letting them in. Smile. Say hello. Engage them in some way. All of this is part of the process of accepting our condition. When we are comfortable looking or feeling different, our social phobias diminish.
Since it is difficult to understand dystonia, I talk about it with as many people as possible. The more people I tell, the more awareness there is and the greater chance I will be better understood. Talking about dystonia also helps eliminate the stigma associated with chronic conditions, and it makes me feel less anxious and self conscious, especially in public.
There are times I can sense that someone is uncomfortable and wants to say something, but doesn’t know what to say or how to say it. In these cases, I try to break the ice with a brief comment, which is typically a lighthearted joke about my particular symptoms at the moment. Whether or not this leads to talking more about dystonia, at the very least it helps reduce the discomfort that I or others might be feeling.
Talking about it also provides an opportunity to help someone else with dystonia who may not know they have it. This has happened to me several times. After bringing it up in conversations, some people have literally said, “That sounds like what my friend has! I need to tell him/her about this. Thank you so much for telling me.”
Considering how unaware the public is about dystonia, not to mention the many people who are undiagnosed and misdiagnosed, I see it as a responsibility to tell people about it. How is dystonia going to get more awareness if we who have it remain silent? We live with a condition that is not as well known as conditions that affect fewer people. We need to speak up and play a part in dystonia becoming a household name by telling people about it, both friends and strangers. It matters to those of us living with dystonia to keep talking and answering all the puzzled expressions.

Read more:

Acadia Pharmaceuticals submits new FDA for Parkinson's psychosis drug


Acadia Pharmaceuticals said Thursday it has submitted a New Drug Application to the U.S. Food and Drug Administration for its Nuplazid treatment for psychosis associated with Parkinson's Disease. "NUPLAZID holds promise for patients with Parkinson's disease psychosis who currently have no FDA-approved treatment options," said Steve Davis, who was named Chief Executive of Acadia in a separate statement early Thursday. Davis joined the company in July 2014 as chief financial officer, and became interim CEO in March. He has previously worked at Heron Therapeutics, Ardea Biosciences Inc. and at Neurogen, said the statement. About one million people in the U.S. suffer from Parkinson's, according to the National Parkinson Foundation. Acadia shares were indicating higher in light, premarket trade, but are up 20% in the year so far, while the S&P 500 has lost 5.3%.

ACADIA Pharmaceuticals Inc:Announces it has submitted a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) seeking approval for NUPLAZID (pimavanserin) for the treatment of psychosis associated with Parkinson's disease.

Cynapsus Therapeutics Enrolls First Patient in Pivotal Phase 3 Safety Study of APL-130277 for the Treatment of OFF Episodes in Patients With Parkinson's Disease

