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How do you design clinical trials to test neuroprotective therapeutics? Responses (10) 30 Jun 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. How to develop pharmacological approaches to mimic effects of DBS? Responses (3) 23 May 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. What is the pathological role of Alpha Responses (6)16 Apr 2008 Synuclein in PD? Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. What is the mechanism of DBS? Responses (3) 23 Mar 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. What is the impact on fetal tissue transplants in PD of the recent ndings of synuclein pathology? Responses (3) 23 Feb 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. What are the best preclinical models to test neuroprotection?
Responses (6) 16 Jan 2008
Recent Contributions
Disease modifying therapies must not ignore compensation mechanisms James Wilson, NINDS 12 Jun 2008 A major goal of Parkinson's disease research is to develop therapies which slow or stop disease progression and/or restore dopamine cell function. The rate of clinical progression of Parkinsons disease is highly variable and currently unpredictable. Genetics loads the gun but environment pulls the trigger Carly Tanner, NSF 14 Jun 2008 A major goal of Parkinson's disease research is to develop therapies which slow or stop disease progression and/or restore dopamine cell function. The rate of clinical progression of Parkinsons disease is highly variable and currently unpredictable.
Next Step for LRRK2: identifying substrates Mark Cookson, NIH
30 Mar 2008
Rules for assessing the funding portfolio and setting priorities Anne Persona, MJFF 21 Feb 2008 The health of cell replacement therapies Jeffrey Kordower, Rush University
14 Feb 2008
The damaging effect of an MBA mentality on research funding David Sulzer, Columbia University 23 Jan 2008 The health of cell replacement therapies Jeffrey Kordower, Rush University
14 Feb 2008
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The damaging effect of an MBA mentality on research funding David Sulzer, Columbia University 23 Jan 2008
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Sick Transplants and the health of cell replacement therapies 30 Jun 2008
A major goal of Parkinson's disease research is to develop therapies which slow or stop disease progression and/or restore dopamine cell function.The rate of clinical progresion of Parkinsons disease is variable and currently unpredictable. Reprogrammed Cells Reduce Parkinson's Symptons in Rats 30 Jun 2008 Neurons derived from reprogrammed adult skin cells successfully integrated into foetal mouse brains and reduced symptoms in a Parkinsons disease rat model, according to a study published on April 7 in the online Early Edition of ...
Parkinson's cure in the nose 30 Jun 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. FDA approves RequipXL 30 Jun 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Azilect slows Parkinson's Disease Progression 30 Jun 2008 Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendisse tristique. Cras et sem at odio porttitor mattis.
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PD Guide
The PD Guide is a comprehensive outline of the current basic science and clinical understanding of PD
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Cannabinoids and neuroprotection in basal ganglia disorders
J. Fernandez-Ruiz, Ciuidad Universitaria, Madrid 6 May 2008
Etiopathogenesis Risk Factors Genetic factors Causative Genetic Factors Autosomal Inheritance of PD Autosomal Dominant Mutations PARK1 (SNCA/Alpha-Synuclein) PARK3 (Sepiapterine?) PARK4 (SNCA/Alpha-Synuclein duplications/triplications) PARK5 (UCHL1/ubiquitin carboxyterminal hydrolase 1) PARK8 (LRRK2/dardarin) PARK13 (Omi/HtrA2) Autosomal Recessive PARK2 (Parkin) PARK6 (PINK1) PARK7 (DJ-1) PARK 9 (ATP13A2) Sex-Linked Inheritance X-linked PARK12 Other potential monogenic loci/genes PARK10 PARK11 Synphilin-1 Nurr1/NR4A2 POLG/DNA Polymerase gamma Genetic Susceptibility Factors Non-genetic/Environmental Factors Environmental toxins Biological pathogenic agents Recreational/Pharmacological drug use Dietary Factors Metabolites Cancer Brain Injury Occupation Physical activity Pathogenic pathways Dopamine metabolism/toxicity Protein handling Translation/transcription Promoter haplotype REP1 allele Misfolding Chaperones -synuclein Post-translational modification Phosphorylation and Nitration Trafficking Lipid membranes Microtubules Protein/protein interactions Aggregation Oligomerization Fibril formation Degradation Proteosome (ubiquitin) Lysosomal function Implicated Genes/Proteins -synuclein Parkin Uchl1
Existing anti-inammatory agents are ineffective or dangerous

