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

Contact: Lisa Merkl lkmerkl@uh.edu 713-743-8192 University of Houston

HOUSTON, Aug. 23, 2012 Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson's disease.

Affecting more than 500,000 people in the U.S., Parkinson's disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.

"LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system," said CNRCS director and professor Jan-ke Gustafsson, whose lab discovered LXRbeta in 1995. "The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders."

To better understand the relationship between LXRbeta and Parkinson's disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson's in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.

The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.

"LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons," Gustafsson said. "Microglia are the police of the brain, keeping things in order. In Parkinson's disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson's disease."

###

Gustafsson, professor Margaret Warner, research assistant professor Xin-Jie Tan, and postdoctoral fellows Wanfu Wu and Yubing Dai authored the PNAS study, which is available at http://www.pnas.org/content/early/2012/07/18/1210833109.abstract.

Here is the original post:
Therapeutic avenues for Parkinson's investigated at UH

Researchers have shown that people with Parkinson's disease performed markedly better on a test of working memory after a night's sleep, and sleep disorders can interfere with that benefit.

While the classic symptoms of Parkinson's disease include tremors and slow movements, Parkinson's can also affect someone's memory, including "working memory."

Working memory is defined as the ability to temporarily store and manipulate information, rather than simply repeat it. The use of working memory is important in planning, problem solving and independent living.

The findings underline the importance of addressing sleep disorders in the care of patients with Parkinson's, and indicate that working memory capacity in patients with Parkinson's potentially can be improved with training. The results also have implications for the biology of sleep and memory.

"It was known already that sleep is beneficial for memory, but here, we've been able to analyze what aspects of sleep are required for the improvements in working memory performance," said postdoctoral fellow Michael Scullin, who is the first author of the paper.

The performance boost from sleep was linked with the amount of slow wave sleep, or the deepest stage of sleep. Several research groups have reported that slow wave sleep is important for synaptic plasticity, the ability of brain cells to reorganize and make new connections.

Sleep apnea, the disruption of sleep caused by obstruction of the airway, interfered with sleep's effects on memory. Study participants who showed signs of sleep apnea, if it was severe enough to lower their blood oxygen levels for more than five minutes, did not see a working memory test boost.

54 study participants had Parkinson's disease, and 10 had dementia with Lewy bodies: a more advanced condition, where patients may have hallucinations or fluctuating cognition as well as motor symptoms. Those who had dementia with Lewy bodies saw no working memory boost from the night's rest. As expected, their baseline level of performance was lower than the Parkinson's group.

Participants with Parkinson's who were taking dopamine-enhancing medications saw their performance on the digit span test jump up between the fourth and fifth test. On average, they could remember one more number backwards. The ability to repeat numbers backward improved, even though the ability to repeat numbers forward did not.

Patients needed to be taking dopamine-enhancing medications to see the most performance benefit from sleep. Patients not taking dopamine medications, even though they had generally had Parkinson's for less time, did not experience as much of a performance benefit. This may reflect a role for dopamine, an important neurotransmitter, in memory.

Link:
Sleep improves memory in Parkinson's patients

PHILADELPHIA Researchers at the Perelman School of Medicine will receive $11.9 million over the next five years from the National Institute of Neurological Disorders and Stroke (NINDS) for the Penn Udall Center for Parkinsons Disease (PD) research. This grant is a renewal of an NINDS funded PD center that successfully completed its research program over the last five years.

Parkinsons is one of the most common neurodegenerative diseases, second only to Alzheimer's disease in the number of people affected. Estimates suggest that approximately 1,000,000 Americans have PD.

Cognitive impairment, executive dysfunction and dementia add to the burden of PD and increase mortality, but the underlying basis of dementia in PD is unclear. There are no effective disease modifying therapies. Despite important research advances, the exact causes of PD, Parkinsons with dementia (PDD), and dementia with Lewy Bodies (DLB) are unknown. To address this, a NINDS Morris K. Udall Parkinsons Disease Research Center of Excellence was launched at Penn in 2007.

This renewal for years six through ten of the Penn Udall Center builds on recent progress advancing researchers understanding of the progression of PDD from normal cognition to cognitive impairment, executive dysfunction and dementia in PDD, and disease progression in DLB, in addition to central nervous system degeneration mediated by progressive accumulations of pathological alpha-synuclein.

Recent Penn Udall Center studies raise the provocative, but highly plausible possibility that the progression of PD/PDD/DLB is linked to the cell-to-cell spread of pathological alpha-synuclein. Therefore, the overarching goals of the Penn Udall Center are to explore mechanisms of disease progression and alpha-synuclein transmission through collaborations between basic and translational research projects that work with each of the cores to implement the mission of the Penn Udall Center in the renewal period.

"The Penn Udall Center will elucidate mechanisms of cognitive impairment, executive dysfunction and dementia in Parkinsons Disease as well as mechanisms of neurodegeneration that are mediated by the transmission of alpha-synuclein pathologies, said Center Director John Trojanowski, MD, PhD, director of Penn's Institute on Aging and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine. By using new approaches and model systems to achieve its goals, the Penn Udall Center will investigate novel disease mechanisms in Parkinsons and advance efforts to develop new interventions and better diagnostics for this disorder.

