Parkinson’s Disease Biomarkers Are Target of New Research Effort

Michael J. Fox Foundation-funded study aims to find clinical way of detecting disease in early stages

 DECEMBER 10, 2015 BY CAROLINA HENRIQUES

Researchers at University of California, San Diego School of Medicine, are using a $375,000 grant from the Michael J. Fox Foundation (MJFF) to support work aiming to identify blood biomarkers that might finally lead to an early diagnosis of Parkinson’s disease.

“One of the really unmet needs with Parkinson’s disease is the creation of a simple diagnostic test that can identify the disease early on,” said study leader Paula Desplats, PhD, assistant professor in the Department of Neurosciences at the UCSD, in a university press release. “Like other neurodegenerative disturbances, by the time a Parkinson’s patient has outward symptoms, many neurons are lost.”

No diagnostic tests currently exist for Parkinson’s disease (PD), a condition that affects approximately 1 million people in the United States. Physicians now rely on patients’ symptoms, medical history and neurological exams. Finding biomarkers — unique signs that indicate the existence or progress of a disease — could greatly advance Parkinson’s research.

The study will investigate DNA methylation, an epigenetic cell signaling mechanism used to switch genes on or off, which affects a cell’s physiology. “The most important thing in our study is identifying a biomarker that could be easily tested in the clinic,” Dr. Desplats said. “You can’t probe the brain of the patient; you need to be able to look at tissue that is easily accessible. So we began to investigate changes in methylation that can be read in blood.”

Dr. Desplats’ research is based on two previous, smaller studies that showed unique epigenetic changes in the blood of PD patients compared to controls. One, from 2013-14, involved 46 people and was also financed by MJFF. That study’s findings were “highly sensitive and specific,” she said. “We found a group of genes that, when taken together, show a particular pattern in Parkinson’s disease. They (MJFF) invited us to continue.” The new study, set to begin this month, involves 216 Parkinson’s patients and 216 healthy controls. The Harvard Neurodiscovery Biomarker Program, a study partner, will provide the blood samples to be analyzed. “This is the first longitudinal study of blood methylation for Parkinson’s disease,” concluded Dr. Desplats. “That’s important because these changes may not only help us determine who has Parkinson’s disease, but also help us monitor how a person is progressing in the disease.”

The research team expects to publish study results in 2017.

http://parkinsonsnewstoday.com/2015/12/10/uc-san-diego-receives-michael-j-fox-foundation-grant-to-identify-parkinsons-biomarkers/

For Parkinson’s Management, Deep Brain Stimulation May Complement Drugs

BY MARGARIDA AZEVEDO  
December 9, 2015
DBS offers alternative to high-dose medications in advancing stages of disease, doctor says

In a recent Medical Minute, a weekly health news feature from Penn State’s Milton S. Hershey Medical Center, Dr. James McInerney discusses developments in Parkinson’s disease research and the different approaches to symptom management, with special focus on deep brain stimulation (DBS).

Parkinson’s disease (PD) is a progressive and debilitating neurodegenerative disease, characterized by the loss of control of balance, movement, and coordination as well as progressive impairment of intellectual function. Symptom onset usually occurs when 50% to 80% of the patient’s neurons have died, but replacing dying cells through stem cell therapy, for example, is not yet effective, making these cells also vulnerable to degeneration.

Initial treatment involves dopaminergic medication that temporarily replaces dopamine levels or mimics this neurotransmitter action, since most PD symptoms are caused by the lack of dopamine in the brain. These drugs usually help to reduce tremors, improve overall motor skills and coordination of movements, all symptoms that tend to get worse as disease progresses and hinder basic activities such as sleep, movement, eating, and dressing. Frequently, PD is also associated with clinical depression that also requires treatment with antidepressants. Correct management of mood disturbances often leads to motor improvements in PD patients.

