Research News for Those With Parkinson’s Disease

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Diagnosed Illnesses in Veterans Needs More Transparency

As I compile this information from other sources, I hope that it keeps our readers updated and that they share with others that need to be kept informed.  I wonder how many veterans of the Vietnam War and how many veterans of the Gulf War 90-91 have Parkinson’s Disease.  I know a few Gulf War Veterans 90-91 that have been diagnosed with Parkinson’s Disease for several years.  There is no presumption of service connection for Parkinson’s for Gulf War Veterans. 

The author becomes frustrated because there is no place to find data on how many Gulf War Veterans (90-91) have Parkinson’s Disease.  Why cann’t the VA be more open on how many illnesses are being seen in the different groups of Veterans?  How many Vietnam Veterans have Parkinson’s Disease?  This holds firm also for other diagnosed illnesses.  The VA ought to have this information available on their web site for each diagnosed illness be it Parkinson’s Disease, any type of Cancer, Cardiac Disease, etc.

Maybe if this was on the central VA website, the american public and the veteran would know the facts of how many diagnosed illnesses veterans experience and what the normal civilian occurrence data of number per 100,000 in the population is for the same illness.  This would indeed show transparency in our government!  Our veterans and our fellow civilians need this information.

Below are several (7) articles on Parkinson’s Disease research that will be important for those that have that illness.  The information came from a review of 3 months of publications and the help of Medical News Today. Articles 1-3 (VA Puget Sound Health Care System was involved in this study) explore a huge study that was done that is tremendously important in identifying the link that Parkinson’s Disease has with the immune system and autoimmune disorder (including MS), the other studies look at connections to Alzheimer’s Disease and Molecular Mechanisms that trigger Parkinson’s Disease, Pesticide exposure interaction, and Gastrointestinal problems in Parkinson’s Disease.  So as the reader can quess this review has implications for Vietnam Veterans exposed to Agent Orange and also to Gulf War Veterans (90-91).  The research also explores biomarkers and potentials for new treatment modalities.

We need the VA to place more information on the research that is being done on their website.  We need the VA to provide more data sharing on their main website on the occurrence of Parkinson’s Disease, MS, ALS, and other autoimmune disorders, as well as all diagnosed illnesses, in the veterans population by war re Vietnam and Gulf War and the comparison figures for civilian populations.

1.  New Parkinson’s Gene Is Linked To Immune System

2.  Genetic Link Discovered Between Immune System,

3.   Immune System Genes Linked To Parkinson’s Disease 

4.  New Pathway To Parkinson’s And Alzheimer’s Diseases

5.  Study Identifies Molecular Mechanism Triggering Parkinson’s Disease

6.  Genes And Pesticide Exposure Interact To Increase Men’s Risk For Parkinson’s Disease

7.  New Study Showed The Impact Of Gastrointestinal Disorders In Patients With Parkinson’s Disease
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1.  New Parkinson’s Gene Is Linked To Immune System
A hunt throughout the human genome for variants associated with common, late-onset Parkinson’s disease has revealed a new genetic link that implicates the immune system and offers new targets for drug development.

The long-term study involved a global consortium, including Johns Hopkins researchers from the Center for Inherited Disease Research who performed genome-wide association studies on more than 4,000 DNA samples half from unrelated patients with Parkinson’s and half from healthy “controls.” The team confirmed that a gene in the human leukocyte antigen (HLA) region was strongly linked with Parkinson’s disease; this region contains a large number of genes related to immune system function.

The new data, published August 17 in Nature Genetics, bolster previous studies that hinted about a role for infections, inflammation and autoimmunity in Parkinson’s disease. This genetic finding demonstrates that inflammation isn’t simply a result of having the disease, but somehow is involved as a player in its origin.

“This is an exciting finding from a genome-wide association study (GWAS)which is completely hypothesis-independent and bias-free, based solely on looking at the whole genome and finding out what genes might be related to Parkinson’s,” says Kimberly Doheny, Ph.D., assistant professor, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine; assistant director of the Center for Inherited Disease Research (CIDR); and director of the CIDR Genotyping Lab, Johns Hopkins University.