The Penn Udall Center is based on 20 years of basic research on neurodegenerative diseases within the Center for Neurodegenerative Disease Research and clinical programs at the Parkinsons Disease and Movement Disorders Center, both within Penn Medicine.

The Udall Centers of Excellence were developed in honor of former Congressman Morris K. Udall, who died in 1998 after a long battle with Parkinsons disease. The first center was named in 1997.

The Udall Center renewal grant (P50 NS053488) will include four core groups focusing on clinical care: neuropathology, biomarker and genetics; data management, biostatistics and bioinformatics; and administration. Planned projects will look for an immune therapy to block PD transmission in animal models, biomarkers to evaluate and predict cognitive decline in Lewy Body spectrum disorders, language and executive dysfunction in PD, and how transmission of alpha-synuclein occurs in neurons. The Penn Udall Center team includes John Trojanowski, MD, PhD, Howard Hurtig, MD, Dan Weintraub, MD, Vivianna Van Deerlin, MD, PhD, Edward B. Lee, MD, PhD, Sharon Xie, PhD, Li-San Wang, PhD, Alice Chen-Plotkin, MD, Murray Grossman, MD, PhD, Rachel Gross, MD, Kelvin Luk, PhD, and Virginia M-Y Lee, PhD, MBA.

The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 fiscal year.

Continued here:
Perelman School of Medicine Granted $11.9 Million Renewal of NINDS Support for Morris K. Udall Parkinson's Disease ...

Ed McCaskey has lived with Parkinsons disease for six years, and now hes trying to help others like him mitigate some of their symptoms through exercise.

McCaskey, 59, was diagnosed with Parkinsons in 2006. He lives in Roscoe, Ill., and he joined the Stateline Family YMCA Roscoe Branch the same year, and he typically works out five days a week.

Exercise has been found to help reduce some of the symptoms like shaking and tremors associated with Parkinsons. That is why the YMCA of Greater Cleveland in Ohio developed a program called Pedaling for Parkinsons with the help of Cleveland Clinic physician Dr. Jay L. Alberts, a staff member with the Biomedical Engineering Center for Neurological Restoration.

The program in which participants exercise on indoor spin/cycling bikes and tandem bikes launched earlier this year, and McCaskey read about it in a Parkinsons newsletter and pitched it to his local YMCA. Research by Cleveland Clinic showed a 35 percent reduction in symptoms with the act of pedaling a bicycle at a rapid pace optimally 80 to 90 revolutions per minute.

The YMCA staff in Roscoe, Ill., agreed, and the one-hour class will meet three days a week starting Sept. 24 through Nov. 16. Its free to YMCA members and nonmembers alike.

Some class participants may need a relative or friend to drive them to the class, and McCaskey said YMCA officials will let those people use the Y facilities free of charge while they wait during the class.

More than 1 million people nationally are living with Parkinsons disease, and nearly 60,000 new cases are diagnosed each year, according to the National Parkinson Foundation. Parkinsons is a chronic degenerative disease that occurs when nerve cells in parts of the brain stem die or degenerate.

McCaskey recently traveled to Washington state and tried the Pedaling for Parkinsons class there. It was pretty easy for the marathon runner and regular spin-class participant, but he said its a great opportunity for Parkinsons patients to get moving and realize the benefits of exercise.

Im still pretty lucky because my symptoms are minimal, McCaskey said. After a good workout, a lot of those symptoms dissipate for a good part of the day. The exercise recommendation came from my doctor, but following up on it really reinforces what he says. Im experiencing the positive benefits.

Melissa Westphal: 815-987-1341; at mwestpha@rrstar.com

Continue reading here:
Pedaling for Parkinson's: A workout that can help reduce shaking, tremors

ScienceDaily (Aug. 23, 2012) Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson's disease.

Affecting more than 500,000 people in the U.S., Parkinson's disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.

"LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system," said CNRCS director and professor Jan-ke Gustafsson, whose lab discovered LXRbeta in 1995. "The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders."

To better understand the relationship between LXRbeta and Parkinson's disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson's in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.

The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.

"LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons," Gustafsson said. "Microglia are the police of the brain, keeping things in order. In Parkinson's disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson's disease."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Houston.

Read more:
Therapeutic avenues for Parkinson's investigated

Editor's Choice Main Category: Alzheimer's / Dementia Also Included In: Parkinson's Disease;Sleep / Sleep Disorders / Insomnia Article Date: 13 Aug 2012 - 14:00 PDT

Current ratings for: Rejected Drug Could Protect Against Parkinson's And Alzheimer's

4.75 (4 votes)

Over 5 million people worldwide suffer from Alzheimer's disease, an incurable, progressive neurodegenerative disease that is the leading cause of dementia in the elderly, whilst around 1 million people in the U.S. suffer from Parkinson's disease, a progressive disorder that leads to muscle stiffness, tremors and slowed movements and gait.

