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

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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

Recommendation and review posted by Fredricko

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

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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

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

Recommendation and review posted by Fredricko

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

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

Recommendation and review posted by Fredricko

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

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