It was long believed that common, late-onset Parkinson’s had no genetic components that environmental factors were the exclusive cause. Since genes were first implicated almost two decades ago, Parkinson’s has proven itself a “tough nut to crack,” Doheny says, adding that a handful of GWAS done prior to this one revealed nothing new other than to confirm genes that previously had been found to confer risk.

Setting this GWAS study apart, Doheny says, was the investigators’ meticulous choosing of patients and care of the DNA samples tested. The study’s principal investigator, Haydeh Payami Ph.D., of the New York State Department of Health, describes CIDR’s contribution as “huge.”

It took 18 years to build the study, according to Payami, at whose insistence the collection of DNA and clinical information was standardized using the most rigorous research criteria. Patients from whom samples were taken were tracked for at least a dozen years after their initial diagnoses to assure that they indeed had Parkinson’s, Payami adds, explaining that about 20 percent of PD patients’ diagnoses are actually misdiagnoses.

A neurodegenerative disease affecting between 1 and 2 percent of people over the age of 65, Parkinson’s disease can be difficult to diagnose as no definitive test exists. Its symptoms, which include tremors, sluggish movement, muscle stiffness and difficulty with balance, can be caused by many other things, including other neurological disorders, toxins and even medications. 

The GWAS itself took about four months, Doheny says, and cost about $400 per sample tested; whole-genome sequencing costs about $10,000 per sample. Since 1996, CIDR has provided high-quality genotyping services and statistical genetics consultation to gene hunters: researchers who are working to discover genes that contribute to common diseases by ferreting out variants in the genome. Its role in the Parkinson’s study was to assure that the genotyping dataset was of high quality, that data cleaning was done appropriately and that association analysis was stringent.

“We now have another window into what may be going on in Parkinson’s,” Payami says. “This finding anchors the idea of immune system involvement in genetics and brings it out to the forefront in terms of where research should be directed.”

Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are protective against Parkinson’s disease, according to the study. However, not everyone benefits from them to the same degree. The amount of risk reduction conferred by NSAIDs may vary widely depending on genetic differences, say the researchers. Investigating the connection between Parkinson’s disease and inflammation, especially in the context of the variable genetic make-ups of individuals, likely would lead to better, more selective medicines for treatment.

The study was funded by the National Institute of Neurological Disorders and Stroke, the Michael J Fox Foundation for Parkinson’s Disease Research, the Department of Veterans Affairs, the National Institute on Aging, the National Institute of Mental Health, the Intramural Research Program of the NIH at National Library of Medicine, and the Close to the Cure Foundation.

Authors of the study are Taye H. Hamza, Alain Laederach, Jennifer Montimurro, Dora Yearout, Denise M. Kay, Victoria I. Kusel, Randall Collura and Haydeh Payami, all of the New York State Department of Health; Cyrus P. Zabetian and Ali Samii from the University of Washington, Seattle; lbert Tenesa of the University of Edinburgh, Scotland; Kimberly F Doheny and Elizabeth Pugh, Center for Inherited Disease Research, Johns Hopkins University School of Medicine; John Roberts, Virginia Mason Medical Center; Alida Griffith, Evergreen Hospital Medical Center; William K. Scott, University of Miami; John Nutt, Oregon Health & Sciences University; and Stewart A. Factor, Emory University School of Medicine, Atlanta, GA .

Source: Johns Hopkins Medicine

Copyright: Medical News Today
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2.  Genetic Link Discovered Between Immune System, Parkinson’s Disease
Article Date: 16 Aug 2010 – 2:00 PDT 
A team of researchers has discovered new evidence that Parkinson’s disease may have an infectious or autoimmune origin. “Common genetic variation in the HLA region is associated with late-onset sporadic Parkinson’s disease” appears online in Nature Genetics.

The study was conducted by the NeuroGenetics Research Consortium, an international team of researchers led by Haydeh Payami, research scientist at the New York State Department of Health Wadsworth Center. The clinical directors for the study were Dr. Cyrus Zabetian, associate professor of neurology at the University of Washington and VA Puget Sound Health Care System, Stewart Factor at Emory University and John Nutt at Oregon Health and Sciences University.

