A Moving New Parkinson's Disease Campaign Aims to Stamp Out Inequalities in Treatment and Care Across Europe

The "Awareness Campaign" Visualises Daily Challenges Faced by People

With Parkinson's as Revealed by New European Research

MADRID, August 25 /PRNewswire/ -- The European Parkinson's Disease Association (EPDA) today urged European decision makers and politicians to end inequalities in care and treatment access for people with Parkinson's disease.

The plea was made during the launch of EPDA's latest campaign, 'Parkinson's is visible, make it livable', intended to visualise the daily challenges faced by those with Parkinson's, increase people's knowledge and understanding of the disease and influence decision makers.

EPDA's campaign follows new research* highlighting the extent to which everyday activities are negatively impacted by Parkinson's. The research, Real Life, Real PD, conducted by EPDA among 3,000 people living with the disease, showed that eating, dressing, washing and speaking are some of the daily tasks significantly affected and that the majority of people do not feel in control of their symptoms. Almost half of all respondents described how their depression and mood swings placed an added strain on relationships with partners and families.

Speaking at the event, EPDA president Stephen Pickard commented, "Parkinson's is a costly disease and places a huge burden on carers and society as a whole. We need governments to realise that taking action to reduce this burden by ensuring people receive the best care and treatment available makes the most economic and social sense."

He continued, "There are nearly 1.2 million people living with Parkinson's in Europe, and with an ageing population this figure is set to rise. It's time to address inequalities in care and treatment of the disease and improve the lives of those affected by Parkinson's now and in the future."

The campaign was launched at the 12th Congress of the European Federation of Neurological Societies (EFNS) in Madrid where delegates heard from EPDA representatives and watched a series of emotive short films featuring people with Parkinson's battling with everyday tasks such as shopping and crossing the road.

The campaign, 'Parkinson's is visible, make it livable', is the first step towards eradicating inequalities in care and treatment access across Europe and a summit meeting is scheduled to take place in Brussels next year where MEPs will discuss the practical steps required to improve management of the disease.

Campaigner, Tom Isaacs (40), who has lived with Parkinson's disease for 12 years, commented at the event, "It always amazes me how Parkinson's is so visible socially and yet seemingly invisible to society. This is a ruthless condition and help is needed throughout Europe. This EPDA initiative is crucial. We need to increase understanding. We need to raise the profile. We need people not just to see, but to act."

To watch EPDA's short films and find out more about the campaign, please follow this link:

http://www.parkinsonsdecisionaid.eu.com/awarenessCampaign/2008/video.asp

*The full research report has been submitted for publication to the International Journal of Clinical Practice and is currently under review

Extracellular dopamine induces the oxidative toxicity of SH-SY5Y cells

Yuhua Jiang ^{1 2}, Lin Pei ¹, Shupeng Li ¹, Min Wang ¹, Fang Liu ^{1 3 *}

¹Department of Neuroscience, Centre for Addiction and Mental Health, Clarke Division, University of Toronto, Toronto, Ontario, Canada M5T 1R8
²Department of Radiation Oncology, Qilu Hospital, Shandong University, Ji-Nan 250012, People's Republic of China
³Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada M5T 1R8

email: Fang Liu (f.liu.a@utoronto.ca)

^*Correspondence to Fang Liu, Department of Neuroscience, Centre for Addiction and Mental Health, Clarke Division, 250 College Street, Toronto, Ontario, Canada M5T 1R8

Abstract

Dopamine-induced neuronal cytotoxicity has been proposed as a leading pathological mechanism underlying many neuronal degenerative disorders including Parkinson disease. Various hypotheses have been proposed including oxidative stress and dopamine (DA)-induced intracellular signal disorder via DA D1 and D2 receptors. The exact mechanism involved in this process is far from clear. In this study, employing a neuronal blastoma cell line, SH-SY5Y, we tried to elucidate the roles of these different suggested mechanisms in this pathological process. The results showed that DA induced cell toxicity in a dose- and time-dependent way. Selective D1 and D2 DA receptor antagonist could not block the cytotoxic effects, whereas reductive reagent ascorbic acid but not GSH could effectively rescue the cell death, suggesting that DA-induced cell toxicity was caused by an extracellular oxidative stress. This was further supported by the enhancing effects of DA transporter blocker, GBR, which could increase the cell death when pretreated. Finally, ascorbic acid could also protect SY5Y cells from DA-induced cellular apoptotic signal changes including PARP and P53. Our studies suggested that DA exerted its cytotoxic effects via an extracellular metabolism, whereas intracellular transportation could reduce its oxidative stress. Cytotoxicity effects induced by extracellular DA could be protected by reductive agents as ascorbic acid. These results help to broaden our understanding of the mechanisms of DA-induced cell death and may provide potentially therapeutical alternative for the neurodegenerative disorders. Synapse 62:797-803, 2008. © 2008 Wiley-Liss, Inc.