J. McGeer, USC 8 Mar 2008
Research Questions
Are there any already-approved antiinammatory drugs that should be tested for PD? 9 Feb 2008
News
Researchers To Simulate And Analyze Brain, Immune System Activity ...
Science Daily 17 Jun 2008
Study shows coffee lowers risk of Parkinson's disease but not cancer deaths
USA Today 16 Jun 2008
Grant opportunities worldwide

Parkinson's Disease Foundation, Inc.
Grant program to support research in neuroinammation, genetics, programmed cell death/GDNF in development of DA neurons
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The PD Guide is a comprehensive outline of the current basic science and clinical understanding of PD
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Cannabinoids and neuroprotection in basal ganglia disorders
J. Fernandez-Ruiz, Ciuidad Universitaria, Madrid 6 May 2008
Etiopathogenesis Risk Factors Genetic factors Causative Genetic Factors Autosomal Inheritance of PD Autosomal Dominant Mutations PARK1 (SNCA/Alpha-Synuclein) PARK3 (Sepiapterine?) PARK4 (SNCA/Alpha-Synuclein duplications/triplications) PARK5 (UCHL1/ubiquitin carboxyterminal hydrolase 1) PARK8 (LRRK2/dardarin) PARK13 (Omi/HtrA2) Autosomal Recessive PARK2 (Parkin) PARK6 (PINK1) PARK7 (DJ-1) PARK 9 (ATP13A2) Sex-Linked Inheritance X-linked PARK12 Other potential monogenic loci/genes PARK10 PARK11 Synphilin-1 Nurr1/NR4A2 POLG/DNA Polymerase gamma Genetic Susceptibility Factors Non-genetic/Environmental Factors Environmental toxins Biological pathogenic agents Recreational/Pharmacological drug use Dietary Factors Metabolites Cancer Brain Injury Occupation Physical activity Pathogenic pathways Dopamine metabolism/toxicity Protein handling Translation/transcription Misfolding Post-translational modification Trafficking Protein/protein interactions Degradation Implicated Genes/Proteins Animal Models Therapeutic Strategies Mitochondrial dysfunction Implicated Genes/Proteins Animal Models Therapeutic Strategies Oxidative Stress Implicated Genes/Proteins Animal Models Therapeutic Strategies Neuroinflammation Implicated Genes/Proteins Animal Models Therapeutic Strategies
Existing anti-inammatory agents are ineffective or dangerous

