Patients with symptoms of Parkinson's disease have often been misdiagnosed and told they're merely feeling the physical affects of the aging process. A new guideline developed for Canadian doctors by Parkinson's specialists hopes to reduce the number of misdiagnoses. (iStock)

A specialist with the Ottawa Hospital has helped to develop the first ever national guidelines for diagnosing Parkinson's, an often-misdiagnosed disease with subtle symptoms.

Accurately diagnosing the degenerative disorder of the central nervous system is confusing for some physicians because many of the symptoms such as tremors or a general slowing down can be brushed off as gradual physical wear-and-tear from old age, said Dr. David Grimes, director of Ottawa Hospital's Parkinson's Disease and Movements Disorders Clinic.

"It's not like having a stroke, where something dramatic happens all of a sudden, and so it's one of those conditions where symptoms creep into the picture and go on for many months, or sometimes years," Grimes said. "They're seeing their family doctor, and they're saying their sore shoulder is from this, or the hand's not moving because they have just a little bit of Arthritis, and so it can take quite a while before they're able to come up with the right diagnosis."

In a bid to help patients get the timely treatment and therapies they need, Grimes worked with other specialists for five years to create a tool for doctors across Canada that would help them more accurately diagnose Parkinson's patients in the early stages, before the disease progresses.

Paul Wing and Nick Kaethler count themselves among those who feel they may have lost time as far as being able to manage the disease due to delayed diagnosis.

Wing, whose doctor told him he was likely suffering from anxiety, didn't find out he actually had Parkinson's for eight months.

"It's really disconcerting. You're thinking, do I have AHLS, do I have MS, am I depressed? Is it cancer? It could be anything," Wing said. "It's hard to fight the good fight. It's hard when you don't have an enemy to fight."

Kaethler said he was told by his doctor, "You're just getting old. Live with it."

It took Kaethler five years to discover his enemy was Parkinson's.

Continued here:
Parkinson's diagnosis guide created for Canadian MDs

A new, small study found people with Parkinson's disease who took caffeine pills saw slight but noticeable improvements in movement problems related to the condition.

The findings warrant further study, Canadian researchers said. And there are still questions - such as if patients would develop a caffeine tolerance, eventually blunting the benefits of coffee or caffeine pills.

"It's a bit too early to say, Everybody should be drinking coffee,'" said lead researcher Dr. Ronald Postuma, from McGill University in Montreal.

"Does it really make a difference over years of Parkinson's disease? I don't think we know."

Still, he said, caffeine is generally safe, so it could be worth trying for some patients with Parkinson's who aren't doing great and also have trouble with sleepiness.

About 50,000 to 60,000 people in the United States are diagnosed with Parkinson's disease every year, according to the National Parkinson Foundation. Typical symptoms include shaking and trouble with movement and coordination.

There's no cure for the disease, but some medications can make symptoms less severe.

As much as four cups of coffee

For the new study, Postuma and his colleagues randomly assigned 61 people with Parkinson's and in their mid-60s, on average, to six weeks of caffeine pills or identical drug-free placebo pills.

Participants in the caffeine group took 100 milligrams when they woke up and again after lunch for the first three weeks, then were bumped up to 200 milligrams twice a day for the rest of the study.

Continued here:
Caffeine may provide some Parkinson's relief

By Serena Gordon HealthDay Reporter

WEDNESDAY, Aug. 1 (HealthDay News) -- Caffeine has previously been linked to a lower risk of developing Parkinson's disease, but now new research says the ubiquitous stimulant may also help treat disease symptoms.

In a small study of 61 people with Parkinson's disease, Canadian researchers found that giving the caffeine equivalent of about three cups of coffee per day improved motor symptoms, such as slow movement and stiffness. Interestingly, caffeine didn't significantly improve daytime sleepiness, a common symptom in Parkinson's disease.

"Caffeine treats Parkinson's disease," said the study's lead author, Dr. Ronald Postuma, an associate professor in the department of neurology at McGill University in Montreal.

"There was a modest effect on sleepiness that didn't reach statistical significance, but I think it was clear that it helps patients," he said. "Where we saw the most potential benefit from caffeine was on motor aspects and symptoms. People felt better and were more energetic. You could see on the exam that they were better."

Parkinson's disease is a degenerative disorder that causes shaking, stiffness, slow movements and difficulty with balance. More than one million Americans have Parkinson's disease, and more than 50,000 people are diagnosed with the disease each year, according to the National Parkinson Foundation.

In the current study, published in the Aug. 1 online edition of the journal Neurology, half of the group of Parkinson's patients was randomly assigned to receive caffeine treatment, while the other half received an inactive placebo.

To be included in the study, the volunteers had to consume less than 200 milligrams (mg) of caffeine daily -- about two cups of coffee -- and they couldn't have any heart rhythm problems, uncontrolled high blood pressure, or an active ulcer.

For the first three weeks of the study, those receiving caffeine were given 100 mg of caffeine twice daily -- once when they got up and again at lunchtime.

During the second three weeks, the dose was increased to 200 mg twice daily.

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Caffeine May Help Treat Parkinson's Disease

iStockphoto.com

Getting a diagnosis for Parkinson's disease might be as easy as placing a phone call.

There's currently no cure for Parkinson's, a debilitating neurological disease. There's also no blood test that can detect it, meaning early intervention is almost impossible.

But soon there might be a shockingly easy way to screen for Parkinson's disease. It would be as simple as picking up the telephone and saying "ahhh."

One of these voices tests positive for Parkinson's disease. Can you tell the difference? Find out if you're right at the bottom of this story.

"There's some evidence, admittedly weak, that voice disturbances may well be one of the first or early indicator of the disease," mathematician Max Little tells weekends on All Things Considered host Guy Raz.

Little is head of the Parkinson's Voice Initiative and he's created an algorithm that can determine whether or not a person has Parkinson's just by the sound of their voice.

Right now, the algorithm has a 99 percent success rate.

A Surprising Result

Little worked on this algorithm while he was getting his PhD at Oxford. It didn't occur to him that it could be used to detect Parkinson's disease until a chance encounter with a researcher from Intel.

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Say 'Ahhh': A Simpler Way To Detect Parkinson's

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

Current ratings for: Severe Flu Increases Risk Of Parkinson's

1 (1 votes)

5 (1 votes)

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

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

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

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

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

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.

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

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

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."

###

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

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.

The rest is here:
Speaker offers insights into Parkinson's

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

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

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

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

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 ...

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

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 Nurelin™ Program At Cambridge Healthtech Institute's Parkinson's Conference