Mild cognitive impairment in Parkinson’s disease: the challenge and the promise

Abstract: This review addresses the literature surrounding Parkinson’s disease (PD) and mild cognitive impairment (MCI).

It discusses the neuropsychological, pharmaceutical, and pathological overlap, the socioeconomic impact of PD and MCI, and the value of recognizing,understanding, and treating MCI in PD.

It is concluded from this review that MCI in PD does exist and should be considered in clinical and research investigations. Due to the lack of accepted clinical criteria, an inclusive operating definition of MCI in PD is proposed.

Research guidelines for studying the presence of MCI in PD and evaluating the efficacy of pharmaceutical interventions are also suggested.

Abstract: This review addresses the literature surrounding Parkinson’s disease (PD) and mild cognitive impairment (MCI). It discusses the neuropsychological, pharmaceutical, and pathological overlap, the socioeconomic impact of PD and MCI, and the value of recognizing,understanding, and treating MCI in PD. It is concluded from this review that MCI in PD does exist and should be considered in clinical and research investigations. Due to the lack of accepted clinical criteria, an inclusive operating definition of MCI in PD is proposed. Research guidelines for studying the presence of MCI in PD and evaluating the efficacy of pharmaceutical interventions are also suggested.

See full article.......

Authors:

Hubert H Fernandez1
Gregory P Crucian1
Michael S Okun1
Catherine C Price2
Dawn Bowers2
1Department of Neurology,
2Department of Clinical and Health
Psychology, University of Florida,
Gainesville, FL, USA

Etiquetas de Technorati: Parkinson,Investigación,Información,Blog,PD

WE MOVE - Movement Disorders Mime Video

 

Rasagiline (Azilect) as Disease-modifying Treatment for Parkinson’s Disease?

From M.J. FOX Foundation (http://www.michaeljfox.org/)

Original article.....

On Monday, June 16, 2008, Israeli drugmaker Teva issued a press release reporting that Azilect (rasagiline) was on track to become the first disease-modifying treatment for Parkinson’s disease. The company has completed the ADAGIO Phase 3 clinical trial, in which Azilect tablets met three clinical endpoints demonstrating that the drug could slow progression of Parkinson’s disease.

The Michael J. Fox Foundation spoke with Karl Kieburtz, MD, PhD, Professor of Neurology and Community and Preventive Medicine at the University of Rochester Medical Center and chair of the Parkinson Study Group, about how patients should interpret the news.
NOTE: The medical information contained in this article is for general information purposes only. The Michael J. Fox Foundation has a policy of refraining from advocating, endorsing or promoting any drug therapy, course of treatment, or specific company or institution. It is crucial that care and treatment decisions related to Parkinson’s disease and any other medical condition be made in consultation with a physician or other qualified medical professional.

MJFF: In the simplest terms, what is Teva reporting and why is it potentially important for people with Parkinson’s?

KK: Teva’s press release reported that rasagiline, which Teva sells under the brand name Azilect, can slow functional decline in early-stage PD patients who have not yet been treated with dopamine-replacement therapies, such as levodopa. This means that rasagiline could be the first PD treatment to receive the label “disease-modifying” from the Food and Drug Administration (FDA).
MJFF: Do we know for sure that rasagiline is disease-modifying?
KK: No, we don’t know that with certainty yet. I want to emphasize strongly that the press release was not a scientific one. Commercial entities are obligated by the Securities and Exchange Commission (SEC) to put out communications such as this when they have information that they know may affect their share prices. As of this week, the scientific data resulting from the trial have not been made public. In the future, when the data have been made public, the results of this trial may be seen differently.
The good news is that at least some scientific results should be forthcoming as soon as within the next few weeks. Some of the data from the ADAGIO trial will be presented during the week of June 23 at the Movement Disorders Society Congress in Chicago, and we would also expect to see publication in a peer-reviewed journal within a relatively short timeframe. [Editor’s note: Watch the MJFF Web site for further updates in coming weeks.]
MJFF: What kind of drug is rasagiline? Are there other similar drugs that could exert a similar effect?
KK: Rasagiline belongs to a class of drugs called monoamine oxidase inhibitors (MAO-Is). To date these drugs have typically been used alone or in combination with levodopa as a symptomatic therapy for both early- and late-stage Parkinson’s patients. Another drug in the same class is called selegiline. At this point it’s impossible to extrapolate Teva’s rasagiline results to selegiline, because selegiline has not yet been tested in the same ‘delayed start’ design. Perhaps there is some unique quality to rasagiline that allows it to potentially slow PD progression. We’ll know more when we see the data.
MJFF: Are there negative side effects or other concerns people should have before asking their doctor for Azilect? Should everyone with PD now consider taking the drug?