The research team studied more than 2,000 Parkinson’s disease patients and 2,000 healthy volunteers from clinics in Oregon, Washington, New York and Georgia, assessing clinical, genetic and environmental factors that might contribute to the development and progression of Parkinson’s disease and its complications. Some of the research subjects were tracked for nearly two decades.

“Over the years, there have been subtle hints that immune function might be linked to Parkinson’s disease” said Zabetian. “But now we have much more convincing evidence of this and a better idea of which parts of the immune system might be involved.”

In the study, researchers detected a new association with the HLA (human leukocyte antigen) region, which contains a large number of genes related to immune system function in humans. With the new findings, and link to HLA, researchers will now be encouraged to take a fresh look at the possible role of infections, inflammation and autoimmunity in Parkinson’s disease.

HLA genes are essential for recognizing foreign invaders from the body’s own tissues. Similarly, HLA molecules are supposed to recognize a body’s own tissue as itself and prevent immune reactions against them. But the system doesn’t always work perfectly. HLA genes are highly variable from individual to individual. Certain variants of the genes are associated with increased risk or protection against infectious disease, while other variants can induce autoimmune disorders in which the immune system attacks the body’s own tissues. Multiple sclerosis, a neurological disease caused by autoimmunity, is also associated with HLA-DR. The genetic variant that is associated with Parkinson’s disease is in the same region as the one associated with multiple sclerosis.

People who take non-steroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen) have a reduced risk of developing Parkinson’s disease, which also supports an immune-related mechanism. The protective effect of NSAIDs is not the same for everyone, likely because of genetic differences, and NSAIDs can have side effects. Pursuing the connection between Parkinson’s disease and inflammation, especially in the context of variable genetic makeup, may lead to better, more selective drugs for treating Parkinson’s disease.

Consortium leaders recognize the study would not have been possible without the precious help from volunteer patients. “This type of research could not be done if it weren’t for the willing and dedicated individuals who volunteer as research subjects,” said Payami, who acknowledged that some study subjects participated for nearly two decades.

What’s next for the team? “Our results also pointed to several other genes that might play a role in developing Parkinson’s disease, and these findings need to be confirmed, so we have a lot of work ahead of us” said Zabetian. He and others in the consortium will now mine the data even more for gene-environment interactions, with a goal of finding environmental triggers and protectors to develop genetically-personalized therapeutics for treatment and prevention of Parkinson’s disease.

The study was funded by the National Institute of Neurological Disorders and Stroke and the Edmond J. Safra Global Genetic Consortium grant from the Michael J. Fox Foundation for Parkinson’s Disease Research.

Source:
Mary Guiden
University of Washington

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3.  Immune System Genes Linked To Parkinson’s Disease 

Article Date: 16 Aug 2010 – 2:00 PDT

 An international team of researchers conducting a genome-wide association study (GWAS) has discovered that common variants in immune system genes are linked to Parkinson’s disease.

The study was the work of the NeuroGenetics Research Consortium, led by Dr Haydeh Payami, a research scientist at the Health Wadsworth Center and professor in the School of Public Health, both in the New York State Department of Health. The Consortium wrote a paper on the study that was published online in Nature Genetics on 15 August.

One of the Consortium clinical directors, Dr Cyrus Zabetian, associate professor of neurology at the University of Washington and VA Puget Sound Health Care System, Stewart Factor at Emory University, told the media that for some years now scientists have seen “subtle hints” that immune function and Parkinson’s disease might be linked:

“But now we have much more convincing evidence of this and a better idea of which parts of the immune system might be involved,” he added.

For the study, the researchers examined over 2,000 volunteer patients with Parkinson’s and nearly 2,000 healthy volunteers from clinics in Oregon, Washington, New York and Georgia.

Payami thanked the volunteers for their help, many of whom had been with the study for nearly 20 years: “This type of research could not be done if it weren’t for the willing and dedicated individuals who volunteer as research subjects,” she said.

Payami and colleagues scanned the genomes of all 4,000 volunteers. They also assessed a number of clinical and environmental factors that might contribute to the development and progress of Parkinson’s disease and its complications.

They wrote that they replicated already published links with three genes: SNCA, MAPT, and GAK, and detected new links with common variants in the HLA region that was “uniform across all genetic and environmental risk strata and was strong in sporadic … and late-onset [Parkinson’s] disease”.

