Severe Flu Increases Risk Of Parkinson’s

Editor's Choice Main Category: Parkinson's Disease Also Included In: Flu / Cold / SARS Article Date: 28 Jul 2012 - 0:00 PDT

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British Columbia University researchers have discovered that the odds of developing Parkinson's disease later in life doubles with severe influenza, although the discovered that those who contracted a typical case of red measles as children have a 35% lower risk.

The findings of the collaboration between researchers from UBC's School of Population and Public Health and the Pacific Parkinson's Research Center are published online in the July issue of Movement Disorders.

The researchers led by Anne Harris surveyed 403 Canadian Parkinson's patients and 405 healthy Canadian controls to determine whether occupational exposure to vibrations, like operating construction equipment, had any impact on the risk of developing Parkinson's. Harris and her team demonstrated in an earlier study, which appeared online in this month's edition of American Journal of Epidemiology, that occupational exposure actually lowered the risk of developing Parkinson's by 33% in comparison with those who were not exposed to vibrations during their work.

The team discovered in the meantime that people exposed to high-intensity vibrations, as caused by driving snowmobiles, military tanks or high-speed boats, had a consistently higher risk of developing Parkinson's compared with those exposed to lower-intensity vibrations like operating road vehicles. Harris states that although the higher risk was statistically not significant to establish a correlation, it was nevertheless adequately strong enough and consistent to warrant further investigations.

Harris, who is working on her doctorate at UBC, concludes:

Written by Petra Rattue Copyright: Medical News Today Not to be reproduced without permission of Medical News Today

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Severe Flu Increases Risk Of Parkinson's

Patient-Derived Stem Cells Could Improve Drug Research For Parkinson’s

NIH-funded study shows cells from different patients have unique drug responses

Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.

The researchers collected skin cells from patients with genetically inherited forms of Parkinsons and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.

The results were published in Science Translational Medicine.

"These findings suggest new opportunities for clinical trials of Parkinsons disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).

A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.

The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.

Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.

Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.

Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.

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Patient-Derived Stem Cells Could Improve Drug Research For Parkinson's

Lee Judge Simpson says he’s still effective justice despite Parkinson’s disease

Photo by David Ahntholz .da

Joe Simpson

FORT MYERS A Lee circuit judge who hasn't presided over a hearing for a year, but reviews cases and signs orders in an office, contends Parkinson's disease doesn't prevent him from working as a judge and calls his critics misinformed or swayed by stereotypes.

Judge Joseph Simpson, seeking a second six-year term, says it wasn't his choice to be removed from the courtroom last July and given a handicap-accessible office, where he works on a paperwork docket, reviewing domestic violence petitions for temporary injunctions, uncontested divorces, probate files and orders.

"I have been asked why run for re-election and be subjected to ridicule for carrying out my judicial duties with Parkinson's, especially after having spent thousands of dollars to be defended against claims of inability to sit as judge," Simpson wrote in a letter to the Daily News, noting that his mind is still sharp and he uses aids to ensure his voice is clear.

"It is my sincere belief that the public suffers when a judiciary does not include persons with disabilities, with the insight, common sense and experience they bring to the bench," he wrote. " My ability to handle complex legal matters and render sound decisions remains constant."

Simpson detailed his situation in a recent five-page letter to Daily News after the newspaper published a story May 13 about how lawyers and others couldn't understand him, his lack of a hearing docket and the burden it places on judges who share his caseload.

Neither Simpson nor his judicial assistant agreed to interviews for the May 13 story. A Daily News reporter was unable to find or see him because his office isn't accessible without an escort, which wasn't provided.

Circuit Chief Judge Jay Rosman has called Simpson's docket "valuable work" that provides more time for other judges, an accommodation beneficial to the community, the judiciary and Simpson.

But it comes at a time when the state reduced Lee's request for three additional circuit judges to two this year. Lee's circuit civil and probate cases totaled 1.17 million last fiscal year, not including thousands of criminal cases circuit judges hear.

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Lee Judge Simpson says he's still effective justice despite Parkinson's disease

Painting in park raises Parkinson’s awareness

IRVINE Dozens gathered at Mason Regional Park on Saturday to paint pieces of what will be an art installment to raise awareness for Parkinson's disease.

The second annual Unity Barbecue featured artist Jack Knight, who will take the pieces of tubing, tiles and canvas and create a piece to hang on the walls of Aliso Viejo-based Parkinson's in Balance.

Visitors are shown a tile to be painted at the 2nd Annual Painting for Parkinson's and Parkinson's Unity BBQ event held at Mason Regional Park in Irvine on Saturday.

STUART PALLEY, THE ORANGE COUNTY REGISTER

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The event drew those affected by the disease and offered an afternoon of escape.

"I try to pick something that is therapeutic," said Allison Conway, founder of Parkinson's in Balance. "I find it so calming to be able to sit here and create something."

Her painted tile read, "I make Parkinson's look good."

This is the second year Conway, 35, has held the Unity Barbecue in an effort to raise awareness for an illness she knows well.

Conway was diagnosed with an auto-immune disease at age 13, colon cancer at age 24 and young onset Parkinson's at age 32.