KK: Certainly MAO-inhibitors are not without side effects, and there are some warnings associated with prescribing them. They have possible interactions with certain other drugs, including selective serotonin reuptake inhibitors (SSRIs), which are widely prescribed to treat depression. They may interact with a chemical called tyramine found in foods including alcohol and certain cheeses, which can result in blood pressure changes. As a result, people on some of these drugs must adhere to a restricted diet, and this can be difficult. Studies suggest that rasagiline may be less prone to interact with tyramine in this way, but it is still important that patients speak with their doctors to address all the potential issues that surround starting a course of treatment with rasagiline.

MJFF: Was there earlier evidence that rasagiline could be disease-modifying?
KK: Yes, there were preliminary results which Teva was following up on with the ADAGIO study. In 2004 the Parkinson Study Group conducted the TEMPO trial on rasagiline, with results similar to the news out this week, though TEMPO’s overall duration was shorter.
MJFF: How did the researchers design the ADAGIO trial to test for disease modification?
KK: It’s important to note that the endpoints for the trial were clinical outcomes, not biochemical measures. In other words, we still don’t have a way to “look inside” a patient’s brain and check to see how well the dopamine neurons are doing. What this means is that the clinicians were assessing trial participants for observable changes in their PD symptoms — i.e., did their movement not slow as much over the course of the trial? Trial participants were measured against the Unified Parkinson’s Disease Rating Scale (UPDRS), the standard validated tool used in PD clinical trials.
The ADAGIO researchers employed a design known as a “delayed-start trial.” As recently as April 28, at a meeting co-sponsored by MJFF, the Parkinson Study Group, the Food and Drug Administration (FDA) and the American Association of Pharmacological Scientists, FDA has suggested that, in the absence of a biological marker, a delayed-start trial is the design most likely to satisfactorily demonstrate disease modification.
MJFF: What is a delayed-start trial and how does it work?
KK: A delayed start trial works like this: At the outset of the trial, participants are divided into two groups. One group receives the actual treatment, and one receives a placebo. Neither the patients nor the clinicians know which group is which. Results are carefully tracked for a certain period of time — in the case of the ADAGIO trial, 36 weeks.
When the 36 weeks have elapsed, the placebo group is switched to the actual treatment. At this point the clinicians are looking for a very specific result. If the treatment being tested is exerting a disease-modifying effect, then the improvements seen in the group that started on placebo should not be able to “catch up” with the improvements seen in the group that received actual treatment from the beginning. Even though the “delayed start” group may see some improvement once they switch from placebo to the drug, there will always be a “gap” between the two groups. If you can demonstrate that the gap exists and that it remains over an extended period of time, FDA has suggested that it’s reasonable to claim that your treatment is slowing the progression of the disease.
MJFF: Bottom line: How excited should patients and their loved ones feel about this news?
KK: Results that come out in a business-oriented press release aren’t sufficient to make a judgment on implications for patients. We need to really evaluate the science and we need to know exactly what the study found. For example, what were the side effects experienced by patients in the trial? How many dropped out? Did they have to follow a special diet? How did they feel about that?
So, while the news reported this week is potentially very exciting, it is not yet actionable. The clinical and research community awaits further understanding of the trial results in order to effectively advise patients on best next steps.

Etiquetas de Technorati: Parkinson,Medicamentos,Investigación,Información,Blogging

Teva's AZILECT(R) 1 mg Tablets Meet End Points in ADAGIO Phase III Trial

JERUSALEM - (Business Wire) Teva Pharmaceutical Industries Ltd. (NASDAQ: TEVA) announced today the successful completion of ADAGIO, the phase III study designed to demonstrate that AZILECT^® 1 mg tablets can slow down the progression of Parkinson's disease. In the trial, the currently marketed AZILECT^® 1 mg tablets met all three primary end points, as well as the secondary and additional end points, all with statistical significance. The study also confirmed the safety and tolerability of AZILECT^®.

