Published: Wednesday, October 17, 2012 at 5:40 p.m. Last Modified: Wednesday, October 17, 2012 at 5:40 p.m.

A decade ago, deep-brain stimulation for Parkinsons disease was considered a risky procedure. Today, its on the cutting edge of personalized medicine, and researchers at the University of Floridas McKnight Brain Institute are at the forefront of its evolution.

When we started in 2002, there were only a handful of places in the U.S. that did it. There was a lot of skepticism about the operation from internists and neurologists, said Dr. Michael Okun, a neurologist at UF. Now it has gone from crazy to cool to completely accepted.

Okun published an article today in the New England Journal of Medicine that explains how the procedure is helping with Parkinsons disease and other neurological conditions such as obsessive compulsive disorder, Tourettes syndrome and depression.

Okun and Dr. Kelly Foote, a neurosurgeon at UF, have performed more than 800 procedures in the past decade, mostly in Parkinsons patients whose medications have become less effective, leading to complications such as on-off fluctuations.

During the off periods, the medication stops working and patients symptoms such as tremors or immobility worsen. This happens in most patients after about five years, said Okun, and patients with off periods of more than three hours a day are good candidates for deep-brain stimulation.

During the procedure, doctors first identify the part of the brain to target. For most patients, that will be either the subthalamic nucleus or the globus pallidus, two tiny sites involved in controlling movement.

Doctors then drill a dime-sized hole in the skull so they can place a lead that delivers electric current to the troublesome spot responsible for the degeneration caused by the disease.

You want to make sure that you take your time and get it right. Those leads have to be within a half-millimeter to work their magic, Okun said.

Deciding where to place the lead also depends on the patient. If you see a patient and tremors are important maybe they are a dentist or a chef, they might choose one target in the brain. If its a singer or trial litigator, they may target another part of the brain.

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UF: Deep-brain stimulation helping with OCD, Tourette's, along with Parkinson's

Newswise BIRMINGHAM, Ala. For decades, patients with Parkinsons disease (PD) have had the same experience. Their hands start to shake uncontrollably, their limbs become rigid and they lose their balance. Years before those movement problems set in, many begin struggling with fainting, incontinence, sexual dysfunction, anxiety and depression. Many patients are still treated with a 42-year-old drug called L-DOPA, which temporarily staves off symptoms but can itself cause heart arrhythmias, stomach bleeding and hallucinations.

This punishing experience may explain in part why patients with PD die at twice the rate of those without the disease in the years after their diagnosis. In this light, its best to tread carefully when talking about early study results that promise something better. That said, a team of researchers at the University of Alabama at Birmingham is excited.

The UAB team has identified a set of experimental drugs called LRRK2 inhibitors that may go beyond symptom relief to directly counter the inflammation and nerve cell death at the root of Parkinsons. At least, these effects have been suggested in mouse and cell culture studies meant to approximate human disease. UAB researchers reported on these findings today in a presentation at Neuroscience 2012, the annual meeting of the Society for Neuroscience in New Orleans.

We dont yet know what percentage of patients might benefit from LRKK2 inhibitors, but LRRK2 is without a doubt the most exciting target for neuroprotection to have ever been identified in Parkinsons disease, says Andrew West, Ph.D., associate professor in the Department of Neurology within the UAB School of Medicine, who gave the presentation at Neuroscience 2012. We will repeat our experiments many times before drawing final conclusions, but our ultimate goal is see our compound or something like it enter toxicology studies, and ultimately, clinical trials as soon as is prudent.

While Wests compounds are promising, they still face many crucial tests that will decide whether or not they reach human trials. But the field is excited, because this is the first time such a drug target has been found for any neurodegenerative disease. Along with evidence that LRRK2 plays a crucial role in the mechanisms of Parkinsons disease, it is a protein kinase, the same kind of enzyme (although not the same one) that has been safely and potently targeted by existing treatments for other diseases, including the cancer drugs Herceptin, Tarceva and Erbitux.

Why LRRK2? LRRK2 stands for leucine-rich repeat kinase 2. Kinases are enzymes that attach molecules called phosphates to other molecules to start, stop or adjust cellular processes. Past studies found that the most common LRRK2 mutation, called G2019S, makes LRRK2 slightly over-active. The idea is to dial LRRK2 back with drugs.

Whether its a bad version of a gene, an unlucky flu infection, a head injury or just age, something makes a protein called alpha-synuclein build up in the nerve cells of Parkinsons patients, contributing to their self-destruction. Unfortunately, alpha-synuclein and proteins like it are not part of a traditional set of drug-able targets. Once alpha-synuclein builds up, the question becomes whether the brain will handle it well or amplify the disease.

LRRK2, to Wests mind, is a critical decision-maker in the bodys answer to that question. He thinks it operates at the intersection between alpha-synuclein, neurotransmission and immune responses, which fight infectious diseases but also create disease-related inflammation when unleashed at the wrong moment, or in the wrong place or amount. Not everyone who has a LRRK2 mutation develops the disease, but Wests team thinks it becomes important when combined with other factors.

Past studies have shown that alpha-synuclein build-up in nerve cells activates nearby immune cells of the brain called microglia, and that these microglia express high levels of LRRK2. Recent cell studies in Wests lab suggest that mutated, overactive LRRK2 strengthens inflammatory responses in microglia and that inhibiting LRRK2 reduces them. Preliminary data also suggests LRRK2-driven inflammation raises the rate of nerve cell death. Its worth noting, however, that neither these mechanisms nor their relationships with each other and Parkinsons disease have been fully confirmed.