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Painting in park raises Parkinson's awareness

FOXO1 gene may play important role in Parkinson’s disease

ScienceDaily (June 29, 2012) A recent study led by researchers at Boston University School of Medicine (BUSM) revealed that the FOXO1 gene may play an important role in the pathological mechanisms of Parkinson's disease.

These findings are published online in PLoS Genetics, a peer-reviewed open-access journal published by the Public Library of Science.

The study was led by Alexandra Dumitriu, PhD, a postdoctoral associate in the department of neurology at BUSM. Richard Myers, PhD, professor of neurology at BUSM, is the study's senior author.

According to the Parkinson's Disease Foundation, 60,000 Americans are diagnosed with Parkinson's disease each year and approximately one million Americans are currently living with the disease.

Parkinson's disease is a complex neurodegenerative disorder characterized by a buildup of proteins in nerve cells that lead to their inability to communicate with one another, causing motor function issues, including tremors and slowness in movement, as well as dementia. The substantia nigra is an area of the midbrain that helps control movement, and previous research has shown that this area of the brain loses neurons as Parkinson's disease progresses.

The researchers analyzed gene expression differences in brain tissue between 27 samples with known Parkinson's disease and 26 samples from neurologically healthy controls. This data set represents the largest number of brain samples used in a whole-genome expression study of Parkinson's disease to date. The novel aspect of this study is represented by the researchers' emphasis on removing possible sources of variation by minimizing the differences among samples. They used only male brain tissue samples that showed no significant marks of Alzheimer's disease pathology, one of the frequently co-occurring neurological diseases in Parkinson's disease patients. The samples also had similar tissue quality and were from the brain's prefrontal cortex, one of the less studied areas for the disease. The prefrontal cortex does not show neuronal death to the same extent as the substantia nigra, although it displays molecular and pathological modifications during the disease process, while also being responsible for the dementia present in a large proportion of Parkinson's disease patients.

Results of the expression experiment showed that the gene FOXO1 had increased expression in the brain tissue samples with known Parkinson's disease. FOXO1 is a transcriptional regulator that can modify the expression of other genes. Further examination of the FOXO1 gene showed that two single-nucleotide polymorphisms (SNPs), or DNA sequence variations, were significantly associated with age at onset of Parkinson's disease.

"Our hypothesis is that FOXO1 acts in a protective manner by activating genes and pathways that fight the neurodegeneration processes," said Dumitriu. "If this is correct, there could be potential to explore FOXO1 as a therapeutic drug target for Parkinson's disease."

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FOXO1 gene may play important role in Parkinson's disease

Personalized Medicine for Parkinson’s Disease

Washington, D.C. - infoZine - Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.

The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability -- in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.

The results were published in Science Translational Medicine.

"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).

A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.

The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.

Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.

Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.

Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.

Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy. The researchers found that oxygen consumption rates were lower in patient cells with LRRK2 mutations, and higher in cells with the PINK1 mutation. In PINK1 mutant cells, the researchers also found increased vulnerability to oxidative stress, a damaging process that in theory can be counteracted with antioxidants.

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Personalized Medicine for Parkinson's Disease

Patient-derived stem cells may improve treatments for Parkinson’s

Washington, July 5 : Researchers have taken a major step in drug research for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments.

The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability - in particular, abnormalities in the cellular energy factories known as mitochondria.

At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.

"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).

The study was conducted by a consortium of researchers led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston with primary funding from NINDS.

The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.

Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.

Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.

Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.

Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy.

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Patient-derived stem cells may improve treatments for Parkinson's

BUSM researchers identify role of FOXO1 gene in Parkinson’s disease

Public release date: 28-Jun-2012 [ | E-mail | Share ]

Contact: Jenny Eriksen Leary jenny.eriksen@bmc.org 617-638-6841 Boston University Medical Center

(Boston) A recent study led by researchers at Boston University School of Medicine (BUSM) revealed that the FOXO1 gene may play an important role in the pathological mechanisms of Parkinson's disease. These findings are published online in PLoS Genetics, a peer-reviewed open-access journal published by the Public Library of Science.

The study was led by Alexandra Dumitriu, PhD, a postdoctoral associate in the department of neurology at BUSM. Richard Myers, PhD, professor of neurology at BUSM, is the study's senior author.

According to the Parkinson's Disease Foundation, 60,000 Americans are diagnosed with Parkinson's disease each year and approximately one million Americans are currently living with the disease.

Parkinson's disease is a complex neurodegenerative disorder characterized by a buildup of proteins in nerve cells that lead to their inability to communicate with one another, causing motor function issues, including tremors and slowness in movement, as well as dementia. The substantia nigra is an area of the midbrain that helps control movement, and previous research has shown that this area of the brain loses neurons as Parkinson's disease progresses.

The researchers analyzed gene expression differences in brain tissue between 27 samples with known Parkinson's disease and 26 samples from neurologically healthy controls. This data set represents the largest number of brain samples used in a whole-genome expression study of Parkinson's disease to date. The novel aspect of this study is represented by the researchers' emphasis on removing possible sources of variation by minimizing the differences among samples. They used only male brain tissue samples that showed no significant marks of Alzheimer's disease pathology, one of the frequently co-occurring neurological diseases in Parkinson's disease patients. The samples also had similar tissue quality and were from the brain's prefrontal cortex, one of the less studied areas for the disease. The prefrontal cortex does not show neuronal death to the same extent as the substantia nigra, although it displays molecular and pathological modifications during the disease process, while also being responsible for the dementia present in a large proportion of Parkinson's disease patients.

