Journal of Parkinson's Disease

Journal of Parkinson’s Disease

ISSN print
1877-7171
ISSN online
1877-718X
Volume
4; 4 issues
Status
Last issue (4:3) published on 2 September 2014
Next issue
4:4 scheduled for November 2014
Back volumes
1-3
Website
www.journalofparkinsonsdisease.com
Subject
Biochemistry, Medicine & Health, Neurosciences
Institutional subscription for 2014 €545 / US$720 Excluding VAT
Subscription Rates Free Sample Copy
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Book Launch: The Case of the Frozen Addicts: How the Solution of a Medical Mystery Revolutionized the Understanding of Parkinson's Disease (2014)
JPD Editor-in-Chief Bill Langston and Social Media Editor Jon Palfreman, in association with IOS Press, have published the second edition of The Case of the Frozen Addicts: How the Solution of a Medical Mystery Revolutionized the Understanding of Parkinson's Disease. This spellbinding account illuminates how the solution to a baffling mystery of the brain’s chemistry opened a new frontier in medicine and restored life to people without hope. This new updated edition of the classic neurological mystery tale can now be ordered in print, epub or pdf format.

New Sister Journal: Journal of Neuromuscular Diseases
JPD welcomes a new sister journal: Journal of Neuromuscular Diseases (JND), edited by Carsten G. Bönnemann and Hanns Lochmüller. The second issue of JND is now freely available online. This journal is accepting papers

The Journal of Parkinson’s Disease is dedicated to providing an open forum for original research in basic science, translational research and clinical medicine that will expedite our fundamental understanding and improve treatment of Parkinson’s disease. The journal is international and multidisciplinary and aims to promote progress in the epidemiology, etiology, genetics, molecular correlates, pathogenesis, pharmacology, psychology, diagnosis and treatment of Parkinson’s disease. It will publish research reports, reviews, short communications, and letters-to-the-editor and offers very rapid publication and an affordable open access option.

 

 

 

 

 

 

Editors-in-Chief

Patrik Brundin, MD, PhD
Van Andel Research Institute
Grand Rapids, MI, USA
Wallenberg Neuroscience Center
Lund University, Lund, Sweden
Email: patrik.brundin@iospress.com

J. William Langston, MD
The Parkinson's Institute and Clinical Center
Sunnyvale, CA, USA
Email: bill.langston@iospress.com

Associate Editor for Reviews

M. Angela Cenci
Lund University, Lund, Sweden

Associate Editors

Roger Barker
University of Cambridge, Cambridge, United Kingdom

Bastiaan Bloem
University Medical Centre St Radboud, Nijmegen, The Netherlands

Mark R. Cookson
NIH, Bethesda, USA  

Dennis Dickson
Mayo Clinic, Scottsdale, USA

Robert H. Edwards
University of California San Francisco, San Francisco, USA  

Howard Federoff
Georgetown University, Washington, USA

Thomas Gasser
University of Tuebingen, Tuebingen, Germany

Glenda Halliday
The University of New South Wales, Sydney, Australia

Jan Petter Larsen
University of Stavanger, Stavanger, Norway

Peter A. LeWitt
Wayne State University, Detroit, USA
Henry Ford Hospital, Detroit, USA

Tamas Revesz
University College London, London, United Kingdom

Eng King Tan
Duke NUS Graduate Medical School, Singapore, Singapore

Jens Volkmann
Universitätsklinikum Wurzburg, Wurzburg, Germany

Nick Wood
University College London, London, United Kingdom

Social Media Editor

Jon Palfreman
University of Oregon, Eugene, USA

Managing Editor

Bethany Kumar
Case Western Reserve University, Cleveland, USA
Email: jpd@iospress.com

Editorial Board

Dag Aarsland
University of Stavanger, Stavanger, Norway

Asa Abeliovich
Columbia University College of Physicians & Surgeons, New York, USA

Patrick Aebischer 
École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland   