The beauty is that we dont necessarily need to confirm an exact mechanism to move drugs into clinical trials, says West. One could argue that human PD is too complex to fully model in other animals. Many predict that we will not know if we understand Parkinsons disease until we get safe, potent, specific drugs into human studies and until one of them halts or reverses the disease process.

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UAB Team Sets Sights on Neuroprotective Treatment for Parkinson's Disease

Ever since Roy Roden was diagnosed with Parkinsons disease three years ago, hes been on a race to get the most out of life while his body still can.

He has skydived, traveled, zip-lined.

Now, the South Florida native is putting his relay into higher gear, planting his foot firmly on a bike pedal.

Roden and his wife Lynn, of North Miami Beach, will take off Thursday with their two dogs on a cross-country bike ride from Seattle to Miami, to raise awareness and money for Parkinsons.

If you found out you have a degenerative disease, what are you going to do with the next 10 years of your life? Roden said. I want to do something.

Roden, 54, plans to spread the word about clinical trials and share his experience with his most recent treatment, deep brain stimulation.

His doctors are behind him.

I give it the thumbs up, said Dr. Carlos Singer, professor of neurology at the University of Miami School of Medicine and division chief of Parkinsons and movement disorders. It can be inspiring to people. Its neat. It shows how active a person with Parkinsons can be.

A progressive, neurodegenerative brain disorder, Parkinsons is the second most common degenerative disease of the brain, after Alzheimers. It affects one million people in the United States, including an estimated 35,000 in South Florida, according to the National Parkinson Foundation, which is based in Miami.

Each year, about 50,000 to 60,000 cases of Parkinsons are diagnosed, with an average age at diagnosis of 62.

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Couple to bike cross-country for Parkinson’s charities

Pilot Study in Neurosurgery Shows Safety and Benefits of Extradural Stimulation

Newswise Philadelphia, Pa. (October 16, 2012) Electrical stimulation using extradural electrodesplaced underneath the skull but not implanted in the brainis a safe approach with meaningful benefits for patients with Parkinson's disease, reports the October issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

The technique, called extradural motor cortex stimulation (EMCS), may provide a less-invasive alternative to electrical deep brain stimulation (DBS) for some patients with the movement disorder Parkinson's disease. The study was led by Dr. Beatrice Cioni of Catholic University, Rome.

Study Shows Safety and Effectiveness of Extradural Brain Stimulation The researchers evaluated EMCS in nine patients with Parkinson's disease. Over the past decade, DBS using electrodes implanted in specific areas within the brain has become an accepted treatment for Parkinson's disease. In the EMCS technique, a relatively simple surgical procedure is performed to place a strip of four electrodes in an "extradural" locationon top of the tough membrane (dura) lining the brain.

The electrodes were placed over a brain area called the motor cortex, which governs voluntary muscle movements. The study was designed to demonstrate the safety of the EMCS approach, and to provide preliminary information on its effectiveness in relieving the various types of movement abnormalities in Parkinson's disease.

The electrode placement procedure and subsequent electrical stimulation were safe, with no surgical complications or other adverse events. In particular, the patients had no changes in intellectual function or behavior and no seizures or other signs of epilepsy.

Extradural stimulation led to small but significant and lasting improvements in control of voluntary movement. After one year, motor symptoms improved by an average of 13 percent on a standard Parkinson's disease rating scale, while the patient was off medications.

'Remarkable' Improvement in Walking and Related Symptoms The improvement appeared after three to four weeks of electrical stimulation and persisted for a few weeks after stimulation was stopped. In one case where the stimulator was accidentally switched off, it took four weeks before the patient even noticed.

Extradural stimulation was particularly effective in relieving the "axial" symptoms of Parkinson's disease, such as difficulties walking. Patients had significant improvement in walking ability, including fewer problems with "freezing" of gait. The EMCS procedure also reduced tremors and other abnormal movements while improving scores on a quality-of-life questionnaire.

Although DBS is an effective treatment for Parkinson's disease, it's not appropriate for all patients. Some patients have health conditions or old age that would make surgery for electrode placement too risky. Other patientsincluding four of the nine patients in the new studyare eligible for DBS but don't want to undergo electrode placement surgery.

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Less-Invasive Method of Brain Stimulation Helps Patients with Parkinson's Disease

Public release date: 17-Oct-2012 [ | E-mail | Share ]

Contact: Jessica Mikulski jessica.mikulski@uphs.upenn.edu 215-349-8369 University of Pennsylvania School of Medicine

PHILADELPHIA - Changes in the ability to smell and taste can be caused by a simple cold or upper respiratory tract infection, but they may also be among the first signs of neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. Now, new research from the Perelman School of Medicine at the University of Pennsylvania has revealed an association between an impaired sense of smell and myasthenia gravis (MG), a chronic autoimmune neuromuscular disease characterized by fluctuating fatigue and muscle weakness. The findings are published in the latest edition of PLOS ONE.

"This study demonstrates, for the first time, that myasthenia gravis is associated with profound dysfunction of the olfactory system dysfunction equivalent to that observed in Alzheimer's disease and Parkinson's disease," said senior study author Richard Doty, PhD, director of the Smell and Taste Center at Penn. "The results are the strongest evidence to date that myasthenia gravis, once thought of as solely a disorder of the peripheral nervous system, involves the brain as well."