J. McGeer, USC 8 Mar 2008
Research Questions
Are there any already-approved antiinammatory drugs that should be tested for PD? 9 Feb 2008
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Etiopathogenesis Risk Factors Pathogenic Pathways Neuron health/death processes Neuroinflammation Clinical and Biological Signs Clinical Symptoms Biological Signs Neuroimaging Therapeutic Approaches Symptomatic Relief Disease Modification Mechanisms of neuroprotection For full context go to
PD Guide
Neuroinflammation
By Chris Scientist, Clinician, Washington University
The brain has generally been considered to be immune privileged and thus largely protected from immune factors. However, it is now recognized that the brain can initiate injury responses including neuroinflammation as a means to reduce injury and clean up injured brain tissue. The main cellular responders to brain injury are microglia, which produce a number of factors to regulate the injury response including cytokines and protective factors. Although neuroinflammation may have initial protective effects, prolonged and chronic neuroinflammation may lead to prolonged neurodegeneration such as that seen in PD. Whether neuroinflammation acts as an initial trigger of PD pathogenesis or is a downstream result of another triggering pathogenic event is unclear. Neuroinflammation may lead to increased oxidative stress. Evidence for neuroinflammation in PD includes presence of activated microglia, increased expression of cytokines and pro-inflammatory signaling cascades (e.g., NF-kB). Furthermore, epidemiological data supports a reduce risk of PD in users of anti-inflammatory drugs (e.g., NSAIDS).
References
Tansey MG, Frank-Cannon TC, McCoy MK, Lee JK, Martinez TN, McAlpine FE, Ruhn KA, Tran TA. Neuroinflammation in Parkinson's disease: is there sufficient evidence for mechanism-based interventional therapy? Front Biosci. 2008 Jan 1;13:709-17. PubMed Wilms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R. Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause and therapeutic implications. Curr Pharm Des. 2007;13(18):1925-8. PubMed
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Cannabinoids and neuroprotection in basal ganglia disorders J. Fernandez-Ruiz, Ciudad Universitaria, Madrid Existing anti-inflammatory agents are ineffective or dangerous J. McGeer, USC 6 May 2008 8 Mar 2008

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Are there any already-approved anti-inammatory drugs that should be tested for PD? 9 Feb 2008
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Neuroinflammation
By Chris Scientist, Clinician, Washington University
The brain has generally been considered to be immune privileged and thus largely protected from immune factors. However, it is now recognized that the brain can initiate injury responses including neuroinflammation as a means to reduce injury and clean up injured brain tissue. The main cellular responders to brain injury are microglia, which produce a number of factors to regulate the injury response including cytokines and protective factors. Although neuroinflammation may have initial protective effects, prolonged and chronic neuroinflammation may lead to prolonged neurodegeneration such as that seen in PD. Whether neuroinflammation acts as an initial trigger of PD pathogenesis or is a downstream result of another triggering pathogenic event is unclear. Neuroinflammation may lead to increased oxidative stress. Evidence for neuroinflammation in PD includes presence of activated microglia, increased expression of cytokines and pro-inflammatory signaling cascades (e.g., NF-kB). Furthermore, epidemiological data supports a reduce risk of PD in users of anti-inflammatory drugs (e.g., NSAIDS).
Etiopathogenesis Risk Factors Pathogenic Pathways Neuron health/death processes Neuroinflammation Clinical and Biological Signs Clinical Symptoms Biological Signs Neuroimaging Therapeutic Approaches Symptomatic Relief Disease Modification Mechanisms of neuroprotection For full context go to
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Tansey MG, Frank-Cannon TC, McCoy MK, Lee JK, Martinez TN, McAlpine FE, Ruhn KA, Tran TA. Neuroinflammation in Parkinson's disease: is there sufficient evidence for mechanism-based interventional therapy? Front Biosci. 2008 Jan 1;13:709-17. PubMed Wilms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R. Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause and therapeutic implications. Curr Pharm Des. 2007;13(18):1925-8. PubMed
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Cannabinoids and neuroprotection in basal ganglia disorders J. Fernandez-Ruiz, Ciudad Universitaria, Madrid Existing anti-inflammatory agents are ineffective or dangerous J. McGeer, USC 6 May 2008 8 Mar 2008

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Are there any already-approved anti-inflammatory drugs that should be tested for PD? 9 Feb 2008
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Which symptoms are most in need of new therapies? Which are the most troubling to quality of life, and which treatment routes have specic blockages? How to develop pharmacological approaches to mimic effects of DBS?
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10 Jun 2008
Would continuous delivery of L-DOPA allow for MJFF symptomatic benet without development of dyskinesia? What is the mechanism of DBS? Is regulated gene therapy needed? What technologies may be available? How can direct brain infusion of therapeutic agents be made more controlled and predictable? What is the impact on fetal tissue transplants in PD of the recent ndings of synuclein pathology? What are the metrics used to assess efcacy of behavioral therapies? What are the clinical criteria that indicate these therapies? MJFF question: Is inammation a primary or secondary factor in PD pathogenesis? How do you design clinical trials to test neuroprotective therapeutics? What is the pathological role of Alpha Synuclein in PD? What are the best preclinical models to test neuroprotection? MJFF MJFF
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Etiopathogenesis Risk Factors PARK1 (SNCA/AlphaSynuclein mutations) Pathogenic pathways -synuclein Clinical and Biological Signs Clinical symptoms Biological signs Anatomical Distribution of pathology Llewy bodies Therapeutic Approaches Symptomatic relief Disease modification PD as proteinopathy Browse full contents
What is the pathological role of Alpha Synuclein in PD?