Yves Agid
Institut du Cerveau et de la Moelle épinière, Paris, France

Alberto Albanese
National Neurological Hospital Carlo Besta, Milan, Italy

Ernest Arenas
Karolinska Institute, Stockholm, Sweden

Alberto Ascherio
Harvard School of Public Health, Boston, USA

M. Flint Beal
Weill Medical College of Cornell University, New York, USA

Alim Benabid
University of Grenoble, Grenoble, France

Hagai Bergman
The Hebrew University, Jerusalem, Israel

Anders Björklund
Lund University, Lund, Sweden

Vincenzo Bonifati
Erasmus MC, Rotterdam, The Netherlands

Heiko Braak
University of Ulm, Ulm, Germany

Alexis Brice   
Pierre and Marie Curie University, Paris, France

David J. Brooks
Hammersmith Hospital, London, United Kingdom

Robert Burke
Columbia University Medical Center, New York, USA

Paolo Calabresi
University of Perugia, Perugia, Italy

Piu Chan
Beijing Institute of Geriatrics, Beijing, China

K. Ray Chaudhuri
Kings College Hospital, London, United Kingdom

Marie Francoise Chesselet
University of California Los Angeles, Los Angeles, USA

Cynthia Comella
Rush University Medical Center, Chicago, USA

Ted M. Dawson
Johns Hopkins University School of Medicine, Baltimore, USA  

Valina L. Dawson
Johns Hopkins University School of Medicine, Baltimore, USA

David Eidelberg
The Feinstein Institute for Medical Research, New York, USA

Omar M. El-Agnaf
United Arab Emirates University, Al-Ain, United Arab Emirates

Stanley Fahn
Columbia University College of Physicians & Surgeons, New York, USA

Matt Farrer
University of British Columbia, Vancouver, Canada

Joaquim Ferreira   
Hospital de Santa Maria, Lisbon, Portugal

Nir Giladi
Tel Aviv University, Tel Aviv, Israel

Ann M. Graybiel
MIT, Cambridge, USA

J. Timothy Greenamyre
University of Pittsburgh, Pittsburgh, USA

James G. Greene
Emory University, Atlanta, USA

Katrina Gwinn
NIH, Bethesda, USA

Mark Hallett
NIH, Bethesda, USA

John Hardy
University College London, London, United Kingdom

Nobutaka Hattori
Juntendo University School of Medicine, Tokyo, Japan

Etienne C. Hirsch
Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, Paris, France

Joseph Jankovic
Baylor College of Medicine, Houston, USA  

Christine Klein
University of Lübeck, Lübeck, Germany

Amos D. Korczyn
Tel Aviv University, Ramat Aviv, Israel

Jeffrey H. Kordower
Rush University, Chicago, USA

Seung-Jae Lee  
Konkuk University, Seoul, South Korea

Virginia Lee
University of Pennsylvania School of Medicine, Philadelphia, USA

Olle Lindvall
Lund University, Lund, Sweden

Andres Lozano
University of Toronto, Toronto, Canada

Laura Marsh
Baylor College of Medicine, Houston, USA

Mark P. Mattson
National Institute on Aging, Baltimore, USA

Eldad Melamed
Tel Aviv University, Tel Aviv, Israel

Alice Nieuwboer
Catholic University Leuven, Leuven, Belgium

Robert Nussbaum
University of California San Francisco, San Francisco, USA

Ronald F. Pfeiffer
University of Tennessee Health Science Center, Memphis, USA

Pierre Pollak
University of Grenoble, Grenoble, France

Serge Przedborski
Columbia University Medical Center, New York, USA

Niall Quinn
University College London, London, United Kingdom

Heinz Reichmann
University of Dresden, Dresden, Germany

Peter Riederer
University of Wuerzburg, Wuerzburg, Germany

Trevor Robbins
University of Cambridge, Cambridge, United Kingdom

Anthony Schapira
University College London, London, United Kingdom

Todd Sherer
Michael J. Fox Foundation, New York, USA

Ira Shoulson
Georgetown University, Washington, USA

Andrew Singleton
NIH, Bethesda, USA  

David G. Standaert
University of Alabama at Birmingham, Birmingham, USA

Dennis Steindler
University of Florida, Gainesville, USA

Gerald Stern
University College Hospitals, London, United Kingdom

Fabrizio Stocchi
IRCCS San Raffaele, Rome, Italy

A. Jon Stoessl
University of British Columbia, Vancouver, Canada

Michele Tagilati
Cedars-Sinai Medical Center, Los Angeles, USA

Jun Takahashi
Kyoto University, Kyoto, Japan

Caroline M. Tanner
The Parkinson's Institute and Clinical Center, Sunnyvale, USA

Eduardo Tolosa
University of Barcelona, Barcelona, Spain

John Q. Trojanowski
Hospital of the University of Pennsylvania, Philadelphia, USA

Daniel Weintraub
University of Pennsylvania, Philadelphia, USA

Founding Editors
From the Journal of Alzheimer’s Disease

George Perry
University of Texas at San Antonio, San Antonio, USA

Mark A. Smith†
Case Western Reserve University, Cleveland, USA

See instructions to authors.