The general notion that MG is strictly a peripheral nervous system disease stems, in part, from early observations that the disorder is not accompanied by obvious brain pathology. Behavioral and physiological evidence that has been presented in support of MG's involvement in the central nervous system (CNS) has frequently been discounted due to lack of replicability of findings. For example, while some studies have found MG-related deficits in verbal memory, relative to controls, others have not. Nevertheless, scientists have continued to report CNS-related dysfunctions in MG, including visual and auditory deficiencies in this disease. Further, EEG tests have shown abnormalities in MG patients and MG-related antibodies have been detected in cerebrospinal fluid of patients.

In order to further explore the role of the central nervous system in MG, Doty and colleagues employed a smell test that has been used to assess the underlying connection between sense of smell and other neurodegenerative diseases.

"Our sense of smell is directly linked to numerous functions of the brain," says Doty, one of the original researchers who made the connection between loss of smell and Parkinson's disease. "Olfaction is a good model system for other, more complicated, brain circuits. Understanding our sense of smell, or lack thereof, offers broader insights into brain functions and diseases stemming from the brain."

In the current study, 27 MG patients were individually matched for age and sex to 27 normal controls. Eleven patients with polymyositis, a disorder with debilitating muscle symptoms similar to those of MG, also were tested. All participants were administered the University of Pennsylvania Smell Identification Test (UPSIT) and the Picture Identification Test (PIT), a picture test that is equivalent in content and form to the UPSIT designed to control for non-olfactory cognitive deficits. The research team also monitored each patient during the UPSIT and found no impaired ability to inhale, ruling out physical impediments to sniffing the odors.

Researchers found that the UPSIT scores of the MG patients were significantly lower than those of the age- and sex-matched normal controls, as well as the patients with polymyositis. Of the MG patients, only 15 percent were even aware of a smell problem before testing.

"The marked difference in smell dysfunction between the MG patients and the controls cannot be explained by any other physical or cognitive differences," says Doty. "Although we are still exploring the physiological basis of this dysfunction in MG, it's important to note that the extent of the diminished ability to identify odors found in this study is of the same magnitude as that observed in a range of CNS-related diseases, including Alzheimer's and Parkinson's."

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Association between rare neuromuscular disorder and loss of smell, Penn Study finds

The nuclei of brain stem cells in some Parkinson's patients become misshapen with age. The discovery opens up new ways to target the disease.

Nubby nucleus: Brain cells from a deceased Parkinsons patient have deformed nuclei (bottom) compared with normal brain cells from an individual of a similar age. Merce Marti and Juan Carlos Izpisua Belmonte

Stem cells in the brains of some Parkinson's patients are increasingly damaged as they age, an effect that eventually diminishes their ability to replicate and differentiate into mature cell types. Researchers studied neural stem cells created from patients' own skin cells to identify the defects. The findings offer a new focus for therapeutics that target the cellular change.

The report, published today in Nature, takes advantage of the ability to model diseases in cell culture by turning patient's own cells first into so-called induced pluripotent stem cells and then into disease-relevant cell typesin this case, neural stem cells. The basis of these techniques was recognized with a Nobel Prize in medicine last week.

The authors studied cells taken from patients with a heritable form of Parkinson's that stems from mutations in a gene. After growing several generation of neural stem cells derived from patients with that mutation, they saw the cell nuclei start to develop abnormal shapes. Those abnormalities compromise the survival of the neural stem cells, says study coauthor Ignacio Sancho-Martinez of the Salk Institute for Biological Studies in La Jolla, California.

Today's study "brings to light a new avenue for trying to figure out the mechanism of Parkinson's," says Scott Noggle of the New York Stem Cell Foundation. It also provides a new set of therapeutic targets: "Drugs that target or modify the activity [of the gene] could be applicable to Parkinson's patients. This gives you a handle on what to start designing drug screens around."

The strange nuclei were also seen in patients who did not have a known genetic basis for Parkinson's disease. The authors suggest this indicates that dysfunctional neural stem cells could contribute to Parkinson's. While that conclusion is "highly speculative," says Ole Isacson, a neuroscientist at Harvard Medical School, the study demonstrates the "wealth of data and information that we now can gain from iPS cells."

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Parkinson's cells

CAMBRIDGE, Mass., Oct.17, 2012 /PRNewswire/ --NeuroPhage Pharmaceuticals, Inc. announced today positive data with NPT001 in an alpha-synuclein pre-clinical model for Parkinson's disease (PD). The study was funded by The Michael J. Fox Foundation (MJFF). NPT001 is a first-in-class drug candidate with potential disease-modifying activity that disrupts and clears a variety of amyloid aggregates in the brain. In addition to reducing beta amyloid and tau aggregates in Alzheimer's disease (AD) preclinical studies, the new study demonstrates that NPT001 disrupts alpha-synuclein fibrils which are thought to play a critical role in PD.

The study was conducted in collaboration with Dr. Eliezer Masliah at the University of California San Diego (UCSD) and demonstrated that a single NPT001 treatment produced significant reductions in neuropathology along with improved motor performance in the PD model. Specifically, NPT001 significantly reduced alpha-synuclein deposits in the brain and restored dopamine-producing cells to normal function. Deficits in dopamine production are responsible for many of the behavioral dysfunctions in PD. In addition, NPT001 was well-tolerated and produced no observable adverse effects.