Results of the expression experiment showed that the gene FOXO1 had increased expression in the brain tissue samples with known Parkinson's disease. FOXO1 is a transcriptional regulator that can modify the expression of other genes. Further examination of the FOXO1 gene showed that two single-nucleotide polymorphisms (SNPs), or DNA sequence variations, were significantly associated with age at onset of Parkinson's disease.

"Our hypothesis is that FOXO1 acts in a protective manner by activating genes and pathways that fight the neurodegeneration processes," said Dumitriu. "If this is correct, there could be potential to explore FOXO1 as a therapeutic drug target for Parkinson's disease."

###

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BUSM researchers identify role of FOXO1 gene in Parkinson's disease

Speaker offers insights into Parkinson’s

FAIRMONT - It wasn't until celebrities such as Michael J. Fox and Muhammad Ali announced they had Parkinson's Disease that the public began to learn more about this life-altering disease.

While not a terminal illness, Parkinson's does affect the quality of life for those diagnosed.

"About one in 100 people over the age of 60 are diagnosed with Parkinson's Disease," said Rose Wichmann, manager of Struthers Parkinson's Center in Golden Valley. "It goes to two in 100 people over the age of 70. That's more than MS, more than muscular dystrophy and more than ALS-Lou Gehrig's Disease."

Wichmann was in Fairmont on Thursday speaking to a Parkinson's support group at Grace Lutheran Church. She mentioned there are several different types of Parkinson's Disease, and that every person diagnosed has slightly different symptoms.

"Not everyone has the tremors that people associate with Parkinson's," Wichmann said. "We have an acronym called 'TRAP' that lists the four main symptoms, and two or more of these need to be confirmed before receiving a diagnosis."

While tremors are well-associated with Parkinson's, other symptoms are less noticeable, such as rigidity and stiffness in the muscles. There is also the absence or slowing of movements, and posture changes, such as curling over instead of sitting or standing up straight.

"There are about 15 percent of those diagnosed with Parkinson's that never have a tremor," Wichmann said. "But what causes Parkinson's is a group of cells at the base of the brain that produce dopamine. As we age, those cells start to disappear, and about 60 to 80 percent of those disappear before displaying symptoms of Parkinsons."

Dopamine is a chemical that allows the delivery of messages through the brain. Lack of dopamine means signals are not moving as smoothly.

"We say that automatic is broken," Wichmann said. "Those movements you don't even think about, like walking, or rolling over in your sleep. Blinking also goes away, so Parkinson's sufferers have more of a stare. There is a loss of facial expressions because you don't think about if you're going to smile. It's easy for Parkinson's people to be misunderstood because you can't read their facial expressions anymore."

There are also problems with balance.

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Speaker offers insights into Parkinson's

Device Calms Parkinson’s Tremor for 3+ Years

Quality of Life, Daily Living Did Not Improve in Study

By Denise Mann WebMD Health News

Reviewed by Laura J. Martin, MD

June 20, 2012 -- For some people with Parkinson's disease, deep brain stimulation can have immediate and dramatic effects on tremors, rigidity, balance, and other motor symptoms.

Now new research shows that these benefits may last at least three years. The findings appear online in Neurology.

Deep brain stimulation uses a battery-operated device to deliver electrical impulses -- similar to a pacemaker for the heart -- to areas of the brain that control movement. The impulses are thought to block abnormal signals that cause many of the movement problems (motor symptoms) of Parkinson's. This procedure is typically reserved for individuals who no longer respond to their Parkinson's medications or who experience unacceptable side effects from them.

According to the new findings, this treatment helped with motor symptoms such as tremor, but individuals did show gradual declines over time in their quality of life, ability to perform tasks of daily living, and thinking skills.

"This study looked past the immediate 'wow effect,'" says Michele Tagliati, MD. He wrote an editorial accompanying the new study.

"Now we want to know what we can expect over the next 10 years, and this starts to make it clearer," says Tagliati, the director of the Movement Disorders Program at Cedars-Sinai Medical Center in Los Angeles.

"The effect on motor function is sustained," says researcher Frances M. Weaver, PhD. She is the director of the Center for Management of Complex Chronic Care at Edward Hines Jr. VA Hospital in Hines, Ill. But "deep brain stimulation does not have an impact on the other symptoms of the disease, so there will be progression."

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Device Calms Parkinson's Tremor for 3+ Years

uniQure Collaborates with UCSF on GDNF Gene Therapy in Parkinson’s Disease

AMSTERDAM, June 21, 2012 /PRNewswire/ --

uniQure, a leader in the field of human gene therapy, announced today the signing of a collaborative agreement with two leading neurology experts to develop further a gene therapy incorporating uniQure's GDNF (glial cell derived neurotrophic factor) gene for the treatment of Parkinson's disease.