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Terms: Park1 (SNCA/Alpha Synuclein mutations, alpha-Synuclein, Anatomical Distribution of pathology, Llewy bodies, PD as proteinopathy
Misfolding and abnormal aggregation of the neuronal protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease and related neurological disorders, such as dementia with Lewy bodies.
alpha-synuclein is a conventional cytosolic protein and is thought to exert its pathogenic function exclusively in the neuronal cytoplasm in a cell-autonomous manner. However, the current model is being challenged by a series of new observations that demonstrate the presence of alpha-synuclein and its aggregated forms in the extracellular uid both in vivo and in vitro. Extracellular alpha-synuclein appears to be delivered by unconventional exocytosis of intravesicular alpha-synuclein, although the exact mechanism has not been characterized.
References
Windisch M, Wolf H, Hutter-Paier B, Wronski R. The role of alpha-synuclein in neurodegenerative diseases: a potential target for new treatment strategies? Neurodegener Dis. 2008;5(3-4):218-21. Epub 2008 Mar 6. PubMed Lee SJ. Origins and effects of extracellular alpha-synuclein: implications in Parkinson's disease. J Mol Neurosci. 2008;34(1):17-22. Epub 2007 Apr 17. PubMed
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Green tea compound may help prevent PD 31 May 2008 Alpha Synuclein aggreation inhibited by siRNA 2 Feb 2008
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The alpha-synuclein burden hypothesis of Parkinson disease. McGeer EG. Kinsmen Laboratory of Neurological Research 12 Jun 2008
Grant opportunities
MJFF commits up to $4M to study Alpha Synuclein toxicity 12 Jan 2008
The identification of duplicate and triplicate gene copy mutations in familial PD provides significant evidence for excess synuclein being sufficient for PD.
Contributions
Drosophila PD models have lewy bodies, mouse models don't
Michael Rogan, MJFF 22 Jun 2008
Parkinson patient broblasts show increased alpha-synuclein expression

G. Aurberger, USC, Frankfurt 22 Mar 2008
Casein kinase-mediated phosphorylation of alpha-synuclein E

Waxman, U Penn 12 Feb 2008
Events
Webcast: Protein aggregation in Alzheimer's and Parkinson's
AlzForum 12 Jul 2008
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Contents & Navigation

Etiopathogenesis Risk Factors PARK1 (SNCA/AlphaSynuclein mutations) Pathogenic pathways -synuclein Clinical and Biological Signs Clinical symptoms Biological signs Anatomical Distribution of pathology Llewy bodies Therapeutic Approaches Symptomatic relief Disease modification PD as proteinopathy Browse full contents