Latrepirdine was approved in Russia in 1983 as an antihistamine. However, in the 90s, researchers discovered that the drug seemed to be effective in the earliest animal models of Alzheimer's disease. A high- profile Phase II clinical trial in Russia demonstrated that latrepirdine showed a considerable and sustained improvement in cognitive behavior in Alzheimer's patients with minimal side effects. A panel of U.S. clinical experts oversaw the trial. The panel included Mary Sano, PhD, Professor of Psychiatry and Director of the Mount Sinai Alzheimer's Disease Research Center. However, later tests of latripirdine in a U.S. Phase III trial failed to show any improvement in those affected by Alzheimer's, which prompted the sponsors to stop further clinical trials of the drug for Alzheimer's disease.

Prior to the failed trials Sam Gandy, MD, PhD, Professor of Neurology, and Psychiatry, and Director of the Mount Sinai Center for Cognitive Health and his team started investigating the way in which latrepirdine functions. Dr. Gandy declares:

Their new study entailed administering the drug to three different systems, including yeast, mice and mammal cells that all showed a build-up of alpha-synuclein, i.e. a protein that is known to cause neurodegeneration.

They discovered determined that latrepiridine activated autophagy in all three systems, the "self-eating" process of cells that protects the brain from neurodegeneration, which targeted synuclein and protected against its toxicity. They discovered that the drug decreased the amount of synuclein accumulated in the brain of mice through autophagy.

This is the second study published in Molecular Psychiatry by Dr. Gandy's team. Their first study, which appeared in the July 31 issue, revealed that a mice study showed that latrepiridine stopped the toxicity of amyloid-beta protein accumulation by inducing autophagy in animals with Alzheimer's disease. The study entailed randomly administrating latrepirdine or placebo to mice with early stages of Alzheimer's disease, revealed that the drug improved memory through autophagy.

To his surprise, Dr. Petsko, an expert in protein structure, Professor of Neurology and Neuroscience at Weill Cornell Medical College, observed that latrepirdine protects yeast cells from the toxicity of alpha-synuclein and leaves the cells vulnerable so that they can be killed by either the Huntington's disease protein or by either of the two key proteins responsible for ALS-FTD. ALS-FTD is a range of diseases, including Lou Gehrig's disease and frontotemporal dementia.

See the article here:
Rejected Drug Could Protect Against Parkinson's And Alzheimer's

Public release date: 13-Aug-2012 [ | E-mail | Share ]

Contact: Mount Sinai Press Office newsmedia@mssm.edu 212-241-9200 The Mount Sinai Hospital / Mount Sinai School of Medicine

The second of two studies on latrepirdine, recently published in Molecular Psychiatry, demonstrates new potential for the compound in the treatment of Alzheimer's disease, Parkinson's disease, sleep disorders, and other neurodegenerative conditions. An international team led by Mount Sinai School of Medicine scientists found that latrepiridine, known commercially as Dimebon, reduced the level of at least two neurodegeneration-related proteins in mice.

Latrepirdine was initially sold as an antihistamine in Russia, following its approval for use there in 1983. In the 1990s, the compound appeared effective in treating some of the earliest animal models of Alzheimer's disease. In a high profile Phase II clinical trial in Russia, overseen by a panel of top U.S. clinical trial experts, including Mount Sinai's Mary Sano, PhD, Professor of Psychiatry and Director of the Mount Sinai Alzheimer's Disease Research Center, latrepirdine showed significant and sustained improvement in cognitive behavior in Alzheimer's patients with minimal side effects. However, when the drug was tested in the U.S. in a Phase III trial, it did not demonstrate any improvement in people with the disease, causing the sponsors to halt further clinical study of the drug in Alzheimer's disease.

Before the failed trials however, Mount Sinai researchers led by Sam Gandy, MD, PhD, Professor of Neurology, and Psychiatry, and Director of the Mount Sinai Center for Cognitive Health, began studying how latrepirdine worked.

"Despite the failure to replicate the positive Russian trial results in U.S. patients, we found unexpected evidence that latrepirdine had potential as a treatment for a number of neurodegenerative disorders," said Dr. Gandy. "Our study shows that the compound prevents neurodegeneration in multiple ways and should remain a contender for battling these devastating diseases. The anti-amyloid approach most recently exemplified by reports that a second bapineuzumab trial has failed might only help patients if begun before the brain pathology begins to build up."

In the new study, the researchers administered the drug to three different systems: yeast, mice and mammal cells all showing build-up of alpha-synuclein, a protein known to cause neurodegeneration. In all three systems, they determined that latrepiridine activated autophagy, the so-called "self-eating" process of cells that protects the brain from neurodegeneration, which targeted synuclein and protected against its toxicity. In mice, the drug reduced the amount of synuclein accumulated in the brain through autophagy.