Another type of treatment is deep brain stimulation, a surgical procedure intended to treat neurological symptoms and help patients control their movements. A medical device called a neurostimulator is implanted in the brain and delivers electrical stimulation, which can be adjusted by doctors, selecting brain areas that control movement and blocking abnormal nerve signals that cause tremors and other symptoms. This treatment, approved by the U.S. Food and Drug Administration (FDA) for other conditions, such as dystonia and obsessive-compulsive disorder, is usually recommended for patients whose symptoms are worsening and require a more intense medication regimen. Although not a first line of treatment, DBS constitutes a complement to medication. According to Dr. McInerney, “[i]t works better because it is on all the time and it doesn’t cycle on and off the way medications do. And it typically doesn’t produce side effects.”

Dr. McInerney concludes by stressing the importance of symptom awareness for the well-being of the patient. “We want to give them a one-stop shop because if you don’t, you’re not taking care of the whole person. You have to look for these other symptoms and know they are going on,” he said.

The Centers for Disease Control and Prevention (CDC) rates complications caused by PD as the 14th cause of death in the United States, according to the National Parkinson Foundation, although the disease itself is not fatal.

http://parkinsonsnewstoday.com/2015/12/09/the-medical-minute-with-parkinsons-disease-countering-symptoms-is-key/

Cynapsus Therapeutics Announces Positive Data Presentations at World Congress on Parkinson's Disease and Related Disorders Meeting

Dec 8, 2015 

TORONTO, Dec. 8, 2015 (GLOBE NEWSWIRE) -- Cynapsus Therapeutics Inc. ("Cynapsus") (NASDAQ:CYNA) (TSX:CTH), a specialty central nervous system ("CNS") pharmaceutical company developing and preparing to commercialize an easy-to-use, sublingual thin film for the on-demand management of debilitating OFF episodes associated with Parkinson's disease ("PD"), today announced the presentation of updated clinical data from the Phase 2 trial of APL-130277 in five poster presentations at the XXI World Congress on Parkinson's Disease and Related Disorders ("IAPRD") Meeting in Milan, Italy. These results showed APL-130277 significantly improved PD symptoms (as measured by MDS-UPDRS Part III), rapidly turning patients from the OFF to ON state and was generally safe and well-tolerated.

"These additional Phase 2 data presented at the World Congress further support the potential of APL-130277 to rapidly convert patients with motor fluctuations from a debilitating OFF state to ON," said Dr. Albert Agro, Chief Medical Officer of Cynapsus. "We are encouraged by the clinical profile demonstrated to-date and the possibility to offer a treatment alternative for patients who suffer with Parkinson's disease. We continue to enroll patients in our pivotal Phase 3 efficacy and safety studies, and expect to share top-line data in mid-to-late 2016. We also expect to file our New Drug Application for APL-130277 with the U.S. FDA near the end of 2016."

Cynapsus will also host a symposium at the World Congress and is a platinum sponsor. Additional information can be found at the Web site link: http://www.oic.it/iaprd2015/

Phase 2 Clinical Study Design

In the CTH-105 multicenter open-label study, APL-130277 was assessed in 19 patients with PD who experienced the debilitating effects of OFF episodes, with a total duration of OFF of at least two hours daily. By withholding the first dose of levodopa in the morning, patients were dosed in the practically defined OFF state, one of the most difficult to convert to an ON state. Patients were then given escalating doses of APL-130277 until ON was achieved, as documented by study staff and the patient. The MDS-UPDRS Part III score was measured as a secondary endpoint at 15, 30, 45, 60 and 90 minutes after APL-130277 administration.

Poster Presentations

Poster #1: Phase 2 Efficacy Data

The CTH-105 study included PD patients with at least one OFF episode per day and two or more hours of daily OFF time. Patients were dosed in the morning OFF state, starting with APL-130277 10 mg and increased in 5 mg increments until a full ON was achieved, to a maximum of 30 mg. MDS-UPDRS Part III and ON and OFF status was determined pre-dose and 15, 30, 45, 60 and 90 minutes after dosing.

Data presented today at IAPRD showed that 15 of 19 patients dosed achieved a satisfactory full ON following APL-130277 administration. Of the 15 responders, all turned fully ON within 30 minutes of dosing and six within 15 minutes. Thirteen of 15 remained fully ON for at least 30 minutes and 9 of 15 for at least 60 minutes. Mean MDS-UPDRS Part III change from pre-dose to 15, 30, 45, 60 and 90 minutes after dosing for all 19 patients was -11.5, -14.6, -15.0, -13.5 and -9.2, respectively. 