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Few Mild-to-Moderate PD Patients Suffer from Malnutrition, Yet Almost One Third Are at Risk

11 Sep 2014 - Patients with Parkinson’s disease (PD) can experience difficulties with food preparation and ingestion, which could contribute to poor nutrition and place them at risk for malnourishment. Published studies have also suggested that PD is associated with low weight, however, few studies included control groups. A report published in the Journal of Parkinson’s Disease counters this conclusion in patients with mild-to-moderate PD, finding that the incidence or risk of malnutrition is no different for patients with mild-to-moderate PD compared to healthy controls....

Sleep Disturbances, Common in Parkinson’s Disease, Can Be Early Indicator of Disease Onset

11 Jul 2014 - Up to 70% of Parkinson’s disease (PD) patients experience sleep problems that negatively impact their quality of life. Some patients have disturbed sleep/wake patterns such as difficulty falling asleep or staying asleep, while other patients may be subject to sudden and involuntary daytime sleep “attacks.” In the extreme, PD patients may exhibit REM-sleep behavior disorder (RBD), characterized by vivid, violent dreams or dream re-enactment, even before motor symptoms appear. A review in the Journal of Parkinson’s Disease discusses the underlying causes of sleep problems in PD, as well as medications, disease pathology, and comorbidities, and describes the most appropriate diagnostic tools and treatment options....

Deep Brain Stimulation Improves Non Motor Symptoms in Parkinson’s Disease as well as Motor Symptoms

03 Jul 2014 - Deep brain stimulation (DBS) has become a well-recognized non-pharmacologic treatment that improves motor symptoms of patients with early and advanced Parkinson’s disease. Evidence now indicates that DBS can decrease the number and severity of non motor symptoms of patients with Parkinson’s disease (PD) as well, according to a review published in the Journal of Parkinson’s Disease....

Exenatide Has Potential as a Disease Modifying Agent in Parkinson’s Disease

06 May 2014 -

A follow-up study of patients with Parkinson’s disease (PD) who participated in an earlier “proof of concept” clinical trial using exenatide showed that improvements persisted twelve months after discontinuing exenatide therapy. These data provide strong encouragement for the further study of this drug in patients with PD, report researchers in the Journal of Parkinson’s Disease.

Several recent discoveries have highlighted common cellular pathways that potentially relate neurodegenerative processes with abnormal mitochondrial function and abnormal glucose metabolism.

Exenatide, a glucagon-like peptide-1 agonist (GLP-1 agonist) medication marketed as Byetta® and Bydureon® and used in the treatment of insulin resistance in patients with Type 2 diabetes, has been proposed as a disease modifying drug in PD. Earlier studies had shown that exenatide is neuroprotective and promotes functionally beneficial neuroplasticity in animal models of neurodegeneration. Furthermore, exenatide has a favorable safety profile, with only relatively mild gastrointestinal side effects (including nausea and weight loss) as frequent adverse events.

In an earlier “proof of concept” randomized controlled trial published in May 2013, participants were randomized to either self-administer exenatide in addition to their regular PD medications or to act as controls, i.e., receive their conventional PD treatment only. All of the participants had moderate severity PD. In total, 44 patients (20 in the exenatide group and 24 controls) completed the trial. After 12 months the results showed significant and clinically meaningful differences in both motor and cognitive symptoms between those patients receiving exenatide and the controls. At 14 months, when the patients had discontinued exenatide for two months, the exenatide-treated and control groups still differed from each other. The authors concluded that the study supported potential disease-modifying benefits of exenatide in PD, while acknowledging the lack of a placebo arm.

All of the participants took part in a repeat assessment 12 months after the trial ended. The motor and cognitive advantages persisted in the exenatide group. Compared with the control group, those in the exenatide group had an advantage of 5.6 when using the blinded MDS-UPDRS motor subscale and 5.3 points on the Mattis Dementia Rating scale.

“We found that patients on exenatide appeared essentially unchanged throughout and beyond the trial period, while the control group had the expected rate of gradual decline in movement and cognitive ability,” comments senior investigator Thomas Foltynie, MRCP, PhD, of the Sobell Department of Motor Neuroscience, UCL Institute of Neurology, London, UK.