The HLA (human leukocyte antigen) region of the human genome is home to a large number of immune system genes that are important for recognizing foreign agents and differentiating them from the body’s own tissue. HLA molecules also help ensure that the immune system does not attack the body’s own tissue.

However, this part of the immune system does not always work as well as it should: certain HLA variants are linked to increased risk of disease, or higher protection against them, while other variants can trigger autoimmune disorders where the immune system can’t distinguish between the body’s own tissue and foreign agents and attacks both with equal force.

For example, the neurological autoimmune disease multiple sclerosis, is linked to the gene HLA-DR.

Based on this finding, Payami and colleagues said they plan to take a fresh look at the possible role of infection, inflammation and autoimmunity in Parkinson’s disease.

 Their work could help find better drugs for treating Parkinson’s. For example, we already know that some people who take non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, have a reduced risk of developing Parkinson’s, but this effect is not the same in everyone and NSAIDs can also have side effects. A closer investigation of the relevant gene variants could help develop more selective treatments for Parkinson’s.

The team will also be investigating some other genes they came across in their GWAS but they now need to confirm a link with Parkinson’s.  They will also be “mining” the huge piles of data from the study to look for evidence of gene-environment interactions, for instance there may be triggers in the environment that switch certain genes related to Parkinson’s on and off; such discoveries also help in the search for more personalized treatments.

Financial backing for the study came from the National Institute of Neurological Disorders and Stroke and a Edmond J. Safra Global Genetic Consortium grant from the Michael J. Fox Foundation for Parkinson’s Disease Research.

“Common genetic variation in the HLA region is associated with late-onset sporadic Parkinson’s disease.”
Taye H Hamza, Cyrus P Zabetian, Albert Tenesa, Alain Laederach, Jennifer Montimurro, Dora Yearout, Denise M Kay, Kimberly F Doheny, Justin Paschall, Elizabeth Pugh, Victoria I Kusel, Randall Collura, John Roberts, Alida Griffith, Ali Samii, William K Scott, John Nutt, Stewart A Factor & Haydeh Payami.
Nature Genetics, Published online: 15 August 2010
DOI:10.1038/ng.642

Additional source: University of Washington.
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4.  New Pathway To Parkinson’s And Alzheimer’s Diseases
Article Date: 30 Jul 2010 – 1:00 PDT 

Although their genetic underpinnings differ, Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are all characterized by the untimely death of brain cells. What triggers cell death in the brain?

According to a new study published by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) in the July 30 issue of Molecular Cell, the answer in some cases is the untimely transfer of a gaseous molecule (known as nitric oxide, or NO) from one protein to another.

“We and other researchers have shown that NO and related molecules can contribute to either nerve cell death or nerve cell survival. However, these new findings reveal that NO can actually jump from one protein to another in molecular pathways that lead to cellular suicide,” explained Stuart A. Lipton, M.D., Ph.D., senior author of the study and director of the Del E. Web Center for Neuroscience, Aging and Stem Cell Research at Sanford-Burnham. “Now that we have this molecular clue to the cause of nerve cell death in Parkinson’s, Alzheimer’s, and Huntington’s diseases, we can figure out how to use it to better diagnose and treat these diseases.” Dr. Lipton is also a Harvard-trained neurologist who sees many of these patients in his own clinical practice.

In this study, Dr. Lipton and his colleagues, led by Tomohiro Nakamura, Ph.D., found that NO-like molecules are transferred from caspases, proteins that normally initiate cell death, to XIAP, a protein that normally inhibits cell death. In other words, caspases pass NO to XIAP like a ‘hot potato.’ This process occurs by a chemical reaction known as transnitrosylation. When XIAP is left holding NO, the result is a double whammy for brain cells, since cells are programmed to self-destruct when either XIAP has NO attached to it or when caspases don’t. Hence, both brain cell-destroying events occur at the same time. The researchers then found that XIAP holding the NO ‘hot potato’ was much more common in brains of human patients with neurodegenerative diseases than in normal brains, solidifying their suspicion that this protein modification leads to cell damage.