The data will be presented at the upcoming 2013 ADPD meeting in Florence, Italy. "The effects produced by NPT001 are robust and impressive, and the treatment improved the critical functions that are impaired in the brain of Parkinson patients," said Dr. Franz Hefti, PD expert and Chairman of NeuroPhage's Scientific Advisory Board.

"We are excited by the results of this study showing dose-dependent amelioration of neuropathology and functional improvement in a Parkinson's disease pre-clinical model following treatment with NPT001. These results, taken together with our biochemical and cell data for alpha-synuclein, support the development of NPT001 for PD in addition to the ongoing clinical development for Alzheimer's disease," said Dr. Kimberley S. Gannon, NeuroPhage's Senior Vice President of Preclinical Research & Development.

NeuroPhage's technology platform permits the development of therapeutics that target multiple misfolded proteins involved in neurodegeneration such as beta amyloid and tau (involved in AD), as well as alpha-synuclein (involved in PD). In February 2012, NeuroPhage announced that it had received a grant from MJFF for PD research on NPT001.

About Parkinson's Disease

Parkinson's disease is a chronic, progressive disorder of the central nervous system and results from the loss of cells in an area of the brain called the substantia nigra. These cells produce dopamine, a chemical messenger responsible for transmitting signals within the brain. Loss of dopamine causes critical nerve cells in the brain, or neurons, to fire out of control, leaving patients unable to direct or control their movement in a normal manner. The symptoms of Parkinson's may include tremors, difficulty maintaining balance and gait, rigidity or stiffness of the limbs and trunk, and general slowness of movement (also called bradykinesia). Patients may also eventually have difficulty walking, talking, or completing other simple tasks. Symptoms often appear gradually yet with increasing severity, and the progression of the disease may vary widely from patient to patient. There is no cure for Parkinson's disease. Drugs have been developed that can help patients manage many of the symptoms; however they do not prevent disease progression.

About The Michael J. Fox Foundation

The Michael J. Fox Foundation is dedicated to finding a cure for Parkinson's disease through an aggressively funded research agenda and to ensuring the development of improved therapies for those living with Parkinson's today. The Foundation has funded over $304 million in research to date.

About NeuroPhage

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NeuroPhage Reports Beneficial Effects of its Drug Candidate in a Pre-clinical Study of Parkinson's Disease Funded by ...

The sixth annual North Shore Walk for Parkinsons Disease will be held on Saturday, Oct. 20. The 3-mile walk starts at the First Church Congregational, 40 Monument Ave. in Swampscott. Registration is $25 and starts at 10 a.m.; the walk begins at 10:30 a.m. Free T-shirts will be provided for the first 100 walkers.

The North Shore Walk for Parkinsons Disease was started by the Wistran family of Swampscott in honor of Dr. Daniel Wistran, who has been battling Parkinsons disease since 1997.

All donations support the Michael J. Fox Foundation, which is dedicated to finding a cure for Parkinsons disease within the decade. Five million people worldwide are living with Parkinsons disease a chronic, degenerative neurological disorder. In the United States, 60,000 new cases will be diagnosed this year alone. There is no known cure for Parkinsons disease.

For more information, call 781-307-5804 or email northshorewalk@gmail.com. Donations may be made online teamfox.org/goto/northshorewalk.

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Parkinson’s walk set for Saturday in Swampscott

Pig cells will be transplanted into the brains of New Zealanders with Parkinson's disease as part of an experimental treatment of the neurological disorder.

Kiwi scientists will undertake the clinical trial after Living Cell Technologies, which has its research and development based in this country, got the go-ahead to test the treatment in humans next year.

Government approval was given this week for the trial.

'Receiving regulatory approval to conduct clinical trials is a critical step in developing a treatment for this debilitating condition,' said the company's chief executive Andrea Grant said in a statement.

She says pre-clinical trials suggest the treatment, known as NTCELL, can protect brain tissue which would otherwise die, potentially delaying or preventing the effects of Parkinson's.

Only those who have been diagnosed with the neurodegenerative disease for at least four years will be part of the study, which will last for up to 60 weeks.

The trial will involve patients getting either the pig cells or the current gold standard of treatment - deep brain stimulation.

The leader of Auckland District Health Board's movement disorder clinic, Barry Snow, will oversee the trial.

'This represents an exciting new potential option for patients,' Dr Snow said.

Pre-clinical studies had shown improvement in movement and neurological defects and a rise in dopamine-producing neurons within two weeks of treatment.

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Pig cell Parkinson's treatment okayed

NOKOMIS, Fla.--(BUSINESS WIRE)--

Stem cell research may hold the key to a cure for Parkinsons disease. The only problem is, stem cell research hasnt advanced as quickly as patients need it to. Rainbow BioSciences, the biotech subsidiary of Rainbow Coral Corp. (RBCC) is working to market an advanced stem cell growth solution that could potentially energize the worldwide search for a cure.

Currently, government restrictions and ethical dilemmas serve as roadblocks to fast-paced stem cell research, but even when these roadblocks are absent, controlling the behavior of stem cells in a laboratory isnt easy. One way to help speed research projects up and make them more efficient is to raise the number of high-quality adult stem cells available for that research.

RBCC is working to do just that. The company has engaged Regenetech in discussions regarding the potential acquisition of a license to perform cell expansion using that companys Rotary Cell Culture SystemTM.