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Terms: Park1 (SNCA/Alpha Synuclein mutations, alpha-Synuclein, Anatomical Distribution of pathology, Llewy bodies, PD as proteinopathy
Misfolding and abnormal aggregation of the neuronal protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease and related neurological disorders, such as dementia with Lewy bodies.
alpha-synuclein is a conventional cytosolic protein and is thought to exert its pathogenic function exclusively in the neuronal cytoplasm in a cell-autonomous manner. However, the current model is being challenged by a series of new observations that demonstrate the presence of alpha-synuclein and its aggregated forms in the extracellular uid both in vivo and in vitro. Extracellular alpha-synuclein appears to be delivered by unconventional exocytosis of intravesicular alpha-synuclein, although the exact mechanism has not been characterized.
See Also
References
Add Reference
News
Green tea compound may help prevent PD 31 May 2008 Alpha Synuclein aggreation inhibited by siRNA 2 Feb 2008
Windisch M, Wolf H, Hutter-Paier B, Wronski R. The role of alpha-synuclein in neurodegenerative diseases: a potential target for new treatment strategies? Neurodegener Dis. 2008;5(3-4):218-21. Epub 2008 Mar 6. PubMed Lee SJ. Origins and effects of extracellular alpha-synuclein: implications in Parkinson's disease. J Mol Neurosci. 2008;34(1):17-22. Epub 2007 Apr 17. PubMed
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The alpha-synuclein burden hypothesis of Parkinson disease. McGeer EG. Kinsmen Laboratory of Neurological Research
12 Jun 2008
MJFF commits up to $4M to study Alpha Synuclein toxicity 12 Jan 2008
Contributions
Drosophila PD models have lewy bodies, mouse models don't
Michael Rogan, MJFF 22 Jun 2008
The identification of duplicate and triplicate gene copy mutations in familial PD provides significant evidence for excess synuclein being sufficient for PD.
Parkinson patient broblasts show increased alpha-synuclein expression

G. Aurberger, USC, Frankfurt 22 Mar 2008
Casein kinase-mediated phosphorylation of alpha-synuclein E

Waxman, U Penn 12 Feb 2008
Events
Webcast: Protein aggregation in Alzheimer's and Parkinson's
AlzForum 12 Jul 2008
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Neuroimaging progression markers are required to validate ... [Edit] Lorem ipsum dolor sit amet consectateur nonummy lorenzino... Published DRAFT (15 Jan 2008) 23 Feb 2008 Published 3 Jun 2008 Published 12 Jul 2008
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Original article Neuroimaging progression markers are required to validate clinical scales By Chris Scientist * Title Summary Re: Neuroimaging progression markers are required to validate clinical enter text
Scientific Framework
Etiology & Pathogenisis Risk Factors Pathogenic Pathways PD as proteinopathy Neuron health/death processes scales Mitochondrial dysfunction Oxidative Stress Immune response Neuroinflamation Clinical & Biological Signs Biological signs Biomarkers Neuroimaging
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Ken Marek, INDD Disease Modification 30 Mar 2008 Imaging is certainly developing as a Mechanisms of neuroprotection Related Resources diagnostic tool for Parkinson disease Thomas Jovin, Max Planck 21 Feb 2008 Learning from NMR of alpha synuclein aggregation
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Avid Pharmaceuticals 14 Feb 2008 Phase 1: PET imaging compound for PD Inst. Neurodegenerative Disorders 23 Jan 2008 Impact on behavior of disclosing imaging data to trial participants
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NIH NINDS, USA Neuroimaging, Depression, Cognitive function MJFF, USA Browse... Therapeutics Development Initiative Welcome Trust, UK EU 23 Jan 2008 Stem Cells: measures of success
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Original article What is the pathological role of Alpha Synuclein in PD? By MJFF * Title * Body Re: What is the pathological role of Alpha Syniclein in PD? WYSIWYG Tools enter text
Etiology & Pathogenisis Risk Factors Pathogenic Pathways PD as proteinopathy Neuron health/death processes Mitochondrial dysfunction Oxidative Stress Immune response Neuroinflamation Clinical & Biological Signs Biological signs Biomarkers Neuroimaging Therapeutic Approaches Disease Modification Mechanisms of neuroprotection
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alpha synuclein
Author David Sulzer Type Article Updated 23 Feb 2008 Responses 6
Reprogrammed cells reduce Parkinson's symptoms ...

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Neuroimaging progression markers are required to ...