To calculate which protein is more likely to end up with the NO ‘hot potato,’ caspases or XIAP, the researchers created a new version of the Nernst equation – a 19th century mathematical equation taught in every general chemistry class. This power of prediction might allow doctors to diagnose neurodegenerative disorders like Parkinson’s or Alzheimer’s disease earlier.

“We are currently analyzing cerebrospinal fluid and brain tissue from Parkinson’s, Alzheimer’s and other patients to determine if we can use the NO-tagged proteins as biomarkers for the disease,” Dr. Lipton said.

In order to develop therapies to treat Parkinson’s, Alzheimer’s and Huntington’s diseases based on their new findings, Dr. Lipton’s laboratory is also applying the robotic technology in Sanford-Burnham’s Conrad Prebys Center for Chemical Genomics to screen thousands of chemicals for potential drugs that prevent the aberrant or excessive transfer of NO from one protein to another, and thus to prevent nerve cell injury and death.

This study was supported by grants from the National Institutes of Health (NIH) and the San Diego chapter of the American Parkinson’s Disease Association.  Original paper:
Nakamura T, Wang L, Wong CCL, Scott FL, Eckelman BP, Han X, Tzitzilonis C, Meng F, Gu Z, Holland EA, Clemente AJ, Okamoto S, Salvesen GS, Riek R, Yates JR 3rd, Lipton SA. Transnitrosylation of XIAP regulates caspase-dependent neuronal cell death. Molecular Cell. Published online July 30, 2010.

Source:
Sanford-Burnham Medical Research Institute

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5.  Study Identifies Molecular Mechanism Triggering Parkinson’s Disease

Article Date: 30 Jul 2010 – 0:00 PDT  

Scientists at the Stanford University School of Medicine have identified a molecular pathway responsible for the death of key nerve cells whose loss causes Parkinson’s disease. This discovery not only may explain how a genetic mutation linked to Parkinson’s causes the cells’ death, but could also open the door to new therapeutic approaches for the malady.

In a study to be published July 29 in Nature, investigators used an animal model, the common fruit fly, to show that the mutation results in impaired activity of recently discovered molecules called microRNAs, which fine-tune protein production in cells. This impairment, in turn, leads to the premature death of nerve cells specifically involved in the secretion of the brain chemical dopamine. The degeneration of these so-called dopaminergic nerve cells in the brain is a hallmark of Parkinson’s.

“MicroRNA, whose role in the body has only recently begun to be figured out, has been implicated in cancer, cardiac dysfunction and faulty immune response,” said Bingwei Lu, PhD, associate professor of pathology and the study’s senior author. “But this is the first time it has been identified as a key player in a neurodegenerative disease.”

Parkinson’s is a movement disorder characterized outwardly by tremor, difficulty in initiating movement, and postural imbalance and, in the brain, by a massive loss of the dopaminergic nerve cells in areas that fine-tune motor activity. It affects an estimated 1 million people in the United States. The incidence of Parkinson’s, rare in younger people, increases dramatically with age, although nobody is sure why. Nor is it known why the most common mutation implicated in Parkinson’s – LRRK2 G2019S, found in about one-third of all Parkinson’s cases occurring among North African Arabs and North American Ashkenazi Jews – increases the likelihood of contracting the disease.

The new findings show that the LRRK2 mutation trips up the normal activity of microRNAs, resulting in the overproduction of at least two proteins that can cause certain cells, like brain cells, to die.

Understanding how microRNA can go wrong requires an understanding of its relationship to its much longer and better-known cousins, “messenger RNA” (or mRNA) molecules. The latter carry genetic recipes from a cell’s DNA to specialized molecular machines that translate the instructions into the proteins that make up a cell. In contrast, a microRNA molecule is a very short string of RNA that doesn’t contain instructions for making proteins but that can bind to parts of messenger RNA sequences that complement its own. As a result, the messenger RNA’s sequence can no longer be read by the cell’s protein-manufacturing apparatus, gumming up assembly of the protein it encodes.

It’s only recently that scientists have started to understand microRNA’s critical role.   

The researchers in Lu’s lab conducted their experiments in Drosophila, the fruit fly, which has previously proved itself a useful model for several neurodegenerative disorders, yielding substantial insights into Parkinson’s, Alzheimer’s and Huntington’s diseases. They observed that certain proteins were being produced at higher-than-normal levels in the fly LRRK2 model of Parkinson’s disease. What particularly drew their attention were two proteins that are important in regulating cell division. Mature nerve cells, which no longer divide, should not have high levels of these proteins; when they do, they are prone to premature cell death.