The investigators did not find evidence in their data to suggest that glucose tolerance is different in PD patients who received exenatide for 12 months.

“Aside from the changes in MDS-UPDRS scores, there was also persistent divergence in cognitive performance between the groups, with significant differences which were sustained along the trial period, far beyond the 12-month period of drug exposure,” says Foltynie. “These data provide continued support for formal double blind trials of GLP-1 agonists as disease modifying drugs in PD.”

“The present study could represent a milestone if future controlled trials provide evidence supporting a disease-modifying effect of exenatide and could lead to a revolution in PD therapy,” comment Tanya Simuni, MD, of Northwestern University Feinberg School of Medicine, Chicago, and Patrik Brundin, MD, PhD, of the Van Andel Research Institute, Grand Rapids, MI. Writing in the same issue, they warn however that: “Notwithstanding the promising nature of the results, it has to be emphasized that placebo effects can be highly significant and long-standing in PD. Therefore one should not jump to premature conclusions, While placebo effects ought to have diminished 12 months after drug withdrawal so that the exenatide-treated and control groups no longer differed, a lingering placebo effect cannot be excluded.”

Tom Isaacs, Co-founder and President of The Cure Parkinson's Trust which funded the follow-up study, says: "Although we have to remain cautious on the estimation of these results, we are encouraged by the findings. This is the first time that I have come across a program that has the potential to make an enduring change for Parkinson’s patients and we are excited by the potential of this scientific research.” 

#  #  #

NOTES FOR EDITORS

Motor and Cognitive Advantages Persist 12 Months After Exenatide Exposure in Parkinson’s Disease,” by Iciar Aviles-Olmos, MD, PhD; John Dickson, PhD, Zinovia Kefalopoulou, MD, PhD; Atbin Djamshidian, MD, PhD; Joshua Kahan, BSc; Peter Ell, FmedSci; Peter Whitton PhD; Richard Wyse; Tom Isaacs; Andrew Lees, MD, FRCP; Patricia Limousin, MD, PhD; and Thomas Foltynie, MRCP, PhD (DOI: 10.3233/JPD-140364). 

Commentary: “Is Exenatide the next big thing in Parkinson’s disease?” By Tanya Simuni, MD, and Patrik Brundin, MD, PhD (DOI: 10.3233/JPD-149001). Openly available at http://iospress.metapress.com/content/c54026233vj43342/fulltext.pdf

Journal of Parkinson’s Disease, published by IOS Press

Contact Daphne Watrin, IOS Press, +31 20 688 3355, d.watrin@iospress.nl for additional information. Journalists wishing to interview the authors should contact Dr. Thomas Foltynie at T.Foltynie@ucl.ac.uk or Patrik Brundin at patrik.brundin@iospress.com.

ABOUT THE JOURNAL OF PARKINSON’S DISEASE (JPD)

Launched in June 2011 the Journal of Parkinson’s Disease is dedicated to providing an open forum for original research in basic science, translational research and clinical medicine that will expedite our fundamental understanding and improve treatment of Parkinson’s disease. The journal is international and multidisciplinary and aims to promote progress in the epidemiology, etiology, genetics, molecular correlates, pathogenesis, pharmacology, psychology, diagnosis and treatment of Parkinson’s disease. It publishes research reports, reviews, short communications, and letters-to-the-editor and offers very rapid publication and an affordable open access option. 

ABOUT IOS PRESS

Commencing its publishing activities in 1987, IOS Press serves the information needs of scientific and medical communities worldwide. IOS Press now (co-)publishes over 100 international journals and about 90 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.

IOS Press continues its rapid growth, embracing new technologies for the timely dissemination of information. All journals are available electronically and an e-book platform was launched in 2005.

Headquartered in Amsterdam with satellite offices in the USA, Germany, India and China, IOS Press has established several strategic co-publishing initiatives. Notable acquisitions included Delft University Press in 2005 and Millpress Science Publishers in 2008.

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2014 Neuroscience Neurology Brochure

31 Jan 2014 - Download the 2014 Neuroscience Neurology Brochure here. ...

Higher Vitamin D Levels Associated with Better Cognition and Mood in Parkinson’s Disease Patients

17 Jan 2014 - A new study exploring vitamin D levels in patients with Parkinson’s disease (PD) opens up the possibility of a new avenue of early intervention that may delay or prevent the onset of cognitive impairment and depression. The findings are published in the Journal of Parkinson’s Disease....