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Misfolding and abnormal aggregation of the neuronal protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease and related neurological disorders
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Neuroimaging progression markers are required to validate new clinical scales

By Bill Clinician, Clinician, Washington University
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Etiology & Pathogenisis Risk Factors Pathogenic Pathways PD as proteinopathy Neuron health/death processes Mitochondrial dysfunction Oxidative Stress Immune response Neuroinflammation Clinical & Biological Signs Biological signs Biomarkers Neuroimaging Therapeutic Approaches Disease Modification Mechanisms of neuroprotection
Terms: Neuron health/death processes, Neuroinflammation, Neuroimaging, Mechanisms of neuroprotection 5 people rated this article highly.
A major goal of Parkinsons disease research is to develop therapies which slow or stop disease progression and/or restore dopamine cell function. The rate of clinical progression of Parkinsons disease is highly variable and currently unpredictable. Several clinical studies have followed large cohorts of patients with Parkinsons disease for several years, but these studies lack an objective measure of disease progression and are frequently confounded by changes in treatment. Imaging studies provide the opportunity to evaluate patients longitudinally from early to late disease using an objective biomarker for dopamine nerve cell degeneration.
In studies evaluating sequential [123I] -CIT and SPECT imaging in patients with Parkinsons disease, there was an approximately 7% reduction in [123I] -CIT and SPECT activity each year. This rate of nerve cell loss is similar to that found in another imaging study using PET and [18F]DOPA. Evidence from studies of hemi-Parkinsons disease subjects provides further insight into the rate of progression of disease. In early hemi-Parkinsons disease, there is a reduction in the [123I] -CIT activity of about 50% in the brain hemisphere opposite the symptomatic side, but also a 25-30% reduction in the brain hemisphere opposite to the presymptomatic side. Since most patients will progress clinically from unilateral to bilateral symtoms in a 3-6 year period, it is therefore likely that the loss of [123I] -CIT activity in the brain hemisphere reflected in the previously presymptomatic side will progress at about 5-10% per year. Progression studies have begun to provide important new insights into the onset and natural history of Parkinsons disease. For example, given the assumption that progression is linear, it is possible to extrapolate back in time from sequential imaging data and reported symptom duration to estimate when the dopamine neuron loss began and at what level of dopamine neuron loss symptoms began. These calculations are fraught with many assumptions, but likely provide an estimate for the duration of time between the start of the disease process and the start of disease symptoms, called the preclincial phase of the illness. Our data from longitudinal imaging studies suggest that disease symptoms start at 70-75% of normal dopamine cell function and it may take a period of 3-6 years from the start of nerve degeneration to the onset of symptoms. While the data available to calculate the estimates of the preclinical phase must be viewed as preliminary, they are consistent with other imaging studies and with pathology studies. If correct, this has tremendous implications for understanding the cause of Parkinsons disease and for developing strategies for disease screening and treatment. For example, if preclinical disease is relatively short, repetitive screening might be required to identify affected individuals in an at risk population. Furthermore, as potential preventative or restorative therapies are developed, these treatments might be directed to the time period from onset of degeneration to onset of symptoms.
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Ken Marek, INDD 30 Mar 2008 Imaging is certainly developing as a diagnostic tool for Parkinson disease Thomas Jovin, Max Planck 21 Feb 2008 Learning from NMR of alpha synuclein aggregation
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Flowers KA, Robertson C: Perceptual abnormalities in Parkinson's disease: top-down or bottom-up processes? Perception 1995, 24:1201-1221. PubMed Djamgoz MB, Hankins MW, Hirano J, Archer SN: Neurobiology of retinal dopamine in relation to degenerative states of the tissue. Vision Res 1997, 37:3509-3529. PubMed | Publisher Full Text Wink B, Harris J: A model of the Parkinsonian visual system: support for the dark adaptation hypothesis. Vision Res 2000, 40:1937-1946. PubMed | Publisher Full Text
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Functional Neuroimaging has unique potential 22 Aug 2007 John Doe, Director, BioBlah The complexities and hazards of PET make it unusable for large scale studies, especially with the protracted longitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it is essential to develop this technology as a non-invasive method to track PD progression. Functional Neuroimaging has unique potential 22 Aug 2007 John Doe, Director, BioBlah The complexities and hazards of PET make it unusable for large scale studies, especially with the protracted longitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it
NIH NINDS, USA Neuroimaging, Depression, Cognitive function MJFF, USA Therapeutics Development Initiative Welcome Trust, UK EU 23 Jan 2008 Stem Cells: measures of success
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Neuroimaging progression markers are required to validate new clinical scales