The researchers looked at the mRNAs containing the genetic recipes for the two overproduced proteins, and predicted that they would be bound by two specific microRNAs: let-7 and miR-184. When they then manipulated the activities of those two microRNA species in flies’ brains, they had results consistent with the damage associated with Parkinson’s.

Diminishing the activity of let-7 in dopaminergic nerve cells, for example, caused both the increased production of one of the suspect proteins and degeneration of the cells.  The researchers showed that toning down the levels of these two proteins, in itself, prevented dopaminergic nerve cell death in the flies. “The flies no longer got symptoms of Parkinson’s,” said Lu. “This alone has immediate therapeutic implications. Many pharmaceutical companies are already making  compounds that act on these two proteins, which in previous studies have been shown to be associated with cancer. It may be possible to take these compounds off the shelf or quickly adapt them for use in non-cancer indications such as Parkinson’s.”

The researchers then went a step further, showing how the genetic mutation of LRRK2 caused interference of microRNA molecules’ ability to inhibit their target mRNAs. It leads to the disruption of a huge complex of molecular machinery that must operate smoothly in order for microRNA to do its job. This link between the common Parkinson’s-producing mutation and consequent microRNA malfunction is a new finding.

“The clinical impact of our findings may be five to 10 years down the road,” Lu said. “But their impact on our understanding of the disease process is immediate. We can now start testing compounds in mammals and cultured human dopaminergic cells to see if they can inhibit overproduction of these proteins and stave off dopaminergic cell death.”

Currently available drugs for Parkinson’s disease temporarily alleviate its symptoms but can have undesirable side effects, and they don’t prevent dopaminergic cells from dying.

The study’s first author is Stephan Gehrke, PhD, a postdoctoral researcher in Lu’s laboratory. Second author Yuzuru Imai, PhD, a former postdoctoral scientist in Lu’s lab, is now an associate professor at Tohoku University in Sendai, Japan. The study received financial support from the National Institutes of Health and the McKnight, Beckman and Sloan foundations.

Source:
Bruce Goldman
Stanford University Medical Center
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6.  Genes And Pesticide Exposure Interact To Increase Men’s Risk For Parkinson’s Disease Article Date: 17 Jun 2010 – 2:00 PDT

 Genetic mutations and workplace exposure to some insecticides together appear to be associated with an increased risk for Parkinson’s disease among men, according to a report in the June issue of Archives of Neurology, one of the JAMA/Archives journals.

“In most cases, the etiology of Parkinson’s disease is likely to be multifactorial, and environmental factors as well as their interaction with susceptibility genes are considered to contribute to the disease,” the authors write as background information in the article. Humans exposed to certain pesticides, including organochlorines such as DDT, have been shown to develop Parkinson’s disease through damage to neurons that produce the neurotransmitter dopamine.

“If environmental chemicals can increase Parkinson’s disease risk, host factors that contribute to variability in their uptake, metabolism and distribution in the body may modulate individual risk,” the authors write.

“Genetic polymorphisms of xenobiotic [compounds not naturally found in the body] metabolizing enzymes may act as susceptibility factors.” The gene ABCB1 may encode the production of compounds essential to this process.

Fabien Dutheil, Ph.D., of Université Paris Descartes, Assistance-Publique Hôpitaux de Paris, and colleagues studied 207 individuals with Parkinson’s disease and 482 matched controls. Participants were assessed to detect two known ABCB1 polymorphisms and classified as never users, users for gardening and professional users of pesticides. For professional users, detailed information on lifelong pesticide use was gathered.

Overall, ABCB1 polymorphisms were not associated with Parkinson’s disease risk. However, among 101 men with Parkinson’s disease and 234 matched controls, the relationship between organochlorine insecticide exposure and Parkinson’s disease was approximately 3.5 times stronger in men who carried two variant alleles (gene copies) compared with those who were not carriers.