This study demonstrated that APL-130277 rapidly converted PD patients from the OFF to the full ON state and provided clinically meaningful improvement in MDS-UPDRS Part III scores. In addition, much of the benefit was sustained through 90 minutes.

Poster #2: Phase 2 Safety Data

The safety data from CTH-105 assessed 19 subjects who received a total of 77 doses of APL-130277, with doses ranging from 10 mg to 30 mg. Subjects were pre-medicated for three days with trimethobenzamide, which was continued during the study.

Data showed that in this study, 13 (68.4%) patients experienced an adverse event "AE", with most experiencing mild AEs. The most common AEs were dizziness (7/19, 36.8%), somnolence (6/19, 31.6%), nausea (4/19, 21.1%) and yawning (3/19, 15.8%). There was one serious AE of dysphagia deemed not related to APL-130277 by the investigator. There were no AEs of local oral irritation and no subjects discontinued due to AEs. 

These results showed that APL-130277 was safe and well-tolerated in PD patients with OFF episodes. The most common AEs were mild to moderate, and are commonly associated with dopaminergic medications. 

Poster #3: Phase 2 Subgroup Analysis 

This CTH-105 subgroup analysis showed that when evaluating patients by number OFF episodes, age, levodopa dose, number of classes of PD medications and years of OFF episodes, the percentage of patients turning ON with APL-130277, absolute MDS-UPDRS improvement and percent MDS-UPDRS improvement were similar between groups. 

Results also showed that APL-130277 rapidly converted 15 of the 19 PD patients dosed from the OFF to the full ON state regardless of disease severity.

Poster #4: Phase 2 Dose Analysis

Results of CTH-105 showed that of the 19 patients dosed, 15 converted from OFF to ON with APL-130277. There was no correlation with baseline levodopa dose, number of daily OFF episodes or number of PD medications and effective dose of APL-130277. In addition, baseline disease severity did not predict the effective doses needed to turn an OFF patient ON. Therefore, all patients should be titrated starting with the lowest possible dose.

Poster #5: Phase 2 MDS-UPDRS Analysis

In CTH-105, the MDS-UPDRS Part III and ON and OFF status was determined pre-dose and 15, 30, 45, 60 and 90 minutes after dosing. This poster showed that of the 19 patients dosed, 15 converted from OFF to full ON with APL-130277. Of nine patients who were ON at 30 minutes but OFF at 15 minutes, the mean MDS-UPDRS Part III absolute and percentage change was -18.0 and -41.4%, respectively, when ON and -10.1 and -24.6%, respectively, when OFF. Of six patients who turned fully ON at 15 minutes, the mean MDS-UPDRS Part III absolute and percentage change was -14.5 and 38.9% at ON, respectively. 

These results showed that APL-130277 rapidly converts PD patients from the OFF state to the ON state. An MDS-UPDRS Part III improvement of over 10 points and 25% change is needed to turn a patient from the morning OFF state to a full ON state.

Cynapsus Sponsored Symposium

The Importance and Impact of OFF Episodes in PD Patients and the Need for Turning ON Therapies

Today's symposium on December 8, 2015, will include discussions on motor complications in PD, current therapies for motor complications and rescue therapies. It will conclude with a key opinion leader panel discussion. It is being held from 12:00 to 13:30 CET in the Silver Hall.

About Parkinson's Disease and OFF Episodes

More than one million people in the U.S. and an estimated four to six million people worldwide suffer from Parkinson's disease. Parkinson's disease is a chronic and progressive neurodegenerative disease that impacts motor activity, and its prevalence is increasing with the aging of the population. OFF episodes are a complication of Parkinson's disease that leave patients rigid and unable to move and communicate. An estimated one quarter to one half of all people with Parkinson's disease whose symptoms are otherwise managed with ongoing drug therapy experience OFF episodes at least once daily and up to six times daily, with each episode lasting between 30 and 120 minutes.