Teva intends to submit these results to the regulatory authorities in the U.S. and Europe. Based on these results, AZILECT^® could become the first Parkinson's disease treatment to receive a label for disease modification.

Full story...

There is no Parkinson disease.

Arch Neurol. 2008 Jun;65(6):705-8.

There is no Parkinson disease.

Weiner WJ.

Department of Neurology, Maryland Parkinson's Disease and Movement Disorders Center, University of Maryland School of Medicine, 22 S Greene St, N4W46, Baltimore, MD 21201, USA. wweiner@som.umaryland.edu

The term Parkinson disease defines a specific clinical condition characterized by a typical history and characteristic signs. This review examines the historical evolution of the concept of Parkinson disease and how the misunderstanding of Parkinson disease may be hindering clinical research trials.

It is proposed that this syndrome be called Parkinson diseases or parkinsonism type 1 through infinity.

PMID: 18541790 [PubMed - in process]

 

Simple, sintetic and clear.

What do you think about?

From blog http://myownarcadia.blogspot.com/

Squamosamide derivative FLZ protects dopaminergic neurons against inflammation

Abstract

Background

Inflammation plays an important role in the pathogenesis of Parkinson's disease (PD) through over-activation of microglia, which consequently causes the excessive production of proinflammatory and neurotoxic factors, and impacts surrounding neurons and eventually induces neurodegeneration. Hence, prevention of microglial over-activation has been shown to be a prime target for the development of therapeutic agents for inflammation-mediated neurodegenerative diseases.

Methods

For in vitro studies, mesencephalic neuron-glia cultures and reconstituted cultures were used to investigate the molecular mechanism by which FLZ, a squamosamide derivative, mediates anti-inflammatory and neuroprotective effects in both lipopolysaccharide-(LPS)- and 1-methyl-4-phenylpyridinium-(MPP⁺)-mediated models of PD. For in vivo studies, a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-(MPTP-) induced PD mouse model was used.

Results

FLZ showed potent efficacy in protecting dopaminergic (DA) neurons against LPS-induced neurotoxicity, as shown in rat and mouse primary mesencephalic neuronal-glial cultures by DA uptake and tyrosine hydroxylase (TH) immunohistochemical results. The neuroprotective effect of FLZ was attributed to a reduction in LPS-induced microglial production of proinflammatory factors such as superoxide, tumor necrosis factor-α (TNF-α), nitric oxide (NO) and prostaglandin E₂ (PGE₂). Mechanistic studies revealed that the anti-inflammatory properties of FLZ were mediated through inhibition of NADPH oxidase (PHOX), the key microglial superoxide-producing enzyme. A critical role for PHOX in FLZ-elicited neuroprotection was further supported by the findings that 1) FLZ's protective effect was reduced in cultures from PHOX^-/- mice, and 2) FLZ inhibited LPS-induced translocation of the cytosolic subunit of p47^PHOX to the membrane and thus inhibited the activation of PHOX. The neuroprotective effect of FLZ demonstrated in primary neuronal-glial cultures was further substantiated by an in vivo study, which showed that FLZ significantly protected against MPTP-induced DA neuronal loss, microglial activation and behavioral changes.

Conclusion

Taken together, our results clearly demonstrate that FLZ is effective in protecting against LPS- and MPTP-induced neurotoxicity, and the mechanism of this protection appears to be due, at least in part, to inhibition of PHOX activity and to prevention of microglial activation.

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Articles from Journal of Neuroinflammation are provided here courtesy of
BioMed Central

Articulo completo en Parkinson's Library - Investigación

Growth Factor Promotes New Neuron Growth in Mouse Model of Parkinson's Disease

A well-known growth factor has been shown to increase the growth of new neurons in mice induced to develop Parkinson's disease. The finding highlights a potential new therapy for the condition.

Newswise — Mice induced to develop Parkinson’s disease (PD) show an increase in the growth of new neurons after they are treated with a well known growth factor. The research, to be published May 16 in The Journal of Neuroscience, based on work by scientists at the Buck Institute, highlights a potential new therapy for this incurable, neurodegenerative disorder that affects 1.5 million Americans.