“Based on a biological hypothesis, we show that organochlorine insecticides may interact with ABCB1 in determining the risk of Parkinson’s disease,” the authors conclude. “These findings support the hypothesis of gene x pesticide interactions in Parkinson’s disease.”

Archives of Neurology . 2010;67[6]:739-745.

Source
Archives of Neurology
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7.  New Study Showed The Impact Of Gastrointestinal Disorders In Patients With Parkinson’s Disease
Main Category: Parkinson’s Disease
Also Included In: GastroIntestinal / Gastroenterology;  Clinical Trials /

Drug Trials;  Conferences
Article Date: 16 Jun 2010 – 2:00 PDT  

New data from a retrospective cohort study showed that up to three quarters of patients with Parkinson’s disease (PD) developed gastrointestinal disorders (GID) that can have a substantial adverse effect on major PD-related clinical and health economic outcomes. These data were presented at the 14th International Congress of Parkinson’s Disease and Movement Disorders in Buenos Aires, Argentina (June 13-17, 2010).

“The new retrospective cohort study suggested that the prevalence of gastrointestinal disorders among patients with Parkinson’s disease was high, increased over time and had a significant impact on clinical and societal outcomes,” said Dr. Florent Richy, Head of Epidemiology, UCB & Adjunct Professor of Epidemiology, University of Liege, Belgium.

“Gastrointestinal disorders can impair the onset of symptom relief by Parkinson’s disease drugs and these data help us to better understand the prevalence and consequences of such disorders amongst patients diagnosed with Parkinson’s disease.”

The study found that gastrointestinal disorders in PD patients were associated with significantly higher rates of neuropsychiatric and motor disorders, as well as increased emergency room admissions, number of concurrent drugs and non-PD healthcare costs.

About the Study

The new findings came from a two year matched retrospective cohort study performed on a U.S. database of patient records (Pharmetrics®)* which included demographic, diagnostic, procedural and prescription information.

Patients with at least two prior diagnoses of Parkinson’s disease and continuous prescriptions of levodopa or dopamine agonists between 1st September 2005 and 1st September 2006 were selected, and health outcomes and health utilization patterns were followed up over a two year period. Outcomes were defined on the basis of a literature review and included neuropsychiatric, motor, urogenital disturbances, healthcare utilization and related costs.

Four hundred and eighty five patients with Parkinson’s disease and GID were matched with 485 patients with Parkinson’s disease and without GID. In the data cut, GID incidence among patients with Parkinson’s disease and no history of GID increased over time, stabilizing at 75% at 92 months. In addition GID was associated with significantly higher rates of neuropsychiatric and motor disorders, including psychosexual dysfunction (RR=8, p=0.05), anxiety (RR=1.61, p<0.01), depression (RR=1.28, p=0.03), ataxia (RR=1.24, p=0.03), pain (RR=1.29, p<0.01), movement disorders (RR=1.39, p=0.02), urinary incontinence (RR=1.43, p=0.01) and risk of fall (RR=1.44, p=0.03). Emergency room admissions (ratio=1.42, p<0.01), number of concurrent drugs (ratio=1.06, p=0.04) and Parkinson’s disease and non-Parkinson’s disease healthcare costs (ratios=1.13 and 1.12, p<0.01 respectively) increased during the observation period in the GID patients.

This study was performed using a licensed IMS Pharmetrics® datacut

Abstract: Gastrointestinal disorders in patients with Parkinson’s Disease: A double-edged sword

Richy F1, Gunn A2, Makaroff L3, Gervasoni C4, Helmers S5 1UCB Pharma SA, Brussels, Belgium & University of Liege, Belgium; 2UCB Pharma SA, Brussels, Belgium; 3Business & Development, Life Sciences, Brussels Belgium; 4Keyrus Biopharma, Lasne, Belgium; 5Emory University School of Medicine, Atlanta, US

Poster Session I, June 14th 2010, 0900-1800

About UCB

UCB, Brussels, Belgium is a biopharmaceutical company dedicated to the research, development and commercialization of innovative medicines with a focus on the fields of central nervous system and immunology disorders. Employing more than 9 000 people in over 40 countries, UCB produced revenue of EUR 3.1 billion in 2009. UCB is listed on Euronext Brussels (symbol: UCB).

Source: UCB

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