Originally developed by NASA, the Rotary Cell Culture SystemTM is a rotating-wall bioreactor designed to facilitate the growth of human cells in simulated weightlessness. Cell cultures, including stem cells, grown inside the bioreactor look and function much closer to human cells grown within the body than the flat cell cultures grown in Petri dishes.

By bringing the bioreactor to emerging research markets where stem cell research faces fewer roadblocks, RBCC hopes to help kickstart billions of dollars worth of research into possible cures for Parkinsons and other neurological disorders.

RBCC plans to offer new technology to compete in the stem-cell research industry alongside Amgen, Inc. (AMGN), Celgene Corporation (CELG), Genzyme Corp. (NASDAQ:GENZ) and Gilead Sciences Inc. (GILD).

For more information on Rainbow BioSciences, please visit http://www.rainbowbiosciences.com/investors.html.

About Rainbow BioSciences

Rainbow BioSciences, LLC, is a wholly owned subsidiary of Rainbow Coral Corp. (OTCBB:RBCC). The company continually seeks out new partnerships with biotechnology developers to deliver profitable new medical technologies and innovations. For more information on our growth-oriented business initiatives, please visit our website at [http://www.RainbowBioSciences.com]. For investment information and performance data on the company, please visit http://www.RainbowBioSciences.com/investors.html.

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RBCC: NASA Bioreactor Could Speed Parkinson’s Research

Editor's Choice Academic Journal Main Category: Parkinson's Disease Also Included In: MRI / PET / Ultrasound Article Date: 05 Oct 2012 - 8:00 PDT

Current ratings for: Brain Scan Can Predict The Course Of Parkinson's Disease

4.25 (4 votes)

The authors explained that this brain scan can identify which Parkinson's patients are at risk of severe disease, thus enabling doctors to better manage and treat their symptoms.

Some specialists already use the DaTscan when confirming a Parkinson's diagnosis after a physical examination.

However, the DaTscan can only help in the diagnosis to a certain extent. It can point towards Parkinsonism, but cannot help the doctor distinguish between many similar disorders, of which classic Parkinson's disease is one.

GE Healthcare announced the availability of DaTscan (Ioflupane I 123 Injection) in June 2011.

When using the DaTscan, the patient is injected with a small quantity of a radioactive contrast agent which binds to dopamine transporters in the brain. Then, a scanner is used to measure how much of the contrast agent there is in the brain, and where exactly it is. People with Parkinson's have fewer neurons with dopamine transporters, thus, lower amounts of the radioactive agent appear in their brain scans, compared to "healthy" individuals.

Bernard Ravina, M.D., M.S.C.E., and team set out to determine whether the DaTscan might be used to predict the long-term progression of Parkinson's disease. They looked at the DaTscan images of 491 individuals who had just been diagnosed with Parkinson's - none of them had yet started on standard medications for the disease. All the patients were participants in the Longitudinal and Biomarker Study in PD (LABS-PD), a clinical trial funded in part by the Parkinson's Disease Foundation.

The LABS-PD study had been a long-term one, thus the team were able to compare participants' DaTscan results, which were taken just after diagnosis and then again 22 months later, with information from their yearly health assessments.

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Brain Scan Can Predict The Course Of Parkinson's Disease

Pig cells will be transplanted into the brains of New Zealanders with Parkinson's disease as part of an experimental treatment of the neurological disorder.

Kiwi scientists will undertake the clinical trial after Living Cell Technologies, which has its research and development based in this country, got the go-ahead to test the treatment in humans next year.

Government approval was given this week for the trial.

"Receiving regulatory approval to conduct clinical trials is a critical step in developing a treatment for this debilitating condition," said the company's chief executive Andrea Grant said in a statement.

She says pre-clinical trials suggest the treatment, known as NTCELL, can protect brain tissue which would otherwise die, potentially delaying or preventing the effects of Parkinson's.

Only those who have been diagnosed with the neurodegenerative disease for at least four years will be part of the study, which will last for up to 60 weeks.

The trial will involve patients getting either the pig cells or the current gold standard of treatment - deep brain stimulation.

The leader of Auckland District Health Board's movement disorder clinic, Barry Snow, will oversee the trial.

"This represents an exciting new potential option for patients," Dr Snow said.

Pre-clinical studies had shown improvement in movement and neurological defects and a rise in dopamine-producing neurons within two weeks of treatment.

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Pig cell treatment for Parkinson's okayed

Washington, October 6 (ANI): Boston University School of Medicine (BUSM) investigators have conducted the first genome-wide evaluation of genetic variants associated with Parkinson's disease (PD).

The study points to the involvement of specific genes and alterations in their expression as influencing the risk for developing PD.

Jeanne Latourelle, DSc, assistant professor of neurology at BUSM, served as the study's lead author and Richard H. Myers, PhD, professor of neurology at BUSM, served as the study's principal investigator and senior author.

A recent paper by the PD Genome Wide Association Study Consortium (PDGC) confirmed that an increased risk for PD was seen in individuals with genetic variants in or near the genes SNCA, MAPT, GAK/DGKQ, HLA and RIT2, but the mechanism behind the increased risk was not determined.

"One possible effect of the variants would be to change the manner in which a gene is expressed in the brains, leading to increased risk of PD," said Latourelle.

To investigate the theory, the researchers examined the relationship between PD-associated genetic variants and levels of gene expression in brain samples from the frontal cortex of 26 samples with known PD and 24 neurologically healthy control samples.