John Steele, PhD, a Mount Sinai neuroscience graduate student, devoted his PhD thesis to these studies. Lenard Lachenmayer, MD, a postdoctoral fellow working under the supervision of Zhenyu Yue, PhD, Associate Professor of Neurology at Mount Sinai, shares first authorship of the new paper with Steele and with Shulin Ju, PhD, a postdoctoral fellow at Brandeis University working under the direction of Greg Petsko, PhD, and Dagmar Ringe, PhD, both professors of biochemistry, chemistry and neuroscience at Brandeis.

This study is the second of two published by Dr. Gandy's team in Molecular Psychiatry. The first, published July 31, 2012, determined that latrepiridine stopped the toxicity of amyloid-beta protein accumulation in mice present with Alzheimer's disease by inducing autophagy. In that study, they randomly administered either latrepirdine or placebo to mice engineered to have the early stages of Alzheimer's disease and found that, through autophagy, the drug improved memory.

Dr. Petsko, an expert in protein structure who is now Professor of Neurology and Neuroscience at Weill Cornell Medical College, noted that, surprisingly, latrepirdine protects yeast cells from the toxicity of alpha-synuclein while leaving the cells vulnerable to killing by either the Huntington's disease protein or by either of the two key proteins responsible for ALS-FTD, a spectrum of diseases that includes both Lou Gehrig's disease and frontotemporal dementia.

Here is the original post:
Rejected drug may protect against toxic substance common to Alzheimer's and Parkinson's diseases

By Jason Napodano, CFA

Parkinson's Disease

Parkinsons disease (PD) is a neurodegenerative brain disorder that results from the death of dopamine-generating cells in the substantia nigra region of the midbrain. PD is also characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons. The cause of PD is generally idiopathic, although some atypical cases have a genetic origin. The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy in 1817.

PD patients often exhibit marked reduction in motor control and an increase in parkinsonism (tremors, hypokinesia, rigidity, bradykinesia, and postural instability). However, as the disease progresses, patients often exhibit non-motor symptoms that include autonomic dysfunction, neuropsychiatric problems (mood, cognition, behavior or thought alterations, psychosis), and sensory and sleep difficulties. Parkinsons disease psychosis (PDP) is common in nearly 50% of PD patients a decade after initial diagnosis. Anxiety and depression are common co-morbidities. Initial signs of PD include shaking, loss of smell, difficulty writing, trouble sleeping, constipation, and poor posture. Diagnosis of a typical case is mainly based on symptoms, with tests such as neuroimaging used for confirmation.

There is no cure for PD. Instead, physicians attempt to manage the symptoms of the disease through a multidisciplinary approach that may include pharmacological, social, and surgical options. The most common pharmaceutical treatment options are those which look to increase the level of dopamine in the brain. These include dopamine replacement therapies (DRT) combined with dopa decarboxylase inhibitors, dopamine agonists, and MAO-B inhibitors. The treatment option is often tailored specifically for the patient based on the stage and severity of the disease and the balance between good symptom control and side-effects resulting from enhancement of dopaminergic function.

Despite these co-formulations, Levodopa carries significant risk of side-effects, including dyskinesia. As a result, despite its effectiveness in reducing motor symptoms associated with Parkinsons disease, physicians often attempt to delay Levodopa therapy until the disease progresses to a more moderate-to-severe stage. Most early-stage PD patients start out on MAO-B inhibitors and / or dopamine agonists, or low-dose Levodopa. However, PD is a progressive and degenerative disease, and patients typically progress to the point where starting Levodopa or increasing the Levodopa dose is necessary in five years after initial diagnosis. After a decade on therapy, almost all PD patients require high doses of Levodopa, as well as surgical options including deep brain stimulation (DBS). As the dose and use of Levodopa increases, the incidence of dyskinesia also increases.

Levodopa also has a relatively short half-life, requiring dosing averaging three to four times a day. Peak plasma concentrations of Levodopa occur 60 to 90 minutes after dosing. Unfortunately, this is also when peak side effects such as dyskinesia occur. The hefty dosing requirement of Levodopa creates compliance issues, especially at night when patients may sleep through their dose schedule dosing every six hours. The peaks and troughs associated with Levodopa create significant on and off treatment times for PD patients.

Levodopa-Induced Dyskinesia

Levodopa-Induced Dyskinesia (LID) is a major side-effect of Levodopa use. LID is characterized by hyperkinetic movements, including chorea (abnormal involuntary movement), dystonia (sustained muscle contraction, abnormal posture), and athetosis (involuntary convoluted movements). It is most common at times of peak L-DOPA plasma concentrations (peak-dose dyskinesia), although it may also occur when plasma concentrations of L-DOPA rise and fall (diphasic dyskinesia) or during off-time (off-period dystonia).

In the U.S., there are an estimated 500,000 to 1 million patients suffering from Parkinsons disease. There are no approved treatment options for PD-LID. Approximately 50% of PD patients will experience LID after 4 to 6 years on L-DOPA therapy. The number rises to 90% after 10 to 15 years on L-DOPA therapy.