New Research Suggests Changes in Parietal Brain Gray Matter Volume Associated with Memory Deficits in Early PD

17 Jan 2014 - Research by a team of investigators in Finland suggests that the free recall memory deficits common even in early stages Parkinson’s disease (PD) are related to structural changes in the brain, specifically parietal cortical gray matter volume. Their findings are published in the current issue of the Journal of Parkinson’s Disease....

New Study Links Depression in Newly Diagnosed Parkinson’s Disease Patients to Reduced Striatal Dopamine Synthesis

10 Oct 2013 - According to the Parkinson’s Disease Foundation, up to 60% of individuals with Parkinson’s disease (PD) exhibit mild to moderate depression, which is often underdiagnosed. It is unclear whether depression results from having a debilitating disease or reflects a parallel abnormal change in the brain caused by PD pathophysiology. ...

PD-Like Sleep and Motor Problems Observed in α-Synuclein Mutant Mice

11 Jun 2013 - The presence of Lewy bodies in nerve cells, formed by intracellular deposits of the protein α-synuclein, is a characteristic pathologic feature of Parkinson’s Disease (PD). In the quest for an animal model of PD that mimics motor and non-motor symptoms of human PD, scientists have developed strains of mice that overexpress α-synuclein. By studying a strain of mice bred to overexpress α-synuclein via the Thy-1 promoter, scientists have found these mice develop many of the age-related progressive motor symptoms of PD and demonstrate changes in sleep and anxiety. Their results are published in the latest issue of Journal of Parkinson’s Disease....

Shedding Light on Early Parkinson’s Disease Pathology

02 Apr 2013 - In a mouse model of early Parkinson’s disease (PD), animals displayed movement deficits, loss of tyrosine-hydroxylase (TH)-positive fibers in the striatum, and astro-gliosis and micro-gliosis in the substantia nigra (SN), without the loss of nigral dopaminergic neurons. These findings, which may cast light on the molecular processes involved in the initial stages of PD, are available in the current issue of Restorative Neurology and Neuroscience....

Blood-Based Biomarkers May Lead to Earlier Diagnosis of Parkinson’s Disease

21 Jan 2013 - Parkinson's disease (PD) is a progressive neurological condition. At present, it is usually diagnosed only when motor features are present. Hence, there is a need to develop objective and measurable biomarkers to improve PD diagnostics during its earlier stage, prior to its motor onset. In this pilot study, researchers identified and tested the first blood-based circulating microRNA (miRNA) biomarkers for PD. Their results are published in the latest issue of Journal of Parkinson’s Disease....

2013 Neuroscience Neurology Brochure

27 Nov 2012 - Download the 2013 Neuroscience Neurology Brochure here. ...

Years before Diagnosis, Quality of Life Declines for Parkinson’s Disease Patients

02 Jul 2012 - Growing evidence suggests that Parkinson’s disease (PD) often starts with non-motor symptoms that precede diagnosis by several years. In the first study to examine patterns in the quality of life of Parkinson’ disease patients prior to diagnosis, researchers have documented declines in physical and mental health, pain, and emotional health beginning several years before the onset of the disease and continuing thereafter. Their results are reported in the latest issue of Journal of Parkinson’s Disease. ...

Sleep Improves Functioning in Parkinson’s Patients, but Reasons Remain Elusive

20 Jun 2012 - Some Parkinson’s patients report that their motor function is better upon awakening in the morning, which is contrary to what would be expected after a night without medication. This phenomenon, known as sleep benefit, has been studied but no consistent variables have been found and in the last decade there has been little new research. A new study, published in the June issue of the Journal of Parkinson’s Disease, assesses a large sample of Parkinson’s disease (PD) patients and confirms that some patients experience sleep benefit, both overnight and following afternoon naps, but finds no significant variables between those who do benefit and those who do not. ...

19th Century Therapy for Parkinson’s Disease May Help Patients Today

23 Apr 2012 - In the 19th century, the celebrated neurologist, Jean-Martin Charcot, developed a “vibration chair” to relieve symptoms of Parkinson’s disease. He reported improvements in his patients, but he died shortly thereafter and a more complete evaluation of the therapy was never conducted. Now a group of scientists at Rush University Medical Center have replicated his work, and they report that while vibration therapy does significantly improve some symptoms of Parkinson’s disease, the effect is due to placebo or other nonspecific factors, and not the vibration. Their study is published in the April issue of Journal of Parkinson’s Disease. ...