The mice, which developed Parkinson-like symptoms after they received the toxin MPTP (which causes PD in humans) were treated with fibroblast growth factor-2 (FGF-2), a naturally occurring protein that has been studied extensively for its neuroprotective properties. In the Buck study, the use of FGF-2 enhanced the neurogenesis, or growth of new neurons, that was already underway in the injured area of the brain. In addition, researchers began to see an increase in the cells that produce dopamine, the neurotransmitter implicated in PD.

“The fact that FGF-2 allowed these new neurons to develop in the principle site of cell loss in the disease is quite exciting,” said Buck faculty member and lead scientist Julie Andersen, PhD. “This suggests that administration of growth factors might be used therapeutically to replace dead or damaged cells. The next step in our research is to see whether treatment with FGF-2 results in any symptomatic improvement in the mice.”

Scientists at the Buck are currently researching FGF-2 as a potential treatment for Huntington’s disease, a fatal hereditary brain disorder that affects approximately 30,000 Americans. In partnership with Neurobiological Technologies, Inc. (NASDAQ: NTII), Buck researchers are seeking to create a form of FGF-2 for human clinical trials. The protein shows particular promise because it is able to cross the blood-brain barrier.
This most recent study highlights the interdisciplinary approach to research at the Buck Institute. This work built on earlier discoveries in the laboratory of David Greenberg, MD, PhD, which showed neurogenesis occurring in the brains of patients diagnosed with Alzheimer’s disease, and the laboratory of Lisa Ellerby, PhD, which showed that FGF-2 promoted new nerve growth and increased survival in mice genetically engineered to develop Huntington’s disease. The work as a whole emphasizes a research focus at the Buck Institute on efforts to enhance the brains ability to heal itself in the face of injury.

Joining Andersen in the study were Jun Peng, Lin Xie, Kunlin Jin, and David A. Greenberg, all of the Buck Institute.
The Buck Institute is an independent non-profit organization dedicated to extending the healthspan, the healthy years of each individual’s life. The National Institute of Aging designated the Buck a Nathan Shock Center of Excellence in the Biology of Aging, one of just five centers in the country. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating age-related diseases such as Alzheimer’s and Parkinson’s disease, cancer, stroke, and arthritis. Collaborative research at the Institute is supported by genomics, proteomics and bioinformatics technology. For more information: www.buckinstitute.org.

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© 2008 Newswise.  All Rights Reserved.

New Treatment Tried For Parkinson's Disease

Like many patients with Parkinson’s disease, over time, medicine becomes less effective. Doctors are now using a new approach.
In the lab they’ve developed a fluid that’s injected directly into the patient’s brain. The fluid contains billions of viruses and delivers a gene that re-establishes some of the normal chemistry in the brain.
This is the first study to use gene therapy on advanced cases of Parkinson’s and early results are impressive. 
Twelve patients were injected with the genes initially and while all of them got better, nearly half showed a surprising response. The patients became more mobile. They were more able to live independently and tremors improved.
Even more promising, one year after the injections, the majority of patients continued to improve, hinting that their brains may actually be trying to reverse the damage caused by the disease.
The next step for this treatment method is a larger study.