More:
Looking At Dipraglurant For Parkinson's Disease

Golden Globe winner and Oscar nominee Bob Hoskins has retired from acting after being diagnosed with Parkinson's disease.

"He wishes to thank all the great and brilliant people he has worked with over the years, and all of his fans who have supported him during a wonderful career," his rep said in a statement to the BBC. "Bob is now looking forward to his retirement with his family, and would greatly appreciate that his privacy be respected at this time."

Hoskins, 69, was diagnosed in the fall.

Check out photos of Bob Hoskins

A native of Suffolk, England, Hoskins started acting in the 1960s and spent the '70s on British TV series, including Villains. His breakthrough role was as gangster Harold Shand in 1980's The Long Good Friday, which co-starred Helen Mirren. He won a Golden Globe, a BAFTA, a Cannes Film Festival award and earned a Best Actor Oscar nomination for his portrayal of George, a criminal who gets involved with a high-class call girl in 1986's Mona Lisa.

He earned a second Globe nomination for perhaps his most memorable role: private investigator Eddie Valiant in the 1998 live-action and animated hit Who Framed Roger Rabbit.

Other credits include Mermaids, Hook, Nixon and 2005's Mrs. Henderson Presents, for which he earned his third Globe nod.

Hoskins' final film was this summer's hit Snow White and the Huntsman, in which he played the dwarf Muir.

View original Bob Hoskins Retires Due to Parkinson's Disease at TVGuide.com

Related Articles on TVGuide.com

Continue reading here:
Bob Hoskins Retires Due to Parkinson's Disease

TORONTO, ONTARIO--(Marketwire -08/14/12)- This year more furry friends will join the 14,000 Canadians who champion Parkinson SuperWalk. Pets are demonstrating their support for Parkinson SuperWalk through a new online contest, Pets for Parkinson's, launched this week by Parkinson Society Canada.

A first for Parkinson SuperWalk, Pets for Parkinson's challenges Canadians to show support for the walk by submitting photos of their pets demonstrating their enthusiasm for the cause to help raise awareness of Parkinson's disease. Winners will be selected weekly between now and September 10th and awarded a $100.00 PetSmart gift card. Friends and family will also have the chance to participate and vote online for their favourite Parkinson's Pet who will be awarded the grand prize of a $250.00 gift card to PetSmart.

"For many people, pets are an integral member of the family, and every year we have a large number of canine companions who attend Parkinson SuperWalk to show their support. We think this is a great way to have some fun and get more pets (and their families) involved in the cause," says Joyce Gordon, Parkinson Society Canada President and CEO.

Visit http://bit.ly/NvtDnM to see some of Canada's pets with personality gearing up for Parkinson's SuperWalk and to enter the weekly prize draw online. Please see contest terms and conditions for more information.

About Parkinson SuperWalk

Parkinson Society Canada's 22nd annual Parkinson SuperWalk is less than a month away! On September 8th-9th, 14,000 volunteers and participants in 95 communities across Canada will walk together with a goal to raise $3 million nation-wide. Parkinson SuperWalk is Parkinson Society Canada's largest fundraising event and since its inaugural walk in 1990 led by a small group of committed volunteers, the nation-wide event has raised more than $25 million for education, support services, research, and advocacy on behalf of Canadians living with Parkinson's. Register online at http://www.parkinsonsuperwalk.ca.

About Parkinson's Disease

Parkinson's is a neurodegenerative disease for which there is no cure. It is estimated that there are more than 100,000 people living with Parkinson's disease across the country(i). Canadians are encouraged to get involved in their community.

To register, donate, or find a walk, visit http://www.parkinsonsuperwalk.ca. Follow Parkinson SuperWalk on Facebook or on Twitter.

For more about Parkinson's disease and Parkinson Society Canada, and where to find support in your community, visit http://www.parkinson.ca or call 1-800-565-3000.

Visit link:
Does Your Dog have What it Takes to Be Parkinson's Top Dog?

By SPECIAL TO HERNANDO | Hernando Today Published: August 09, 2012 Updated: August 09, 2012 - 1:12 PM

Parkinson's disease symptoms and signs may vary from person to person. Early signs may be mild and may go unnoticed. Symptoms often begin on one side of your body and usually remain worse on that side, even after symptoms begin to affect both sides. Parkinson's signs and symptoms may include:

Tremor. Your tremor, or shaking, usually begins in your limb, often your hand or fingers. You may notice a back-and-forth rubbing of your thumb and forefinger, known as a pill-rolling tremor. One characteristic of Parkinson's disease is tremor of your hand when it is relaxed (at rest).

Slowed movement (bradykinesia). Over time, Parkinson's disease may reduce your ability to move and slow your movement. This may make simple tasks difficult and time-consuming. Your steps may become shorter when you walk, or you may find it difficult to get out of a chair. Also, your feet may stick to the floor as you try to walk, making it difficult to move.

Rigid muscles. Muscle stiffness may occur in any parts of your body. The stiff muscles can limit your range of motion and cause you pain.