By Bill Clinician, Clinician, Washington University
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Terms: Neuron health/death processes, Neuroinflammation, Neuroimaging, Mechanisms of neuroprotection 5 people rated this article highly. Give your own rating: [High] [Low]
A major goal of Parkinsons disease research is to develop therapies which slow or stop disease progression and/or restore dopamine cell function. The rate of clinical progression of Parkinsons disease is highly variable and currently unpredictable. Several clinical studies have followed large cohorts of patients with Parkinsons disease for several years, but these studies lack an objective measure of disease progression and are frequently confounded by changes in treatment. Imaging studies provide the opportunity to evaluate patients longitudinally from early to late disease using an objective biomarker for dopamine nerve cell degeneration.
In studies evaluating sequential [123I] -CIT and SPECT imaging in patients with Parkinsons disease, there was an approximately 7% reduction in [123I] -CIT and SPECT activity each year. This rate of nerve cell loss is similar to that found in another imaging study using PET and [18F]DOPA. Evidence from studies of hemi-Parkinsons disease subjects provides further insight into the rate of progression of disease. In early hemi-Parkinsons disease, there is a reduction in the [123I] -CIT activity of about 50% in the brain hemisphere opposite the symptomatic side, but also a 25-30% reduction in the brain hemisphere opposite to the presymptomatic side. Since most patients will progress clinically from unilateral to bilateral symtoms in a 3-6 year period, it is therefore likely that the loss of [123I] -CIT activity in the brain hemisphere reflected in the previously presymptomatic side will progress at about 5-10% per year. Progression studies have begun to provide important new insights into the onset and natural history of Parkinsons disease. For example, given the assumption that progression is linear, it is possible to extrapolate back in time from sequential imaging data and reported symptom duration to estimate when the dopamine neuron loss began and at what level of dopamine neuron loss symptoms began. These calculations are fraught with many assumptions, but likely provide an estimate for the duration of time between the start of the disease process and the start of disease symptoms, called the preclincial phase of the illness. Our data from longitudinal imaging studies suggest that disease symptoms start at 70-75% of normal dopamine cell function and it may take a period of 3-6 years from the start of nerve degeneration to the onset of symptoms. While the data available to calculate the estimates of the preclinical phase must be viewed as preliminary, they are consistent with other imaging studies and with pathology studies. If correct, this has tremendous implications for understanding the cause of Parkinsons disease and for developing strategies for disease screening and treatment. For example, if preclinical disease is relatively short, repetitive screening might be required to identify affected individuals in an at risk population. Furthermore, as potential preventative or restorative therapies are developed, these treatments might be directed to the time period from onset of degeneration to onset of symptoms.
Etiology & Pathogenisis Risk Factors Pathogenic Pathways PD as proteinopathy Neuron health/death processes Mitochondrial dysfunction Oxidative Stress Immune response Neuroinflammation Clinical & Biological Signs Biological signs Biomarkers Neuroimaging Therapeutic Approaches Disease Modification Mechanisms of neuroprotection
Related Resources
Articles
[more]
Ken Marek, INDD 30 Mar 2008 Imaging is certainly developing as a diagnostic tool for Parkinson disease Thomas Jovin, Max Planck 21 Feb 2008 Learning from NMR of alpha synuclein aggregation
Clinical Trials
[more]
Citations