New Findings and Imaging Techniques May Aid Diagnosis of Concomitant Alzheimer’s in Patients with Parkinson’s Disease Dementia

17 Apr 2012 - Dementia is a frequent complication of Parkinson’s disease (PD), but it is clinically impossible to distinguish PD dementia (PDD), which develops from the progression of the Lewy body pathology that underlies PD, from PD with coexistent Alzheimer’s disease (PDAD). Both have similar characteristics. A team of scientists has found that PDAD patients have much denser accumulations of amyloid plaques in the striatal area of the brain than PDD patients. The results suggest that recently developed imaging techniques may be able to identify striatal amyloid plaques in the living brain and could be useful for distinguishing PDD from PDAD. Their results are published in the April issue of the Journal of Parkinson’s Disease....

Journal of Parkinson's Disease Brochure 2012

27 Feb 2012 - Download the Journal of Parkinson's Disease Brochure 2012 here. ...

Scientists Report First Step in Strategy for Cell Replacement Therapy in Parkinson’s Disease

25 Jan 2012 - Induced pluripotent stem cells (iPSC) are a promising avenue for cell replacement therapy in neurologic diseases. For example, mouse and human iPSCs have been used to generate dopaminergic (DA) neurons that improve symptoms in rat Parkinson’s disease models. Reporting in the current issue of the Journal of Parkinson’s Disease, a group of scientists from Japan evaluated the growth, differentiation, and function of human-derived iPSC-derived neural progenitor cells (NPCs) in a primate model, elucidating their therapeutic potential. ...

New Research Reveals How α-Synuclein Interacts with Cell Membranes in Parkinson’s Disease

19 Jan 2012 - The accumulation of α-synuclein, a small, negatively charged protein, in neural cells, is one of the hallmarks of Parkinson’s disease. It has been suggested that oligomeric α-synuclein causes membranes to become permeable, or to form channels on the outer cell membrane. Now, a group of scientists from Sweden has found a way to reliably replicate α-synuclein aggregation on cell membranes to investigate how different forms of α-synuclein interact with membranes under different conditions and to learn if any of the α-synuclein species can penetrate these membranes. Their results are published in the current issue of the Journal of Parkinson’s Disease....

New Study Supports View that Lewy Bodies Are Not the Primary Cause of Cell Death in Parkinson’s Disease

10 Jan 2012 - The pathology of Parkinson’s disease is characterized by a loss of dopamine-producing neurons in the pars compacta of the substantia nigra (SN), an area of the brain associated with motor control, along with the development of α-synuclein (αS) protein in the form of Lewy bodies (LB) in the neurons that survive. The spread of LB pathology is thought to progress along with the clinical course of Parkinson’s disease, although recent studies suggest that they are not the toxic cause of cell death. A new study published in The Journal of Parkinson’s Disease finds no support for a primary pathogenic role of LBs, as neither their distribution nor density was associated with the severity of nigral cell loss. ...

Genetic Factors Can Predict the Progression of Parkinson’s Disease

16 Dec 2011 - Parkinson’s disease is marked by the abnormal accumulation of α-synuclein and the early loss of dopamine neurons in the substantia nigra region of the brain. A polymorphism in the promotor of α-synuclein gene known as NACP-Rep1 has been implicated as a risk factor for the disease. Now, researchers have found that different variants of NACP-Rep1 and its interaction with the microtubule-associated protein tau (MAPT) H1 haplotype can influence the speed of clinical deterioration in patients with Parkinson’s disease. ...

New Study First to Link Mitochondrial Dysfunction and alpha-Synuclein Multiplication in Human Fibroblasts

07 Oct 2011 - A new study in the Journal of Parkinson’s Disease shows for the first time the effects of α-Synuclein (α-syn) gene multiplication on mitochondrial function and susceptibility to oxidative stress in human tissue. Mitochondrial dysfunction has been frequently implicated in the neurodegenerative process that underlies Parkinson’s disease, but the basis for this has not been fully understood. ...

Ability to Ride a Bike Can Aid Differential Diagnosis of Parkinson’s Disease in Any Setting

07 Oct 2011 - In a new study published today in the Journal of Parkinson’s Disease, Japanese researchers report that the ability to ride a bike can differentiate between atypical parkinsonism and Parkinson’s disease, regardless of the environment or situations for bicycling. ...