Gene expression was determined using a microarray that screened effects of genetic variants on the expression of genes located very close to the variant, called cis-effects, and genes that are far from the variant, such as those on a completely different chromosome, called trans-effects.

An analysis of the cis-effects showed that several genetic variants in the MAPT region showed a significant association to the expression of multiple nearby genes, including gene LOC644246, the duplicated genes LRRC37A and LRRC37A2 and the gene DCAKD.

Significant cis-effects were also observed between variants in the HLA region on chromosome 6 and two nearby genes HLA-DQA1 and HLA-DQA1. An examination of trans-effects revealed 23 DNA sequence variations that reached statistical significance involving variants from the SNCA, MAPT and RIT2 genes.

"The identification of the specific altered genes in PD opens opportunities to further study them in model organisms or cell lines with the goal of identifying drugs which may rectify the defects as treatment for PD," said Myers.

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Genes behind Parkinson's disease identified

Editor's Choice Academic Journal Main Category: Parkinson's Disease Also Included In: Rehabilitation / Physical Therapy Article Date: 05 Oct 2012 - 4:00 PDT

Current ratings for: Parkinson's Patients Benefit From Physical Therapy

3.5 (6 votes)

In the USA, the term is Physical Therapy. In the United Kingdom, Ireland, and Australasia people say Physiotherapy.

Parkinson's disease management has traditionally been centered on drug therapy. Recently, however, doctors have been progressively embracing rehabilitation therapies, including physical therapy as a supplement to medications and neurosurgical treatment.

Dr Claire Tomlinson and team set out to determine what effect rehabilitation therapies might have on patients with Parkinson's disease. They gathered data from 39 randomized trials involving 1,827 people. Within those studies they assessed a wide range of physical therapy methods that were used to treat patients, including dance, treadmill training, exercises and physical therapy.

The researchers assessed 18 physical therapy outcomes, which showed clear improvements in nine areas.

They detected three especially positive outcomes from physical therapy treatment in the following areas:

Parkinson's patients demonstrated that they were able to walk faster or maintain their balance more effectively, and without intervention, after undergoing physical therapy sessions.

Dr Tomlinson, said:

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Parkinson's Patients Benefit From Physical Therapy

Editor's Choice Main Category: Parkinson's Disease Also Included In: Stem Cell Research Article Date: 04 Oct 2012 - 11:00 PDT

Current ratings for: Parkinson's Disease Cure May Be In Stem Cell Research, But..

3.67 (3 votes)

An advanced stem cell growth solution that may potentially lead to a search for a Parkinson's cure, according to a communiqu released today by Rainbow Biosciences. The company is working towards having such technology on the market as soon as possible.

Scientists say that ethical dilemmas and government restrictions have made stem cell research breakthrough much more difficult to achieve. Add to this the difficulty in controlling stem cell behavior in the lab, and the task seems even harder.

Rainbow Biosciences says that one way to accelerate research projects and make them advance more efficiently is to increase the availability of top-quality adult stem cells for research.

Rainbow says it is working on this. It is in discussions with Regenetech regarding acquiring a license to perform cell expansion using its Rotary Cell Culture System, which was originally developed by NASA.

Rainbow Biosciences wrote:

The company would like to bring the bioreactor to "emerging research markets" which do not face as many regulatory roadblocks. They say this will help activate "billions of dollars' worth of research" into potential cures for Parkinson's disease, as well as some the disorders of the nervous system.

Rainbow Biosciences says that this new addition to the stem cell research world will compete alongside industry giants, such as Amgen Inc., Celgene Corporation, Gilead Sciences Inc., and Gynzyme Corp.

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Parkinson's Disease Cure May Be In Stem Cell Research, But..

NATICK, Mass., Sept. 28, 2012 /PRNewswire/ --Boston Scientific Corporation (BSX) received CE Mark approval for use of its Vercise Deep Brain Stimulation (DBS) System for the treatment of Parkinson's disease. The Vercise DBS System is the first and only commercially available DBS system to incorporate multiple independent current control, which is designed to selectively stimulate targeted areas in the brain. This system is an innovative technology that is designed to provide physicians fine control of stimulation.

"The launch of the Vercise DBS System represents a key expansion for Boston Scientific,"said Maulik Nanavaty, senior vice president and president of Boston Scientific's Neuromodulation Division. "Vercise DBS is the only system on the market able to finely control stimulation with multiple independent current control. This unique technology underscores our commitment to improving patients' lives."

The first commercial implant of the Vercise DBS System was performed by a team at the University Clinic Wurzburg in Germany that included Prof. Dr. Cordula Matthies, Head of Functional Neurosurgery and Prof. Dr. Jens Volkmann, Director of the Department of Neurology.

"We welcome the Vercise DBS System," said Prof. Dr. Volkmann. "We believe it represents advancement in DBS technology through flexible and unique programming options. We believe the system gives neurologists the ability to precisely target stimulation based on patient needs."

The Vercise System is designed to provide comfort, control, and convenience to the clinician's practice and to patients with Parkinson's disease. It is intended to minimize side effects of stimulation by controlling current at each individual contact on the lead. In addition, the system is designed to offer unique patient benefits including the longest battery life available for DBS therapy and the smallest stimulator footprint.

"The unique technology offered by the Vercise DBS System provides us with new stimulation options we have never had before," said Prof. Dr. Matthies. "I look forward to seeing a positive impact in patients' quality of life."