Add Citation Flowers KA, Robertson C: Perceptual abnormalities in Parkinson's disease: top-down or bottom-up processes? Perception 1995, 24:1201-1221. PubMed Djamgoz MB, Hankins MW, Hirano J, Archer SN: Neurobiology of retinal dopamine in relation to degenerative states of the tissue. Vision Res 1997, 37:3509-3529. PubMed | Publisher Full Text Wink B, Harris J: A model of the Parkinsonian visual system: support for the dark adaptation hypothesis. Vision Res 2000, 40:1937-1946. PubMed | Publisher Full Text
[more]
NIH NINDS, USA Neuroimaging, Depression, Cognitive function MJFF, USA Therapeutics Development Initiative
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Functional Neuroimaging has unique potential 22 Aug 2007 John Doe, Director, BioBlah The complexities and hazards of PET make it unusable for large scale studies, especially with the protracted longitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it is essential to develop this technology as a non-invasive method to track PD progression. Functional Neuroimaging has unique potential 22 Aug 2007 John Doe, Director, BioBlah The complexities and hazards of PET make it unusable for large scale studies, especially with the protracted longitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it
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Original Research Question How do you design clinical trials to test neuroprotective therapeutics? By Michael Rogan
Etiology & Pathogenisis RiskCompleted Factors 23 Feb 2008 23 Feb 2008 20 May 2008Pathogenic Pathways PD as proteinopathy Neuron health/death processes Mitochondrial dysfunction Oxidative Stress Articles Immune response [more] Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Ken Marek, INDD 30 Neuroinflamation Mar 2008 Suspendisse ut purus. Suspendisse tristique. Cras et sem at certainly developing as a Imaging is odio Clinical & for porttitor mattis. Donec dignissim ornare tortor. Donecdiagnostic tool Biological Signs lectus turpis, Parkinson disease Biological signs tempor id, cursus vitae, eleifend in, risus. Aenean turpis. Mauris Biomarkers Thomas Jovin, Neuroimaging ultricies quam malesuada ligula. Vivamus neque. Maecenas arcuMax Planck 21 Feb 2008 Learning from NMR of alpha synuclein lacus, bibendum in, pretium ut, imperdiet a, augue. Vivamus lorem aggregation Therapeutic Approaches velit, placerat non, porta sit amet, iaculis nec, est. Proin Disease Modification scelerisque lectus quis lectus. Integer felis. Duis sagittis auctor Clinical Mechanisms of neuroprotection Trials [more] Avid lorem ut 14 Feb 2008 eros. Vivamus porta lacus id pede. Nulla scelerisque Pharmaceuticals Phase 1: PET imaging compound for quam. Related Resources PD Sent Accepted Declined Delegated Due Inst. Neurodegenerative Disorders 23 Jan 2008 Impact on behavior of disclosing imaging data to trial participants
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Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Neuroimaging progresion markers... [More]

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

Welcome Chris Scientist Prole My Work

Next Step for LRRK2: identifying substrates Mark Cookson, NIH

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Existing anti-inammatory agents are ineffective or dangerous

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Welcome Chris Scientist About

Existing anti-inammatory agents are ineffective or dangerous

Grant opportunities worldwide

Grant opportunities worldwide

Welcome Chris Scientist About

By Chris Scientist, Clinician, Washington University

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Parkinson's Disease Foundation, Inc.

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What is the pathological role of Alpha Synuclein in PD?

Parkinson patient broblasts show increased alpha-synuclein expression

Casein kinase-mediated phosphorylation of alpha-synuclein E

Welcome Chris Scientist About

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What is the pathological role of Alpha Synuclein in PD?

MJFF commits up to $4M to study Alpha Synuclein toxicity 12 Jan 2008

Parkinson patient broblasts show increased alpha-synuclein expression

Casein kinase-mediated phosphorylation of alpha-synuclein E

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How do you Design clinical trials to test neuroprotective ...

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