Professor Krystof Bankiewicz at the University of California, San Francisco (UCSF), a world expert in GDNF gene therapy, and Professor Howard Federoff of Georgetown University, a preeminent physician-neuroscientist, have developed a product approved to start clinical trials in the U.S. using uniQure's GDNF gene incorporated into an adeno-associated virus-2 (AAV-2) delivery vector. The GDNF gene contains the information to produce a protein necessary for the development and survival of nerve cells. The positive effect of GDNF on nerve cells has already been demonstrated in early research by uniQure in collaboration with the University of Lund, Sweden.

UCSF entered into a collaboration with Dr. Russell Lonser, neurosurgeon and Chief of the Neurosurgical Branch of the NINDS, a division of the National Institutes of Health, to commence a Phase I study of the gene therapy in patients with Parkinson's disease. Patient enrollment is expected to begin mid-2012. Collaborating on the study will be Drs. Krystof Bankiewicz of UCSF, Howard Federoff of Georgetown University and NINDS co-investigator neurologists Drs. Mark Hallett and Walter Koroshetz.

"This agreement provides uniQure with access to the data from a Parkinson's disease GDNF clinical study conducted by two of the world's leading medical researchers in the field. If successful, we intend to manufacture the vector construct ourselves and with a partner progress the product into advanced clinical studies," said Jrn Aldag, CEO of uniQure. "GDNF has been shown to be involved in several other CNS disorders so if we reach the proof of concept stage in Parkinson's, we can potentially expand product development quickly and efficiently into clinical trials for other indications, such as Huntington's and Multiple System Atrophy (MSA)."

"The development of AAV2-GDNF, sponsored by both NIH and by Parkinson's foundations, has taken us 10 years to complete. We are very pleased that a path for clinical development of AAV2-GDNF as a possible treatment for PD is now in place," said Dr. Krystof Bankiewicz, UCSF Principal Investigator.

Under the terms of uniQure's agreement with UCSF, uniQure holds the exclusive commercial rights to all UCSF preclinical data and to IND enabling Phase I clinical data provided to UCSF by NINDS. In the event that the Phase 1 study shows proof of concept, uniQure will use its proprietary manufacturing system for future production of the AAV construct and take responsibility for future development of the gene therapy product. uniQure holds the exclusive license to the GDNF gene from Amgen.

About uniQure

uniQure is a world leader in the development of human gene based therapies. uniQure has a product pipeline of gene therapy products in development for hemophilia B, acute intermittent porphyria, Parkinson's disease and SanfilippoB. Using adeno-associated viral (AAV) derived vectors as the delivery vehicle of choice for therapeutic genes, the company has been able to design and validate probably the world's first stable and scalable AAV manufacturing platform. This proprietary platform can be applied to a large number of rare (orphan) diseases caused by one faulty gene and allows uniQure to pursue its strategy of focusing on this sector of the industry. Further information can be found at http://www.uniqure.com.

Certain statements in this press release are "forward-looking statements" including those that refer to management's plans and expectations for future operations, prospects and financial condition. Words such as "strategy," "expects," "plans," "anticipates," "believes," "will," "continues," "estimates," "intends," "projects," "goals," "targets" and other words of similar meaning are intended to identify such forward-looking statements. Such statements are based on the current expectations of the management of uniQure only. Undue reliance should not be placed on these statements because, by their nature, they are subject to known and unknown risks and can be affected by factors that are beyond the control of uniQure. Actual results could differ materially from current expectations due to a number of factors and uncertainties affecting uniQure's business. uniQure expressly disclaims any intent or obligation to update any forward-looking statements herein except as required by law.

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uniQure Collaborates with UCSF on GDNF Gene Therapy in Parkinson's Disease

Research and Markets: Handbook of Parkinson’s Disease – Blue-Ribbon Guide

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/lb6wfj/handbook_of_parkin) has announced the addition of the "Handbook of Parkinson's Disease" book to their offering.

This blue-ribbon guide has long prevailed as one of the leading resources on Parkinson's Disease (PD). Fully updated with practical and engaging chapters on pathology, neurochemistry, etiology, and breakthrough research, this source spans every essential topic related to the identification, assessment, and treatment of PD. Reflecting the many advances that have taken place in the management of PD, this source promotes a multidisciplinary approach to care and supplies new sections on the latest pharmacologic, surgical, and rehabilitative therapies, as well as essential diagnostic, imaging, and nonmotor management strategies for PD.

Key Topics Covered:

Early Iconography of Parkinson's Disease

Epidemiology of Parkinsonism

Differential Diagnosis of Parkinsonism

Pathophysiology and Clinical Assessment of Parkinsonian Symptoms and Signs

Autonomic Dysfunction and Management

Sleep Dysfunction in Parkinson's Disease

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Research and Markets: Handbook of Parkinson's Disease - Blue-Ribbon Guide

Parkinson’s Disease – Smelling Test For Early Detection

Editor's Choice Main Category: Parkinson's Disease Article Date: 16 Jun 2012 - 0:00 PDT

Current ratings for: 'Parkinson's Disease - Smelling Test For Early Detection'

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Researchers have now discovered that the sense of smell provides valuable indications. Hyposmia, i.e. losing the ability to smell for no known cause could be a markers for the non-motor signs of Parkinson's disease. Dr Ulrich Liebetrau, chief physician for Parkinson's consultations at the Neurological Department of Kliniken der Stadt Kln, declared at the 22nd Meeting of the European Neurological Society (ENS) in Prague: "Smelling tests in doctors' offices are suitable for detecting hyposmia but so too are tests conducted in public places such as pedestrian zones."