Parkinson's disease is a progressive neurological disorder which affects 6.3 million people worldwide according to European Parkinson's Disease Association. Deep Brain Stimulators are neurostimulator devices that stimulate specific areas of the brain using electrical signals to treat the symptoms of Parkinson's disease.

Patient Testimonials

To view a patient testimonial about the Vercise DBS System, please CLICK HERE.

"I am really satisfied with the outcome of the DBS surgery and finally back to a normal life. When the Wurzburg team proposed the Vercise DBS system with new capabilities, I thought this was the best solution for me. The recharging system is so convenient, simple and easy to use. I am glad that this new system is expected to minimize the need to undergo regular replacement surgeries and related complications," said Rudolph Roland, a patient with Parkinson's disease from Wurzburg, Germany.

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Boston Scientific Launches Vercise™ Deep Brain Stimulation System in Europe

SUNNYVALE, Calif., Oct. 1, 2012 /PRNewswire/ -- Amarantus BioSciences, Inc. (AMBS), a biotechnology company developing new treatments for brain-related disorders including Parkinson's disease and Traumatic Brain Injuries (TBI) centered on its proprietary anti-apoptotic therapeutic protein known as MANF, today announced the publication of a landmark research paper on MANF, Amarantus' lead development program. The studies were conducted at the University of Helsinki, a research institution based in Helsinki, Finland, performing groundbreaking neuroscience research based in its' Department of Biosciences and Institute of Biotechnology. This research paper, published by Palgi et al., from Dr. Tapio Heino's laboratory at the University of Helsinki in the peer-reviewed journal BMC Genomics is entitled "Gene expression analysis of Drosophila Manf mutants reveals perturbations in membrane traffic and major metabolic changes," in which researchers describe the critical role MANF plays in the endoplasmic reticulum, the unfolded protein response (UPR), and dopaminergic neurons which are affected by Parkinson's Disease. http://www.ncbi.nlm.nih.gov/pubmed/22494833.

"This publication marks a significant advancement in our understanding of how the MANF molecule works in improving overall cellular function," said Dr. John W. Commissiong, Founder & Chief Scientist at Amarantus. "This could be very significant as the MANF Program is advanced for Parkinson's disease"

The MANF-family (MANF and CDNF) of proteins are remarkably conserved in evolution in multicellular organisms. Previous studies in Dr. Heino's laboratory carried out by Palgi et al. demonstrate that fruit fly, Drosophila melanogaster, Manf (DmMANF) is a true orthologue to mammalian MANF, meaning that the proteins have similar biological functions in the two systems. This was most clearly demonstrated by the observation that the lethal effects of the absence of DmMANF observed in Manf mutant flies are fully rescued by human MANF (hMANF). This gene orthology makes Drosophila a powerful genetic model that can be used to study MANF signaling pathways. Furthermore, DmMANF is specifically required for the maintenance of dopaminergic neurites because in Manf mutant embryos and larvae, dopaminergic neurites degenerate and dopamine levels are extremely low. Still, despite these important observations, little is known about the mechanism of action, and about the molecules that interact with the MANF/CDNF proteins.

Dr. Heino's research group has performed an extensive microarray analyses and report interesting genome-wide differences in gene expression between wild type flies, Manf mutant flies, and flies overexpressing Manf. The data obtained from functional annotation clustering, which provides information about biological pathways influenced by these genetic differences, revealed statistically significant enrichment of genes related to metabolism and membrane transport. The observed changes at the gene expression level were further supported by ultrastructural studies of the mutants, which revealed accumulation of vesicles and a structurally disorganized endoplasmic reticulum (ER). Altogether more than 40% of the known Drosophila genes related to the ER and the unfolded protein response (UPR) showed altered expression levels in the mutants. The researchers were also able to demonstrate that lack of DmMANF results in activation of UPR in vivo. Overexpression of DmMANF resulted in upregulation of genes involved in oxidation reduction, an important process that protects dopamine neurons from oxidative stress. Thus, the results support the previously reported findings in mammalian cells that upregulation of MANF is important in the UPR and is protective for the cell. The UPR has been implicated in several human neurodegenerative diseases.

Dr. Mari Palgi, the lead author on the study observed that, "Additionally, this microarray study in Drosophila revealed several other genes and processes implicated in the pathology of Parkinson's disease such as mitochondrial Htra2 and DJ-1, oxidative phosphorylation, and protein ubiquitination. Interestingly, despite the very low dopamine levels in Manf mutants, the genes involved in dopamine synthesis and metabolism showed clear upregulation."

About Amarantus BioSciences, Inc.

Amarantus BioSciences, Inc. is a development-stage biotechnology company founded in January 2008. The Company has a focus on developing certain biologics surrounding the intellectual property and proprietary technologies it owns to treat and/or diagnose Parkinson's disease, Traumatic Brain Injury and other human diseases. The Company owns the intellectual property rights to a therapeutic protein known as Mesencephalic-Astrocyte-derived Neurotrophic Factor ("MANF") and is developing MANF-based products as treatments for brain disorders. The Company also is a Founding Member of the Coalition for Concussion Treatment (#C4CT), a movement initiated in collaboration with Brewer Sports International seeking to raise awareness of new treatments in development for concussions and nervous-system disorders. For further information please visit http://www.Amarantus.com.