TORONTO, Sept. 2, 2015 (GLOBE NEWSWIRE) --

Cynapsus Therapeutics Inc. (NASDAQ:CYNA) (TSX:CTH) (the "Company") today announced enrollment of the first patient in the CTH-301 clinical trial, a pivotal Phase 3 study to examine the safety and tolerability of APL-130277 for the acute treatment of OFF episodes in patients with Parkinson's disease (PD). CTH-300, a pivotal Phase 3 efficacy study, is also ongoing with data expected from both trials in 2016.
Dr. Albert Agro, Chief Medical Officer of Cynapsus, stated, "Enrolling the first patient in the CTH-301 safety study is a significant milestone for Cynapsus. The design and endpoints for this study were based on an End-of-Phase 2 meeting with the FDA earlier this year. The CTH-301 study, together with the CTH-300 efficacy study, will form the basis for our expected NDA submission near the end of 2016. We believe that apomorphine, the only approved drug to rapidly treat OFF episodes, combined with our sublingual film delivery technology, could provide many patients with a rapid, reliable means of turning ON from the OFF state."
The CTH-301 trial is a 6-month, open-label, single arm safety study in PD patients who have at least one OFF episode every 24 hours, with total OFF time of at least two hours per day. The primary endpoint for the study is the safety and tolerability of APL-130277 in patients with PD. The secondary endpoints examine efficacy variables including the change in the MDS-UPDRS Part III scores over the 6-months of treatment. Sites will recruit patients over several months, with each patient being evaluated for six months. An estimated 226 patients will be enrolled, including up to 126 who had been enrolled in the CTH-300 efficacy study and rolled over to this study, plus an additional 100 new patients.
For additional information about the CTH-301 trial and to learn more about eligibility, patients can visit
Anthony Giovinazzo, President and Chief Executive Officer of Cynapsus, said, "Approximately 400,000 people with PD in the U.S. experience debilitating OFF episodes. When PD patients experience an OFF episode, they are often unable to perform simple daily tasks such as eating, bathing and dressing, thus becoming increasingly dependent on caregivers. We believe that APL-130277 can, if approved, change the way a large number of patients around the world manage OFF episodes. While we expect to have 12 weeks of safety data from the CTH-300 efficacy study in early to mid 2016, the 6-month data from the CTH-301 safety study will provide a much more robust assessment of safety."
About Cynapsus
Cynapsus is a specialty Central Nervous System pharmaceutical company developing and preparing to commercialize a fast-acting, easy-to-use, sublingual thin film for the on-demand turning ON of debilitating OFF episodes associated with PD. The Company recently completed a Phase 2 clinical trial for its lead product candidate, APL-130277, a sublingual formulation of apomorphine hydrochloride, or apomorphine. Apomorphine is the only molecule approved for acute, intermittent treatment of OFF episodes for advanced PD patients, but is currently only approved as a subcutaneous injection in the United States. APL-130277 is a "turning ON" medication designed to rapidly, safely and reliably convert a PD patient from the OFF to the ON state while avoiding many of the issues associated with subcutaneous delivery of apomorphine. It is designed to convert all types of OFF episodes, including morning OFF episodes, often considered the most difficult to treat. Cynapsus has initiated its Phase 3 clinical program for APL-130277, relying on the abbreviated Section 505(b)(2) regulatory pathway in the United States, and the Company intends to submit a new drug application in 2016.
Forward-Looking Statements
This announcement contains "forward-looking statements" within the meaning of applicable securities laws, including, without limitation, the expected completion of the CTH-300 and CTH-301 Phase 3 studies of APL-130277 in mid to late 2016, and an NDA submission of APL-130277 in 2016. These forward-looking statements include information about possible or assumed future results of the Company's business, financial condition, results of operations, liquidity, plans and objectives. In some cases, you can identify forward-looking statements by terminology such as "believe," "may," "estimate," "continue," "anticipate," "intend," "should," "plan," "expect," "predict," "potential," or the negative of these terms or other similar expressions. These forward-looking statements are based on the Company's current expectations and beliefs and inherently involve significant risks and uncertainties. Actual results and the timing of events could differ from those anticipated in such forward-looking statements as a result of risks and uncertainties, and include, but are not limited to, those factors identified under the caption "Risk Factors" in the Company's Form 10-Q filed with the United States Securities and Exchange Commission (the "SEC") on August 14, 2015 and its other filings and reports in the United States with the SEC available on the SEC's web site at, and in Canada with the various Canadian securities regulators, which are available online at Furthermore, unless otherwise stated, the forward-looking statements contained in this press release are made as of the date of this press release, and the Company has no intention and undertakes no obligation to update or revise any forward-looking statements, whether as a result of new information, future events, changes or otherwise, except as required by law.
Neither the NASDAQ nor the TSX has approved or disapproved of the contents of this press release.
CONTACT: Company Contacts:
         Cynapsus Therapeutics
         Anthony Giovinazzo
         President and CEO
         (416) 703-2449 x225
         Cynapsus Therapeutics
         Andrew Williams
         COO & CFO
         (416) 703-2449 x253
         Investor Contact:
         The Trout Group
         Marcy Nanus
         Senior Vice President
         (646) 378-2927
         Media Contact:
         Russo Partners LLC
         Matt Middleman
         (212) 845-4272