Parkinson's is a very common neurological slowly progressive disease that usually affects individuals aged between 50 and 60 years. In Germany alone there are about 300,000 people diagnosed with Parkinson's. Scientists still remain uncertain for the reasons of cell death occurring in the substantia nigra in the basal ganglia of the brain of Parkinson's patients, but suspect that genetic factors may be involved. The cell death causes a shortage of dopamine, a neurotransmitter, which leads to loss of control over voluntary and involuntary movements. German neurologists from Cologne have now tested a new early detection method for subtle signs of Parkinson's which focuses on the partial loss of the sense of smell, which they based on previous studies that demonstrated that one in ten people with hyposmia develop Parkinson's in later years.

Dr Liebetrau explained: "Our objective was to reach as many people with hyposmia as we possibly could."

The team used an unusual method for their trial. They performed a public smelling test on a Saturday in a banqueting hall in Cologne's pedestrian district that is well known. Liebetrau described the requirements the venue needed to fulfill, saying:

They asked 187 participants to smell vanilla, lemon, cloves and lavender to smell. Overall, 46 participants were identified as having hyposmia, who were all offered a follow-up at the City of Cologne Clinics (Kliniken der Stadt Kln). Dr Liebetrau explained: "The test was to be followed up by a professional examination done by neurologists and ENT specialists at a separate time and place. After all, hyposmia can be a sign of any number of diseases."

The result revealed that three of the 46 individuals with hyposmia were diagnosed with Parkinson's, even though they had no former knowledge prior to the test that they were affected by the disease.

One of the key advantages of low-threshold tests is that diseases that would otherwise go undetected are identified early, which also prevents these diseases from becoming chronic. Early diagnosis is advantageous, even if they involve severe neurological disorders like Parkinson's.

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Parkinson's Disease - Smelling Test For Early Detection

Treating Orthostatic Hypotension Improves Function In Parkinson’s Disease Patients, According To Braintree …

BOSTON, June 21, 2012 /PRNewswire/ --A new study analyzing patient data from Braintree Rehabilitation Hospital in Braintree, Massachusetts, found that blood pressure fluctuations can worsen symptoms of Parkinson's disease. Conversely, after treating Parkinson's disease patients who experienced blood pressure drops when changing from a sitting to standing position, improvements were noted in cognitive function, balance and walking, according to the researchers at Braintree Rehabilitation Hospital.

Information from the study will be presented today at the Movement Disorder Society's 16th International Congress of Parkinson's Disease and Movement Disorders in Dublin, Ireland. The corresponding abstract, "Treating Orthostatic Hypotension in Patients with Parkinson's and Atypical Parkinsonism Improves Function," will be published as an electronic supplement to The Movement Disorders Journal online edition at http://www.movementdisorders.org.

"This new research sheds light for better Parkinson's disease treatment, as blood pressure can be affected by the disease and problems often worsen over time," said Dr. Anna DePold Hohler, Medical Director of the Movement Disorders Program at Braintree Rehabilitation Hospital and Associate Professor of Neurology at Boston University Medical Center, who participated in the study. "The good news for Parkinson's disease patients is that implementing simple interventions, monitored by a physician, can significantly improve functionality."

In the United States, 1.5 million people suffer from this complex neurodegenerative disorder. For this population, blood pressure drops may occur due to a decrease in the neurotransmitter norepinepherine and as a result of medications used to treat motor symptoms.

Depending on the patient, treatment strategies might include increasing water or salt intake, use of compression stockings, and slow position changes. Specific medications may also be warranted in patients at risk for fainting.

These findings update previous work conducted at Braintree Rehabilitation Hospital recently published in the International Journal of Neuroscience, 2011.

The Movement Disorders Program at Braintree Rehabilitation Hospital, a world-class rehabilitative care provider, allows patients to have physical, occupational and speech therapy along with medication adjustments, blood pressure adjustments, and deep brain stimulation adjustments as needed. As a result, improvements in patients are significant and a large number of individuals can be optimized to return home.

Braintree Rehabilitation Hospital is located at 250 Pond Street in Braintree, Massachusetts. For more information visit http://www.braintreerehabhospital.com, or call (781) 348-2500.

Media contact: CM Communications Lori Moretti or Meg Fitzgerald mfitzgerald@cmcommunications.com 617-536-3400

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Treating Orthostatic Hypotension Improves Function In Parkinson's Disease Patients, According To Braintree ...

Researchers ID Cluster of Genes in Blood that Predict Parkinson’s

Newswise Because there is currently no laboratory test that can diagnose Parkinsons disease, it is practically impossible to detect those individuals who are in the earliest stages of the disease. As a result, Parkinsons disease can only be diagnosed by a clinical neurological examination based on findings suggestive of the disease.