Cell-Based Therapy Shows Promise In Patients With Parkinson's Disease

A novel cell therapy using retinal pigment epithelial (RPE) cells attached to tiny gelatin bead microcarriers implanted in the brain can improve the symptoms of patients with moderate to advanced Parkinson's disease (PD).
Rush University Medical Center neurosurgeon Dr. Roy A. E. Bakay and colleagues from Emory University, Atlanta found the therapy Spheramine was well-tolerated and patients experienced improvement in Parkinsonian symptoms (tremor, rigidity, slowness of movements, and impaired balance and coordination.) These findings were presented at the Annual Meeting of the American Association of Neurological Surgeons in Chicago on April 28, 2008.
The pilot study was initiated at Emory University Hospital and followed six patients with moderate to advanced PD to investigate the safety, tolerability, and efficacy of the Spheramine implantation. The full patient group has been evaluated for four years, and several have been monitored for six years. Bakay and colleagues report long-term improvement or stabilization of symptoms, maintained for a minimum of two years after Spheramine implantation. They note no Spheramine-related serious adverse events were reported and that the most frequent adverse event was postsurgical headache, which spontaneously resolved within one to two weeks.
"The results of this study are very encouraging - Spheramine is well tolerated through several years of follow-up and improvement in parkinsonian symptoms is sustained," stated Bakay.
The cellular product Spheramine consists of RPE cells attached to microcarriers. RPE cells produce levodopa, the precursor of dopamine. Dopamine is a neurotransmitter produced by nerve cells in the brain that progressively declines as the disease progresses.
The RPE cells, which are normally found in the back of the eye, are cultured under standardized conditions and attached to the microscopic beads prior to implantation. The microcarriers are necessary for the cells to survive in the brain. The implanted cells serve as a new potential source of levodopa to enhance dopamine production where it is most needed.
The patients were selected based on disease stage, levodopa responsiveness, and severity of PD symptoms while off medication. An even distribution of Spheramine was surgically implanted into the more affected side of the brain, and patients left the hospital a few days later.
The primary efficacy measure in this trial is the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS) when the patient has been OFF antiparkinsonian medication for at least 12 hours. The researchers report clinical improvements were noted in both UPDRS motor scores off medication (44 percent improvement from baseline at 48 months) and patient-reported quality of life scores (23 percent improvement from baseline of total PDQ-39 score at 48 months). Several of these patients have been monitored for 6 years and the trial has been extended to 10 years of follow-up."
Bakay said positive results in the pilot study prompted the initiation of a Phase IIb, multicenter, double-blind, randomized, sham surgery-controlled study (STEPS) to further evaluate the safety, tolerability and efficacy of Spheramine. Changes from the pilot study included implantation in both sides of the brain and the addition of a sham surgery group. To date, 71 patients have been randomized for either Spheramine or sham surgery and results from the will become available later this year.
Parkinson's Disease
Parkinson's disease is a progressive brain disorder that affects a person's motor skills which worsen as the disease advances. Early in the disease, there is a loss of brain cells that produce the chemical dopamine. Normally, dopamine operates in a delicate balance with other neurotransmitters to help coordinate the millions of nerve and muscle cells involved in movement. Without enough dopamine, this balance is disrupted, resulting in tremor (trembling in the hands, arms, legs and jaw); rigidity (stiffness of the limbs); slowness of movement; and impaired balance and coordination - the hallmark symptoms of PD.
PD affects one in every 100 people over the age of 65. The latest epidemiology studies indicate that worldwide numbers will increase from an estimated 4.1 million in 2005 to 8.7 million people with PD by 2030. There were an estimated 19,500 PD-related deaths in the United States in 2005, an increase of 1,500 deaths from 2004.
It is estimated to cost $23 billion a year in direct and indirect costs and lost productivity. Despite therapeutic advancements, oral medications provide insufficient symptom control after the disease has progressed and new approaches are needed.
Rush University Medical Center

UPDATE 3-UCB recalls Parkinson's patch, reviews 2008 outlook

By Philip Blenkinsop

BRUSSELS, March 20 (Reuters) - Belgian pharmaceutical group UCB (UCB.BR: Quote, Profile, Research) said on Thursday it was recalling its Parkinson's drug Neupro in the United States and some batches from Europe, prompting a review of its 2008 forecast.

UCB shares dropped as much as 18.4 percent to 21.60 euros on Thursday, their lowest level since August 2003.

"Depending on the resolution timeline of this issue, the full effect on UCB's business is not yet known. Therefore, UCB's 2008 financial outlook is under review and will be updated as soon as possible," the company said in a statement.

UCB achieved net sales of 52 million euros ($81.74 million) from the relatively new drug last year.

UCB said the recall decision was not the result of contamination or toxicity but that the clinical performance of some samples on the market was not as required.

"As a result, there will be an out-of-stock situation with Neupro in the United States in late April 2008. In the European Union and most other regions, Neupro supply is sufficient," it continued.

A spokeswoman said it was not clear how long UCB would be out of stock in the United States and likewise when it would be able to give a new 2008 outlook.

KBC Securities said in a research note that it had reduced its forecast for Neupro sales this year to 88 million euros from 110 million, as well as its peak annual sales estimates and cut its target price to 33.50 euros from 35.00 euros.

The Neupro news is the latest in a series of setbacks for the Belgian drugmaker in the past year.

Would-be blockbuster Cimzia is yet to convince regulators that it should be approved for bowel disorder Crohn's disease.

Earlier this month, U.S. health officials warned that its prescription cough medicine Tussionex could be fatal for young children if taken frequently, though it is not approved for those aged under six.