OFF and motor symptoms of Parkinson's disease are measured by MDS-UPDRS Part III. The MDS-UPDRS Part III is used by neurologists to measure the severity of Parkinson's disease.

About Cynapsus

Cynapsus is a specialty Central Nervous System pharmaceutical company developing and preparing to commercialize an easy-to-use, sublingual thin film for the on-demand management of debilitating OFF episodes associated with Parkinson's disease (PD). The Company recently completed a Phase 2 clinical trial for its 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 ("NDA") in 2016.

Forward-Looking Statements

This announcement contains "forward-looking statements" within the meaning of applicable securities laws, including without limitation, the expected sharing of top-line data for Phase 3 efficacy and safety studies in mid to late 2016, and the expected 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 November 12, 2015 and its other filings and reports in the United States with the SEC available on the SEC's web site at www.sec.gov, and in Canada with the various Canadian securities regulators, which are available online at www.sedar.com. 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 Contact:


Kristen Galfetti


Investor Relations


         (416) 703-2499 x



Vice President, 



I246



kgalfetti@cynapsus.ca




Media Contact:



M-4272

matt.middlem



Russo Partners LLC


Matt Middleman

212) 84


5an@russopartnersllc.com

Read more at Reutershttp://www.reuters.com/article/idUSnHUG5vBWcn+1cc+ONE20151208#rd61VJqMxPF6s8Pf.990

http://health.einnews.com/article/300767156/ff42y88i-0EkXPRX

comments

0
inShare

Share More

A

A

War veteran reveals how Parkinson's drug 'changed his life' and speaks of fears after medicine chiefs axe the treatment in Scotland

• BY VIVIENNE AITKEN  8 DEC 2015
• 
  

  SUFFERER David fears he may lose access to the treatment he claims has changed his life, as it is only available for prescription in England.

Veteran David was prescribed Duodopa before it was axed in Scotland

A FALKLANDS veteran whose life was transformed by a Parkinson’s wonder drug has slammed a decision to restrict its use in Scotland. 

The Scottish Medicines Consortium yesterday rejected the drug Duodopa for routine use on the NHS north of the Border – although it is cleared for use in England. 

Sufferer David Taylor, from Edinburgh , gets the treatment because NHS Lothian pay £28,028 a year for it. But he fears he may lose the drug that has given him his life back, 

The SMC decision means doctors will not be allowed to routinely prescribe it and must make a case to their health board for each patient.

Two photographs taken of David on June 6 this year show the staggering difference Duodopa can make.

David endured agonising cramps caused by the disease early on June 6

David after taking Duodopa, he was smiling on the hills later the same day

In the first, he is pictured rolling about in agony with severe cramps. The second – shot after he took the drug – shows him out hillwalking.

David, 58, was diagnosed with the degenerative neural condition in 2008. Conventional treatments did not control his symptoms and he had severe side effects.

Last night, he said: “Life was hell for me, my wife and family.

“Even when I was taking medication every 90 minutes, I still struggled to control really violent involuntary movements that often alternated with painful cramps.

“One minute I’d be on the floor in agony, unable to move because of the cramps, and next thing I’d be up having violent, uncoordinated movements.”

David, who spent 18 years in the Royal Scots, added: “After my consultant argued my case for nearly a year, I was finally granted funding for Duodopa by the health board.

“The uncontrolled movements and cramps have gone.

“Duodopa has given me a quality of life I couldn’t have had on any other medication.”

Eight to 10 people with Parkinson’s in Scotland would benefit from easier access to Duodopa each year. Parkinson’s UK blasted the SMC’s decision.

They have written to the SMC and Health Secretary Shona Robison asking for an urgent meeting.

The charity’s Scotland director Katherine Crawford said: “It is essential that people with severe Parkinson’s symptoms that are not responding to other treatments can access Duodopa easily. Access to this treatment must not be allowed to become a postcode lottery.”

Without the drug, its users would need round-the-clock care, costing £40,000 a year each.