Impaired posture and balance. Your posture may have become stooped, or you may have balance problems as a result of Parkinson's disease.

Loss of automatic movements. In Parkinson's disease, you may have a decreased ability to perform unconscious movements, including blinking, smiling or swinging your arms when you walk. You may no longer gesture when talking.

Speech changes. You often may have speech problems as a result of Parkinson's disease. You may speak softly, quickly, slur or hesitate before talking. Your speech may be more of a monotone, rather than with the usual inflections.

Writing changes. Writing may appear small and become difficult.

Medications typically markedly reduce many of these symptoms. These medications increase or substitute for a specific signaling chemical (neurotransmitter) in your brain: dopamine. People with Parkinson's disease have low brain dopamine concentrations.

See the article here:
Symptoms of Parkinson's disease

His agent said Hoskins, 69, was given the diagnosis in the autumn and planned to spend time with his family Hoskins, from Suffolk in England, has played a range of roles since the 1970s, ranging from gangster films to comedy roles Parkinson's is a neurological condition which is thought to affect around 127,000 people in the UK and has no known cure

By David Wilkes

PUBLISHED: 11:06 EST, 8 August 2012 | UPDATED: 05:43 EST, 9 August 2012

Retiring: Bob Hoskins was given the diagnosis in the autumn. Announcing his retirement the star's agent said he planned to spent time with his family

Actor Bob Hoskins is retiring from showbusiness after being diagnosed with Parkinsons disease.

The announcement brings to an end a silver screen career which spanned four decades and included Hollywood hits such as Who Framed Roger Rabbit.

His most recent appearance was in Snow White and the Huntsman, released this year and starring Kristen Stewart.

Hoskins, 69, revealed his battle with the brain disorder yesterday, several months after his diagnosis.

A statement released by his agent said: 'Bob Hoskins wishes to announce that he will be retiring from acting, following his diagnosis of Parkinsons disease last autumn.

'He wishes to thank all the great and brilliant people he has worked with over the years, and all of his fans who have supported him during a wonderful career.

Read more from the original source:
Bob Hoskins reveals he is suffering from Parkinson's Disease as he announces retirement from acting career

(Reuters) - Veteran British actor Bob Hoskins, the star of Who Framed Roger Rabbit, said on Wednesday he had been diagnosed with Parkinson's disease and was retiring from acting.

"Bob Hoskins wishes to announce that he will be retiring from acting, following his diagnosis of Parkinson's disease last autumn. He wishes to thank all the great and brilliant people he has worked with over the years, and all of his fans who have supported him during a wonderful career," the actor's London representatives said in a statement.

"Bob is now looking forward to his retirement with his family, and would greatly appreciate that his privacy be respected at this time."

Hoskins, 69, started his career in the 1970s on British television shows such as Thick as Thieves and Rock Follies of '77 before moving into bigger film roles, such as 1980's The Long Good Friday and 1986's Mona Lisa, for which he earned a best actor Oscar nomination and won a Golden Globe award.

The Suffolk-born actor became a staple face in the British film industry, often playing Cockney-speaking characters in both comedy and drama genres with his trademark gravelly voice.

His big Hollywood break came in 1988 when he played Eddie Valiant in Who Framed Roger Rabbit, a role for which he received a Golden Globe nomination. He then went on to play roles in 1990's Mermaids and 1991's Hook.

Hoskins' most recent movie role was as one of the eight dwarves in this year's dark fairytale Snow White and the Huntsman, alongside Chris Hemsworth and Kristen Stewart.

Parkinson's disease is an incurable, degenerative neurological disorder whose sufferers include U.S. actor Michael J. Fox and former heavyweight boxing champion Muhammad Ali.

(Reporting By Piya Sinha-Roy in Los Angeles Editing by Jill Serjeant and Leslie Gevirtz)

Copyright (c) Reuters

Read more:
Bob Hoskins has Parkinson's disease, retiring from acting

Veteran British actor Bob Hoskins, the star of films including Who Framed Roger Rabbit, says he has been diagnosed with Parkinson's disease and is retiring from acting.

Hoskins, 69, started his career in the 1970s on British television shows such as Thick as Thieves and Rock Follies of '77 before moving into bigger film roles, such as 1980's The Long Good Friday and 1986's Mona Lisa, for which he earned a best actor Oscar nomination and won a Golden Globe award.

"Bob Hoskins wishes to announce that he will be retiring from acting, following his diagnosis of Parkinson's disease last autumn.

"He wishes to thank all the great and brilliant people he has worked with over the years, and all of his fans who have supported him during a wonderful career," the actor's London representatives said in a statement.

"Bob is now looking forward to his retirement with his family, and would greatly appreciate that his privacy be respected at this time."

The Suffolk-born actor became a staple face in the British film industry, often playing Cockney-speaking characters in both comedy and drama genres with his trademark gravelly voice.

His big Hollywood break came in 1988 when he played Eddie Valiant in Who Framed Roger Rabbit, a role for which he received a Golden Globe nomination.