Forward Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements include, but are not limited to, statements about the possible benefits of MANF therapeutic applications and/or advantages presented by Amarantus' PhenoGuard technology, as well as statements about expectations, plans and prospects of the development of Amarantus' new product candidates. These forward-looking statements are subject to a number of risks, uncertainties and assumptions, including the risks that the anticipated benefits of the therapeutic drug candidates or discovery platforms, as well as the risks, uncertainties and assumptions relating to the development of Amarantus' new product candidates, including those identified under "Risk Factors" in Amarantus' most recently filed Annual Report on Form 10-K and Quarterly Report on Form 10-Q and in other filings Amarantus periodically makes with the SEC. Actual results may differ materially from those contemplated by these forward-looking statements Amarantus does not undertake to update any of these forward-looking statements to reflect a change in its views or events or circumstances that occur after the date of this presentation.

MEDIA CONTACTS Amarantus BioSciences, Inc. Gerald E. Commissiong 408-737-2734 pr@amarantus.com

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Amarantus BioSciences Announces Landmark MANF Genomics Publication

Public release date: 1-Oct-2012 [ | E-mail | Share ]

Contact: Jennifer Brown jennifer-l-brown@uiowa.edu 319-356-7124 University of Iowa Health Care

Diseases that progressively destroy nerve cells in the brain or spinal cord, such as Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), are devastating conditions with no cures.

Now, a team that includes a University of Iowa researcher has identified a new class of small molecules, called the P7C3 series, which block cell death in animal models of these forms of neurodegenerative disease. The P7C3 series could be a starting point for developing drugs that might help treat patients with these diseases. These findings are reported in two new studies published the week of Oct. 1 in PNAS Early Edition.

"We believe that our strategy for identifying and testing these molecules in animal models of disease gives us a rational way to develop a new class of neuroprotective drugs, for which there is a great, unmet need," says Andrew Pieper, M.D., Ph.D., associate professor of psychiatry at the UI Carver College of Medicine, and senior author of the two studies.

About six years ago, Pieper, then at the University of Texas Southwestern Medical Center, and his colleagues screened thousands of compounds in living mice in search of small, drug-like molecules that could boost production of neurons in a region of the brain called the hippocampus. They found one compound that appeared to be particularly successful and called it P7C3.

"We were interested in the hippocampus because new neurons are born there every day. But, this neurogenesis is dampened by certain diseases and also by normal aging," Pieper explains. "We were looking for small drug-like molecules that might enhance production of new neurons and help maintain proper functioning in the hippocampus."

However, when the researchers looked more closely at P7C3, they found that it worked by protecting the newborn neurons from cell death. That finding prompted them to ask whether P7C3 might also protect existing, mature neurons in other regions of the nervous system from dying as well, as occurs in neurodegenerative disease.

Using mouse and worm models of PD and a mouse model of ALS, the research team has now shown that P7C3 and a related, more active compound, P7C3A20, do in fact potently protect the neurons that normally are destroyed by these diseases. Their studies also showed that protection of the neurons correlates with improvement of some disease symptoms, including maintaining normal movement in PD worms, and coordination and strength in ALS mice.

Of mice and worms

Excerpt from:
Potential new class of drugs blocks nerve cell death

A classically trained dancer is using her expertise to raise the spirits and flexibility of people with Parkinsons disease.

Heather Waldon, of Woodside, who has performed at the Kennedy Center for the Performing Arts, recently started teaching therapeutic dance routines in Forest Hills for those with the degenerative disease.

I love seeing the joy of the people who have Parkinsons and seeing them do pretty sophisticated choreography, said Waldon, 41, who has taught at NYU and other universities.

The free classes, which are held on the third Friday of every month, are part of a recent expansion into Queens by the Mark Morris Dance Group and Brooklyn Parkinson Groups Dance for PD program.

We wanted to provide this resource to them in their own neighborhood, said David Leventhal, the program manager.

The class, which is meant to be more recreational than a rigorous physical therapy session, helps people with their coordination, flexibility and rhythm.

All of these seem to fit Parkinsons like a glove, he said.

The BambooMoves yoga studio on Queens Blvd., where the classes are held, donated the space to the program.

Leventhal said he hopes to grow the program into a weekly operation with multiple locations in the borough.

Early adopters of Dance for PD, which began in Forest Hills in July, said they feel empowered during the vibrant sessions.

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Using dance to deal with Parkinson’s

New technology being developed in America analyses tremors, breathiness and other weaknesses in people's voices which are believed to be one of the condition's earliest symptoms.

Experts at the Massachusetts Institute of Technology claim that their computer programme can pick out Parkinson's sufferers with 99 per cent accuracy simply by analysing their speech.

Dr Max Little, a British researcher who is leading the initiative at MIT, now hopes to determine whether the same results could be produced from a patient speaking over the telephone.

By recruiting Parkinson's patients and health volunteers to take part in a three-minute telephone call where they will say "ah", speak some sentences and answer a few questions, he said the system could be programmed to diagnose people remotely, allowing earlier treatment.

He said: "Science tells us voice impairment might be an early sign of Parkinson's. It sounds counterintuitive as Parkinson's is a movement disorder but the voice is a form of movement.

"Neurologists look at changes in the ability to move, which is done with the limbs, but we are looking in the vocal organs the sounds that come out of the mouth. We are fairly confident we can detect the disease over the telephone."

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Parkinson's could be detected by telephone call