NHS Lothian’s geriatric medicine consultant Dr Conor Maguire said: “Although the numbers of patients requiring Duodopa is low, it can be a life-changing treatment.

“Our patients deserve better than this.”

The SMC said they rejected the drug because “the submitting company’s justification of the treatment’s cost in relation to its health benefits was not sufficient and the company did not present a sufficiently robust economic analysis”.

http://health.einnews.com/article/300777353/NWRs4CWzTJCjIY50

Designer dopamine neurons to treat Parkinson's

 Monday, December 7, 2015 - 23:54

New York: In a first, a team involved in Parkinson's disease research at the University at Buffalo (UB) has developed a way to ramp up the conversion of skin cells into dopamine neurons which are normally hidden in the brain.

They have identified - and found a way to overcome - a key obstacle to such cellular conversions.

At the same time, the finding has profound implications for changing the way scientists work with all cells.

The new research, published in the journal Nature Communications, revolves around their discovery that p53, a transcription factor protein, acts as a gatekeeper protein.

"We found that p53 tries to maintain the status quo in a cell, it guards against changes from one cell type to another," explained Jian Feng, professor in the Jacobs School of Medicine and Biomedical Sciences at UB.

The team also found that p53 acts as a kind of gatekeeper protein to prevent conversion into another type of cell.

"Once we lowered the expression of p53, then things got interesting: We were able to reprogramme the fibroblasts into neurons much more easily," Feng said.

This is a generic way to change cells from one type to another.

"It proves that we can treat the cell as a software system, when we remove the barriers to change," Feng added.

The researchers have done multiple experiments to prove that these neurons are functional mid-brain dopaminergic neurons - the type lost in Parkinson's disease.

The finding enables researchers to generate patient-specific neurons in a dish that could then be transplanted into the brain to repair the faulty neurons.

It can also be used to efficiently screen new treatments for Parkinson's disease.

http://health.einnews.com/article/300675486/dgmkoRGM6kicHm6P

Breakthrough in cell conversion could help with Parkinson's treatment

CHRIS WOOD  DECEMBER 7, 2015

The researchers were able to create the dopamine neurons (pictured) more efficiently than ever before (Credit: Jian Feng/University at Buffalo) 

A team of University at Buffalo researchers has identified a key obstacle in the cell conversion process, the manipulation of which allows for much easier transitions between cell types. The breakthrough has big implications for the treatment of Parkinson's disease, with scientists able to create functional neurons to replace those damaged by the condition.

Parkinson's disease is a degenerative disorder that involves the loss of dopamine neurons in the brain, having a significant impact on the patient's motor skills. The new study has seen researchers attack the problem head on, attempting to find an efficient method of producing new dopamine neurons, which could then be transplanted into the patient's brain to help tackle the disease.

In the past, researchers have used embryonic stem cells for the purpose, but not only is the material difficult to obtain, but making dopamine neurons from stem cells is time-consuming and doesn't result in a large enough volume of cells. Researchers have also turned to normal cells, such as skin cells, for conversion, but tested methods have suffered from similar issues, with too small a quantity of dopamine neurons being produced.

The new method takes a similar approach, but benefits from a significant breakthrough made by the Buffalo team. In essence, the researchers were able to identify a key obstacle to cellular conversion, which having been discovered can now be manipulated.

The team identified that a transcription factor protein, known as p53, guards against changes within a cell from one type to another, preventing any conversion. Once the expression of the protein was lowered, cell reprogramming became much more effective.

Cells have the same basic source code, with that code being read differently to generate all cell types in the body. Therefore, identifying p53 as the agent that maintains the status quo is significant to cell biology as a whole.

"It proves that we can treat the cell as a software system, when we remove barriers to change," says senior paper author Jian Feng. "We might be able able to play with the system more quickly and we might be able to generate tissues similar to those in the body, even brain tissue."

With the new knowledge, the team set about transitioning skin cells into dopamine neurons. During the process, timing was found to be key, and that by lowering the expression of p53 at the time in the cell cycle just before it prepared to duplicate, the transition was easily achieved. The team manipulated the cells at the right moment, turning on the a DNA modification enzyme known as Tet1, and dopamine neurons were produced.