"This disruption comes at a crucial time in the launch phase of this important franchise," Deutsche Bank wrote, adding Neupro's launch for restless legs could be significantly delayed by regulators' insistence that quality problems be resolved.

Neupro, delivered to patients in the form of patches stuck on the skin, is approved to treat early stage Parkinson's disease in the United States and early and late stages of the disease in Europe.

The patches were launched in Europe in 2006 and in the United States in July 2007.

It filed for approval to treat restless legs syndrome in both the United States and Europe in December.

UCB last month forecast that revenue would decrease to about 3.4 billion euros in 2008 from 3.6 billion last year. Recurring core profit (EBITDA) would be about 650 million euros and net profit was expected to exceed 100 million. (Reporting by Philip Blenkinsop, editing by Will Waterman)

La razon que nos une ">The reason that links us together

Tempus fugit" decían los latinos. El tiempo vuela. Para las personas con Parkinson esta frase tiene una valencia todavía mas especial. La lucha contra el tiempo que libramos cada día entre toma y toma nos enseña que hay que aprovecharlo todo y que cada momento dejado atrás es un momento perdido. No obstante, en otros aspectos de nuestras vidas, parecemos olvidar esta gran lección de vida que, muy a pesar nuestro, el PK nos ha enseñado. Un año mas se acerca la fecha que los afectado por el PK tenemos marcada en el calendario y un año mas aplazaremos "sine die" (otra perla del latín que significa "sin fecha") el arranque de una movilización real, unitaria y coordinada de las personas y asociaciones para despertar la sensibilidad de la opinión publica y de la administración hacia la problemática del colectivo PK. Para un recién incorporado a este nueva visión del mundo, resulta francamente difícil de entender como un numero tan grande de personas y de asociaciones, con los medios que la tecnología nos pone a disposición, no hayan conseguido superar los limites de "nuestro proprio jardín" para lanzarse a la exploración de mas grande prados.

">Tempus fugit "said Latinos.
Time flies.

For people with Parkinson's this phrase has a valence even more special.

The fight against time to book every day between takes and takes teaches us that we must take advantage of everything but each time left behind is a moment lost.

However, in other aspects of our lives, we seem to forget this great lesson of life that, despite our very, PK has taught us.

Once again it's aproaching the date that affected by the PK we marked on the calendar and another year defer "indefinitely" (another pearl of Latin meaning "no date") boot of a real mobilization, unified and coordinated individuals and associations to raise awareness of public opinion and the administration to the problem of collective PK.

For a newly incorporated into this new vision of the world, it is frankly difficult to understand how such a large number of individuals and associations, with the resources that technology makes available to us, have not managed to overcome the limits of our own garden " to engage in the exploration of bigger pastures.

¿Estamos todos tan satisfechos de la situación actual para no considerar necesaria ninguna acción? Entonces, ¿a que vienen tantas quejas en todos los foros? ¿Esta alguien realmente convencido que unir esfuerzos en favor de unos objetivos concretos y compartidos, puede acabar perjudicándole? Unir esfuerzos, que quede claro, nadie habla de fusionar, federar, asociar, y todo lo que pueda sonar a renunciar a lo que se ha venido construyendo a lo largo de los años y que constituye uno de los valores del movimiento del asociacionismo: la variedad y la proximidad. "Virtus unita fortior!" La virtud unida es mas fuerte. Hay objetivos que están fuera del alcance de cada uno de nosotros como individuos y justamente nos asociamos buscando en la agregación aquella fuerza que como individuos nos falta.

">Are we all so satisfied with the current situation in order not to consider any necessary action? So, how come so many complaints in all forums?
Is anyone really believe that unite efforts for specific and shared targets can harm them at the end of the day?
Joining efforts, let's make it clear, no one talks about merging, federate, associate, and all that may sound to abandon what has been built over the years and that is one of the values of the movement's associations: variety and proximity.

"Virtus unit fortior!" Virtue is stronger united.
There are goals that are beyond the reach of each of us as individuals and we associate looking at the aggregation that strength that we need as individuals.

¿Que fuerza oculta nos impide ahora repetir este mismo camino de unión, aunque solo por un día, para un objetivo que todos compartimos? ¿Si alguien se ofrece para empezar a andar este camino, nos apuntaríamos a acompañarle? Llevo tiempo reflexionando sobre el tema y buscando la manera de encontrar el hilo de la madeja. Me gustaría contar con la participación de todos para una reunión de ideas para actuaciones concretas que nos pongan en marcha "Unidos contra el Parkinson ".