He then went on to play roles in 1990's Mermaids and 1991's Hook.

Hoskins' most recent movie role was as one of the eight dwarves in this year's dark fairytale Snow White and the Huntsman, alongside Chris Hemsworth and Kristen Stewart.

Parkinson's disease is an incurable, degenerative neurological disorder whose sufferers include US actor Michael J Fox and former heavyweight boxing champion Muhammad Ali.

The rest is here:
Bob Hoskins reveals Parkinson's disease, bows out

His agent said Hoskins, 69, was given the diagnosis in the autumn and planned to spend time with his family Hoskins, from Suffolk in England, has played a range of roles since the 1970s, ranging from gangster films to comedy roles Parkinson's is a neurological condition which is thought to affect around 127,000 people in the UK and has no known cure

By David Wilkes

PUBLISHED: 11:06 EST, 8 August 2012 | UPDATED: 05:43 EST, 9 August 2012

Retiring: Bob Hoskins was given the diagnosis in the autumn. Announcing his retirement the star's agent said he planned to spent time with his family

Actor Bob Hoskins is retiring from showbusiness after being diagnosed with Parkinsons disease.

The announcement brings to an end a silver screen career which spanned four decades and included Hollywood hits such as Who Framed Roger Rabbit.

His most recent appearance was in Snow White and the Huntsman, released this year and starring Kristen Stewart.

Hoskins, 69, revealed his battle with the brain disorder yesterday, several months after his diagnosis.

A statement released by his agent said: 'Bob Hoskins wishes to announce that he will be retiring from acting, following his diagnosis of Parkinsons disease last autumn.

'He wishes to thank all the great and brilliant people he has worked with over the years, and all of his fans who have supported him during a wonderful career.

View original post here:
Bob Hoskins suffering from Parkinson's Disease, announces retirement from acting

PARIS European researchers said they are developing a wearable monitoring system that automatically regulates the delivery of medication to Parkinson's patients.

The EU-funded REMPARK (Personal Health Device for the Remote and Autonomous Management of Parkinsons Disease) project aims to develop a Personal Health System, featuring closed loop detection, with response and treatment capabilities, for the improved management of Parkinsons disease patients.

The REMPARK system is composed of two elements. The first element is a bracelet equipped with a sensor for measuring tremor in patients, and an inertial system worn at the waist on a belt made of biocompatible material. The second part, the size of a mobile phone, is equipped with sensors and can process and wirelessly transmit the data collected.

The next step will consist in including a central server where all the data from patients will be stored, processed and analyzed to assess how each patient is evolving. Researchers suggest it will support supervising medical teams in their decision process.

Led by CETpD, the research project gathers Teknon Medical Centre, Telefnica R&D, the European Parkinsons Disease Association, research centers and companies based in Germany, Portugal, Italy, Israel, Ireland, Sweden and Belgium.

The REMPARK project, which will run until 2015, has an overall budget of 4.73 million ($5.2 million).

------------------------ If you found this article to be of interest, visit Medical Designline where you will find the latest and greatest design, technology, product, and news articles with regard to all aspects of clean technologies. And, to register to our weekly newsletter, click here.

Read the original here:
Wearable monitoring system for Parkinson's patients

Drinking too much coffee can give the average Joe the jitters, but scientists say caffeine may have the opposite effect on people with Parkinson's disease.

The Canadian study found that drinking between two and four cups of coffee a day can help control tremors, opening the door to new treatment options for the progressive neurodegenerative condition that affects more than 10,000 Kiwis.

Symptoms can include tremors, stiffness of muscles, depression, disturbance of normal sleep, fatigue and lack of sense of smell.

Parkinson's New Zealand chief executive Deirdre O'Sullivan said she was excited by the research but expressed caution at the small scale of the study.

The effect of caffeine on the healthy human brain was widely known but she had not heard any research into its effects regarding Parkinson's, she said.

Coffee could also lead to negative effects, so she said it was probably not wise for those suffering from the disease to dramatically increase their intake until more research had been done.

The study was one of the first in humans to show that caffeine can help with movement impairment in people who had the disease, said study author Ronald Postuma, of McGill University in Montreal.

Previous studies have found that people who drink caffeine are less likely to develop Parkinson's.

Sixty-one sufferers - whose symptoms included daytime sleepiness and some motor symptoms - were given either a caffeine supplement or placebo pill.

Members of the caffeine group were given 100 milligrams of caffeine twice a day for three weeks, then 200 milligrams twice a day for three weeks, which is the equivalent of between two and four cups of coffee a day.

Original post:
Study finds coffee may calm Parkinson's disease

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/r5jrks/randd_trends_park) has announced the addition of the "R&D Trends: Parkinson's Disease - Pipeline swells but a paradigm shift is unlikely in the mid-term" report to their offering.

Review of key trends in the development of new Parkinson's disease drugs across the seven major markets. Includes detailed analyses of the composition of the pipeline, clinical trial design, target product profile, and future treatment developments.