But researchers from the Technion-Israel Institute of Technology Faculty of Medicine have now identified a biomarker comprised of five genes shown to predict Parkinson's disease with high accuracy. The findings are reported in a research article now published online by the scientific journal Molecular Neurodegeneration.

A predictive biomarker for Parkinson's disease could also help to identify high-risk individuals before symptoms develop a stage where prevention treatment efforts might be expected to have their greatest impact to slow disease progression, says lead researcher Dr. Silvia Mandel. It could allow diagnosis of carriers of the genetic risk factors, or those who may exhibit pre-symptomatic stages of the disease [depression, sleep disturbances or hyposmia (reduced ability to smell)] and are good candidates for neuroprotective treatment.

All five genes that comprise the biomarker play a role in the ubiquitin-proteasome system of protein degradation, whose involvement in the pathology of Parkinson's disease has previously been demonstrated.

The study was conducted on blood samples from 62 early stage Parkinson's disease patients and 64 healthy age-matched control subjects. The selection of the genes and determination of their expression in the blood was based on previous research conducted by Dr. Mandel and Prof. Moussa Youdim on the brains of deceased Parkinson's disease patients.

More strikingly, in 30 patients at advanced stages of Parkinson's disease, the model was 100 percent accurate. It was also able to fully discriminate between Parkinson's disease and Alzheimer's disease.

The researchers believe the blood test could one day be combined with brain imaging and/or biomarkers in the spinal fluid or other peripheral tissues, as a gold standard not only for early diagnosis, but also for the differential diagnosis of Parkinson's disease and motor disorders that often mimick the disease symptoms.

Dr. Mandel, who is Vice Director of the Eve Topf Center of Excellence for Neurodegenerative Diseases Research and Teaching at the Technion, conducted the research together with her PhD student Leonid Molochnikov, Professor Youdim; Prof. Judith Aharon of Rambam Medical Center; and Prof. Martin Rabey of Assaf HaRofeh Medical Center. Scientists from the Universities of Wrzburg and Pisa also contributed to the research.

The Technion-Israel Institute of Technology is consistently ranked among the world's leading science and technology universities. Home to three of Israel's five winners of the Nobel Prize in science, the Technion commands a worldwide reputation for its pioneering work in computer science, nanotechnology, biotechnology, energy, water-resource management, medicine, drug development, and aerospace. Headquartered in New York City, the American Technion Society (ATS) promotes scientific and technological research and education at the Technion.

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Researchers ID Cluster of Genes in Blood that Predict Parkinson's

Adamas Pharmaceuticals Presents Update On Nurelinâ„¢ Program At Cambridge Healthtech Institute’s Parkinson’s Conference

EMERYVILLE, Calif., June 4, 2012 /PRNewswire/ --Adamas Pharmaceuticals, Inc., a privately held company, announced today that it will present an update on its Nurelin (amantadine HCl extended release capsules) program at the Cambridge Healthtech Institute's (CHI) Targeting Parkinson's Disease Symposium being held today in Philadelphia. Nurelin, a once-daily extended release formulation of amantadine intended for night-time administration, is being developed for the treatment of levodopa-induced dyskinesia (LID) in Parkinson's disease (PD) patients. Results from the Company's prior Phase 1 studies, its preclinical program in Parkinson's and other indications, along with a status report on the ongoing Phase 3 study, Extended Release Amantadine Safety and Efficacy Study in Levodopa-Induced Dyskinesia (EASED), will be presented by Gregory T. Went, Ph.D., Co-Founder and Chief Executive Officer of Adamas. The talk is entitled, "Exploring the Potential of Modified Release Aminoadamantanes in Parkinson's Disease and Related Indications."

"We are excited to introduce the Nurelin program at the conference today, and to provide an update on the previous preclinical and clinical studies that have led to our first Phase 2/3 study of Nurelin in Parkinson's patients who experience levodopa-induced dyskinesia," said Dr. Went. "Amantadine is a remarkable drug that has received little attention from the pharmaceutical industry for the past 30 years, and we hope the EASED study of Nurelin, combined with recently presented academic studies in Parkinson's disease, will help establish new treatment indications for Nurelin. We look forward to presenting the results from this study and assessing the potential of Nurelin as our second NDA candidate to Arimenda."

There are no medications currently approved for the treatment of levodopa-induced dyskinesia, thus there is a significant unmet medical need. Pending the outcome of the EASED study and regulatory review, Nurelin may become the first drug indicated for the treatment of levodopa-induced dyskinesia in Parkinson's disease. Nurelin also is being investigated as a therapeutic agent to address the non-motor symptoms of Parkinson's disease, including fatigue.

About Nurelin (ADS-5102)

Nurelin (ADS-5102) is a proprietary formulation of amantadine in development for the treatment of central nervous system (CNS) disorders including LID in PD patients. Nurelin is designed for once daily administration at night and is being investigated at plasma concentrations up to 2.5 fold higher than those achievable with the commercially available immediate release amantadine tablets. Nurelin capsules can be opened and the contents sprinkled on food for ease of administration in patients who have difficulty swallowing capsules.