">What hidden force prevents us now repeat this same path of unity, but only for one day, for a goal that we all share?
If someone offers to start to walk this path, we'll be ready to accompany him?
I have spent time thinking about the issue and seek ways to find the thread of the skein.
I would like to involve all for a reunion of ideas for concrete actions that we put in place
"Unite against Parkinson <http://unidoscontraelparkinson.es/default.htm>."

I’m ill, but Who Really Needs to Know?

February 21, 2008

I’m ill, but Who Really Needs to Know?

By Lisa Belkin, The New York Times

One of the first decisions you make in the emotional hours after a scary diagnosis is whether to tell others. Most of us share the news with our loved ones, but what of the circles beyond, particularly those at work? Your boss?

Read full article

What it's all about (Parkinson's Disease)

What is Parkinson's Disease?

Dr James Parkinson first identified the condition, which he called "shaky palsy", in 1817.

It is a chronic (long-term), non-fatal, degenerative neurological disorder that impairs movement and speech. Though it is most common in the over-50s, one in 20 of those diagnosed is under 40.

Juvenile Parkinson's - affecting those under 18 - is extremely rare.

Men are slightly more likely to develop Parkinson's than women, but no one knows why.


What causes it?

Characterised by muscle rigidity, tremors - commonly referred to as "the shakes" - fatigue and, in extreme cases, total loss of mobility, the primary symptoms are due to a loss of nerve cells in the substantia nigra, part of the brain producing dopamine to aid movement co-ordination.

With depletion of dopamine-producing cells, parts of the brain can't function normally.

Parkinson's symptoms appear when about 80 per cent of dopamine has been lost.

Dopamine levels continue to fall for years. Researchers believe it is caused by genetics - nine genes linked to Parkinson's have been identified - plus environmental factors.


What are the symptoms?

"They vary greatly - a third of patients don't experience tremors," says Professor Ray Chaudhuri, of the Movement Disorders Unit at King's College Hospital, London.

"Other early warnings can include difficulty in writing, performing simple manual tasks such as tying shoelaces and holding cutlery, or the dragging of a limb.

"There is a feeling of stiffness, accompanied by numbness. One almost universal symptom is a loss of sense of smell - sufferers can't smell oregano."

Slowness or difficulty in initiating movement - bradykinesia - is common, as is muscle rigidity.

Disturbed sleep, bowel problems, incontinence, memory problems and depression are common "non-motor" symptoms, all linked to depleted levels of dopamine.

"The progression of the disease is usually slow for the first 15 years, after which decline can be rapid.

"As the disease advances the bottom half of the body can freeze. It's distressing, but not usually painful," says Professor Chaudhuri.

The symptoms of Parkinson's develop gradually.

There are no specific tests to prove if someone has the condition. Patients are diagnosed on medical history and a clinical examination.

The symptoms can have other causes and tests and scans may be needed to rule these out.


Is there a cure?

"There is no cure," says Professor Chaudhuri. "But it is treatable and manageable.

In the early stages, many rely on a healthy lifestyle - diet, exercise and relaxation. Later, drugs can also be used."

A new treatment, licensed for UK use in 2006, is the Neupro patch, made by Schwarz Pharma.

The patch contains a dopamine agonist - an agent that acts directly on the dopamine receptors in the brain - called rotigotine, and delivers a continuous dose of the drug over 24 hours, so patients have to change the patch only once a day.

Medications increase the level of dopamine reaching the brain, stimulate the areas where dopamine works, and block the action of other chemicals that reduce dopamine's effect.

Surgery is also available, depending on symptoms.

Deep-brain stimulation involves implanting a wire, with four electrodes at its tip, into the thalamus, the globus pallidus or the subthalamic nucleus - all parts of the brain connected to movement and co-ordination.

The wire is connected to a small implantable pulse generator (IPG) inserted under the skin, often in the chest, like a pacemaker.

The IPG sends electrical signals to the brain to stop or reduce Parkinson's symptoms.

Lesioning is another option. An electrode is inserted into the brain, causing selective damage to certain cells in the thalamus (thalamotomy) or globus pallidus (pallidotomy).

Unlike deep-brain stimulation, this is irreversible and less common.

There have been promising developments in coaxing human stem cells - premature cells that can become any of a number of mature cells in the body under the right conditions - to form dopamine-producing brain cells in rats, but treatment in humans is still a long way off.

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