Since early 2011, R&D efforts in Parkinson's disease have been met with mixed success. In Q1 2012, the US FDA re-approved UCB's Neupro (rotigotine patch), and accepted the New Drug Application filing for Impax/GSK's IPX066 for idiopathic Parkinson's disease. Meanwhile, the development of eight late-stage pipeline candidates has been discontinued due to lacklustre efficacy.

Scope

Highlights

Key Topics Covered:

OVERVIEW

EXECUTIVE SUMMARY

CLINICAL PIPELINE OVERVIEW

Read the original post:
Research and Markets: R&D Trends: Parkinson's Disease - Pipeline swells but a paradigm shift is unlikely in the mid-term

August 3, 2012

Connie K. Ho for redOrbit.com Your Universe Online

Coffee lovers take note: coffee may have health benefits related to Parkinsons disease. A new study examined the influence coffee has on the disorder. Based on the results, researchers believe that coffee can help control movement, easing the symptoms of Parkinsons. The findings are featured in the online issue of Neurology, a journal of the American Academy of Neurology.

Studies have shown that people who use caffeine are less likely to develop Parkinsons disease, but this is one of the first studies in humans to show that caffeine can help with movement symptoms for people who already have the disease, explained study author Dr. Ronald Postuma, a member of the American Academy of Neurology and a researcher at the Researchers Institute of the McGill University Health Center, in a prepared statement.

In the study, 61 participants who showed symptoms of Parkinsons disease, such as daytime sleepiness, were split into two groups. One group took a placebo and the other group took a pill with 100 milligrams of caffeine twice a day for three weeks then 200 milligrams twice a day for three weeks. The second group consumed the equivalent of caffeine from two to four cups per day.

Following a six-week exam period, the group that was given caffeine supplements showed a five-point average in improvement in Parkinsons severity rating as compared to participants who were given the placebo.

This is a modest improvement, but may be enough to provide benefit to patients. On the other hand, it may not be sufficient to explain the relationship between caffeine non-use and Parkinsons, since studies of the progression of Parkinsons symptoms early in the disease suggest that a five-point reduction would delay diagnosis by only six months, noted Postuma in the statement.

The group that took caffeine also showed an average of three-point improvement in body stiffness and body movement as compared to those who were in the placebo group.

The people who received caffeine supplements experienced an improvement in their motor symptoms (a five-point improvement on the Unified Parkinsons Disease Rating Scale, a rating scale used to measure the severity of the disease) over those who received the placebo, suggested Postuma in the statement. This was due to improvement in speed of movement and a reduction in stiffness.

However, caffeine did not positively improve daytime sleepiness, depression, or quality of life in the participants; its also important to take note that, as the study was done in a short amount of time, the influence of caffeine may decrease over time.

Excerpt from:
Coffee May Help Control Symptoms Of Parkinson's Disease

Scientists have discovered a new avenue for the treatment of vision loss, one of the complications of Parkinson's disease.

Gentle, non-invasive treatment with a soft infra-red light can potentially protect and heal the damage that occurs to the human retina in Parkinson's disease, says Professor Jonathan Stone from The Vision Centre and the University of Sydney.

"Near infra-red light treatment has long been known to promote the healing of wounds in soft tissues such as skin. Our recent studies are showing that it can also protect the retina of the eye from toxins which attack its nerve cells," Professor Stone said.

"We have been studying a mouse 'model' of Parkinson's disease, in which such a toxin is used to create a Parkinson-like condition. The toxin targets brain cells which use a particular signalling molecule called dopamine, and the infrared light - in the right dose and with the right timing - blocks the toxic effect."

The toxin also kills certain key retinal cells which are important in giving sharpness to the retina's coding of visual images. Infrared light also protects these retinal cells and reduces the damage.

The new results suggest that infra-red radiation will be effective in Parkinson's disease, Professor Stone said. Because the radiation is effective at low intensities, with no known toxicity, there are few barriers if any to trials in humans.

"As shown in these studies on mice, protection or rescue of neurons in the brain - and as we know now, in the retina - is better than the best established treatments for Parkinson's disease," Professor Stone said. "The challenge now is to translate these findings, made in mouse models, to human patients suffering from Parkinson's disease.

"Diseases such as Parkinson's are seriously debilitating; for the individual the need is immediate. There is every reason for clinical trials to be carried out as soon as possible."

As to the potential benefits for Parkinson's patients, he says: "Principally, we anticipate there would be a preservation of acuity, the clarity with which we can see detail and contours in the visual world. The same treatment should be protective for the brain as well, preventing or slowing the otherwise relentless progress of the disease. As always, we will need rigorous trials, to know what can be achieved."

It is no surprise, Professor Stone observed, that the same treatment works for both the brain and the retina. "The retina of the eye is really part of the brain - the only part outside the skull. It has to be outside the skull, so it can function as an eye. In many ways the retina is the most accessible part of the brain, and many discoveries about the brain have begun in the retina.

Here is the original post:
New hope for eyes damaged by Parkinson's disease