Nurelin has a pharmacokinetic profile designed to overcome the CNS side effects associated with immediate release forms of amantadine, while offering potential for enhanced efficacy. This novel pharmacokinetic profile of Nurelin is characterized by: i) higher plasma concentrations during the daytime hours when the motor and non-motor symptoms of Parkinson's disease are at their peak; ii) low plasma concentrations overnight, which may reduce sleep disturbance and vivid dreams occasionally associated with amantadine; and iii) a reduced initial rate of rise in plasma concentration, which is expected to improve overall CNS tolerability of amantadine.

The efficacy and tolerability of multiple doses of Nurelin in the treatment of LID in Parkinson's disease patients is currently being studied in a Phase 2/3 study. This study, entitled EASED (Extended Release Amantadine Safety and Efficacy Study in Levodopa-Induced Dyskinesia), is designed to evaluate the efficacy of three dose strengths of Nurelin for the treatment of LID, and to confirm the tolerability of the new formulation (www.easedPD.com).

About LID in Parkinson Disease

Parkinson's disease is a chronic, progressive disorder with prominent motor signs including tremors, rigidity, bradykinesia and postural instability. Levodopa, the most commonly prescribed and effective drug treatment for symptomatic relief in PD is associated with dose limiting motor side effects, including abnormal involuntary, dance-like movements known as dyskinesia. With continued levodopa treatment, and as PD progresses, dyskinesia can become severely disabling and has been associated with a decrease in the quality of life.

About Adamas

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Adamas Pharmaceuticals Presents Update On Nurelinâ„¢ Program At Cambridge Healthtech Institute's Parkinson's Conference

Parkinson’s group to meet

MERIDIAN When the Meridian Parkinson's Disease Support Group first met a few months ago there were only four people in attendance who suffer from the debilitating condition.

The last meeting of the group saw 50 people show up looking for mutual support, information and peace of mind. Needless to say, Jimmy Gossett, one of the founding members of the group, was both astonished and pleased at the response.

"It is so nice to meet so many people who have the same condition as you," said Gossett, explaining he doesn't wish the disease on anyone. "But when you have this kind of problem, having friends and meeting new ones who through sheer numbers can build you back up, that is a nice thing."

With each new group meeting, Gossett said more and more health professionals work to assist in any way they can. Gossett said in the upcoming meeting, set forTuesday, June 12 at 10 a.m.at the Fifteenth Avenue Baptist Church in Meridian, three health professionals will be on hand to lend their expertise in the realm of Parkinson's Disease (PD).

"We will have physical therapists and speech pathologists on hand to help with information on what we face as PD sufferers," Gossett said. "But we will have fun, laugh, and fellowship. That is the best therapy we can have."

Gossett said the therapists will bring with them years of experience in dealing with PD sufferers. He said the health professionals will address such issues as speech deficits including reduced volume in their voices, decreased intelligibility, poor breath support and swallowing. Speech pathologists Angela Ramsey and Lesley Smith will be speaking to the group about oral motor exercises, respiratory exercises, and patterning techniques. The subject of neuromuscular e-stim to improve speech and swallowing will be covered.

Also, Amanda Sayers, a physical therapist, will be on hand to discuss some exercise techniques and different treatment approaches for the group as related to gait patterns, how to deal with "freezing" and tremors, and safety precautions.

"Each of these presentations will be followed by question and answer sessions so each person there can get the answers unique to their conditions," said Gossett.

Gossett said everyone is invited. He said he hopes that all PD suffers, not only in Meridian and Lauderdale County, but also throughout the East Mississippi area, will come and discover this group so they can seek the help and support so many sufferers need.

"It is all up to us, the PD sufferer, to increase our knowledge and understanding of this condition so that we can better cope with it," Gossett said. "We encourage those family members who have a person suffering from PD to come as well so they can get a firm grip on what their loved one is going through."

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Parkinson's group to meet

Robinson diagnosed with Parkinson’s Disease

State Rep. John Robinson (D-Scottsboro) said on Thursday he is in the early stages of Parkinson's Disease.

Robinson said he was diagnosed in January, shortly before the start of the 2012 Alabama Legislative Session.

"I'm on medication," said Robinson. "It's not a death sentence. It's treatable, but not curable."

Currently serving his fifth term in office after first being elected in 1994, Robinson said he only missed two days of the legislative session this year.

Parkinson's Disease is a chronic, degenerative neurological disorder that affects one in 100 people over age 60. It leads to shaking (tremors) and difficulty with walking, movement and coordination.

Robinson said he's had no problems with shaking.

"It gets my voice," he said. "And my coordination when I'm walking."

Robinson said he is going this summer to see a special neurologist in Chicago, one who has treated Muhammed Ali and Michael J. Fox.

Robinson, who retired from the Jackson County District Attorney's Office after entering politics, will complete 20 years in office when his current term ends. His five terms as state representative is the most for a person from Jackson County.

"I'm proud of that," he said.

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Robinson diagnosed with Parkinson's Disease

New research yields insights into Parkinson’s disease

Public release date: 4-Jun-2012 [ | E-mail | Share ]

Contact: Kagan Kerman kkerman@utsc.utoronto.ca 416-287-7249 University of Toronto Scarborough

Researchers at the University of Toronto Scarborough (UTSC) used an innovative technique to examine chemical interactions that are implicated in Parkinson's Disease.