Since production was completed, the researchers have tested the dopamine neurons, confirming that they're fully functional. The method is highly efficient and could, in the long term, allow for doctors to create patient-specific neurons in the lab, before transplanting them into the brain to repair the neurons damaged by Parkinson's disease.

"Our method is faster and much more efficient than previously developed ones," says Feng. "The best previous method could take two weeks to produce 5 percent dopamine neurons. With ours, we got 60 percent dopamine neurons in 10 days."

The researchers published the findings of the study in the journal Nature Communications.

http://health.einnews.com/article/300662803/qwGFcu8NXZMWmzea
````````````````````````````````````````````````````````````````````````````````````````````

Parkinson’s Therapy Aims to Get Brain to Produce Beneficial Molecule

GM1 ganglioside is known to ease symptoms, but isn't yet widely available

Dec. 7, 2015 BY DANIELA SEMEDO, PHD

In a recent study in the journal PLOS ONE, researchers from the Thomas Jefferson University demonstrate a way of helping the brain produce more of its own GM1 ganglioside, a molecule that has shown promise in relieving Parkinson’s symptoms and slowing disease progression.

Numerous preclinical studies have shown that the administration of GM1 ganglioside, a major component of plasma membrane lipid raft signaling domains, results in significant biochemical and behavioral recovery following different types of nervous system lesions, including those in animal models of Parkinson’s disease (PD). “GM1 ganglioside has shown great promise in Parkinson’s patients,” lead author Jay Schneider, PhD, a professor in the Department of Pathology, Anatomy and Cell Biology at the Sidney Kimmel Medical College, said in a news release. “However, considering the difficulties with the manufacture of GM1 and its delivery to the brain, we wanted to see if we could coax the brain to make more of its own GM1.”

GM1 ganglioside is normally produced by brain nerve cells. However, in patients with PD and with other neurodegenerative conditions, the substance is made at much lower levels than are seen in healthy people.

Previous studies have shown that patients given the GM1 ganglioside had clear symptom and disease improvements, but for these studies, the molecule was extracted from cow brains — an approach with both manufacturing challenges and safety concerns. GM1 ganglioside cannot be readily made synthetically. “We were thinking, ‘There’s got to be a way around this,'” said Dr. Schneider. “Instead of putting more GM1 into the brain, why not try to get the brain to make more of it?”

In the study, titled “Intraventricular Sialidase Administration Enhances GM1 Ganglioside Expression and Is Partially Neuroprotective in a Mouse Model of Parkinson’s Disease,” Dr. Schneider and colleagues conducted a search of existing literature and found that an enzyme known as sialidase was able to convert natural ganglioside molecules in the brain into GM1 ganglioside. Investigators then looked at an alternative therapeutic approach for systemic administration of brain-derived GM1, with the intent of increasing GM1 levels in a mouse model while assessing the substance’s neuroprotective potential. The team inserted a pump that constantly injected sialidase into the animals’ brains. They then initiated the onset of PD in the mice, and observed a neuronal protection at levels identical to those displayed in mice injected directly with GM1 ganglioside.

“We were very excited to see that this could work in the mouse model,” said Dr. Schneider, adding that further efforts are underway. “As long-term delivery of sialidase enzymes to the brain would require implantation of a pump system, which might not be optimal, we are currently working on alternative gene therapy approaches to enhance GM1 levels in the brain.”

A clinical way of increasing GM1 ganglioside levels in the brain could potentially benefit patients with other diseases, including Huntington’s and Alzheimer’s. Dr. Schneider is currently studying gene-therapy methods that could enhance the GM1 ganglioside content of neurons and their neuroprotective potential. For now, provisional patents on the  technologies have been filed.

http://parkinsonsnewstoday.com/2015/12/07/protecting-the-brain-from-parkinsons-disease/

Crises Helplines to call.

Please if your are in a Crisis - don't be afraid - you are not alone. You may feel that no one understands what you are going through. There is nothing to be ashamed of - pick up the phone and call. Many have been in your shoes, and they have been or are being helped. So please call.