The work details how a protein called alpha-synuclein interacting with the brain chemical dopamine can lead to protein misfolding and neuronal death.

Parkinson's Disease is a neurodegenerative disease which results in loss of motor control and cognitive function. Although the cause isn't known precisely, the disease involves the death of brain cells that produce dopamine, a chemical important in neuronal signaling. The disease also involves a protein called alpha-synuclein which aggregates in the neurons of people with the disease.

Kagan Kerman, a chemist in the Department of Physical and Environmental Sciences, and Ian R. Brown, a neuroscientist who founded UTSC's Centre for the Neurobiology of Stress in the Department of Biological Sciences, looked at the way dopamine interacts with alpha-synuclein to form aggregates that may be toxic to neurons.

"This is very fundamental," says Kagan Kerman. "It gives us a new point of view of the misfolding proteins and how they are affected by dopamine."

These sorts of interactions are often studied using microscopy. But the UTSC researchers decided to use an electroanalytic technique called voltammetry. By studying tiny changes in electric current as dopamine and alpha-synuclein interacted they were able to determine details about the early phases of the interaction.

Using the technique, they were able to detail how changes in pH levels and ionic strength of the solution affected the interaction. They found that at higher pH levels and higher ionic strengths, dopamine interacted much more strongly with alpha-synuclein, forming aggregates more quickly.

The results could have implications for understanding and treating the disease. Normally dopamine is contained in structures called vesicles, in which pH levels are low and dopamine is unlikely to interact with alpha-synuclein. Outside of the vesicles dopamine encounters higher pH levels and, according to the new research, is much more likely to interact to create aggregates.

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New research yields insights into Parkinson's disease

Study supports urate protection against Parkinson’s disease, hints at novel mechanism

Public release date: 23-May-2012 [ | E-mail | Share ]

Contact: Mike Morrison mdmorrison@partners.org 617-724-6425 Massachusetts General Hospital

Use of the antioxidant urate to protect against the neurodegeneration caused by Parkinson's disease appears to rely on more than urate's ability to protect against oxidative damage. In the May issue of the open-access journal PLoS One, researchers from the MassGeneral Institute for Neurodegenerative Diseases (MGH-MIND) describe experiments suggesting the involvement of a novel mechanism in urate's protection of cultured brain cells against Parkinson's-like damage.

"Our experiments showed, unexpectedly, that urate's ability to protect neurons requires the presence of neighboring cells called astrocytes," says Michael Schwarzschild, MD, PhD, of MGH-MIND, the study's senior author. "The results suggest there may be multiple ways that raising urate could help protect against neurodegeneration in diseases like Parkinson's and further support the development of treatments designed to elevate urate in the brain." Schwarzschild and colleagues in the Parkinson's Study Group currently are conducting a clinical trial investigating one approach to that strategy.

Characterized by tremors, rigidity, difficulty walking and other symptoms, Parkinson's disease is caused by destruction of brain cells that produce the neurotransmitter dopamine. Several epidemiological studies suggested that healthy people with elevated levels of urate, a normal component of the blood, may have a reduced risk of developing Parkinson's disease, and investigations by Schwarzschild's team found that Parkinson's patients with higher naturally occuring urate levels had slower progression of their symptoms.

The current study was designed to investigate whether both added urate and urate already present within the cells protect cultured dopamine-producing neurons against Parkinson-like degeneration. In addition, since previous studies suggested that urate's protective effects depended on the presence of astrocytes star-shaped cells of the central nervous system that provide both structural and metabolic support to neurons the MGH-MIND team explored how the presence of astrocytes affects the ability of urate to protect against damage induced by MPP+, a toxic molecule that produces the same kind of neurodegeneration seen in Parkinson's and is widely used in research studies.

The experiments showed that, while added urate reduced MPP+-induced cell death by about 50 percent in cultured dopamine-producing mouse neurons, urate treatment virtually eliminated neuronal death in cultures containing both neurons and astrocytes. They also showed that reducing intracellular urate levels by induced expression of the enzyme that breaks it down increased neuronal vulnerability to MPP+ toxicity significantly in cultures that included astrocytes but only slightly in neuron-rich cultures. The fact that the presence of astrocytes greatly increases the protection of both externally applied urate and urate produced within cells indicates that the effect depends on more than urate's ability to directly protect neurons against oxidative stress.

"A valuable next step will be determining whether endogenous urate is protective in live animal models of Parkinson's disease," says Schwarzschild. "It also will be important to determine whether we can selectively increase urate levels in brain cells by targeting urate transporter molecules. The approach now in early clinical trials examines whether treatment with the urate precursor inosine, which increases urate levels throughout the body, can slow the progression of the disease. If we could raise urate levels in brain cells without changing them in the rest of the body, we could avoid the risks of of excessive urate, which when accumulated in joints can cause gout."

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Schwarzschild is an associate professor of Neurology at Harvard Medical School. Sara Cipriani, MD, of MGH-MIND is the lead and corresponding author of the PLoS One report. The study was supported by grants from the National Institutes of Health, the Department of Defense and the American Parkinson's Disease Association.

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Study supports urate protection against Parkinson's disease, hints at novel mechanism