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PD Online Research The Michael J. Fox Foundation for Parkinson’s Research

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D Online Research is a community of scientists, clinicians, and professionals from the Industry,unding, and Financial sectors. We are working to identify and fund high impact PD research, and weo this by posing and answering Research Questions, writing commentary and opinions. The contentn the site is freely available to members and non-members alike.

ow do you design clinical trials to test neuroprotective

erapeutics? Responses (10) 30 Jun 2008

rem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse utrus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec

gnissim ornare tortor.

ow to develop pharmacological approaches to mimic

fects of DBS? Responses (3) 23 May 2008



hat is the pathological role of Alpha Responses (6)16 Apr 2008

ynuclein in PD?rem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse utrus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec


hat is the mechanism of DBS? Responses (3) 23 Mar 2008



hat is the impact on fetal tissue transplants in PD of the recent

dings of synuclein pathology? Responses (3) 23 Feb 2008

rem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut

rus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donecgnissim ornare tortor.

hat are the best preclinical models to test neuroprotection?

Responses (6) 16 Jan 2008

orem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse utrus. Suspendisse tristique. Cras et sem at odio porttitor mattis. Donec


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esearch Questions

Tell us where to put the money"

Next Step for LRRK2: identifying substratesMark Cookson, NIH 30 Mar 2008

Rules for assessing the funding portfolio and setting prioritiesAnne Persona, MJFF 21 Feb 2008

The health of cell replacement therapiesJeffrey Kordower, Rush University 14 Feb 2008

The damaging effect of an MBA mentality on research fundingDavid Sulzer, Columbia University 23 Jan 2008



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Recent Contributions

Disease modifying therapies must not ignorecompensation mechanismsJames Wilson, NINDS 12 Jun 2008

A major goal of Parkinson's disease research is todevelop therapies which slow or stop disease progressionand/or restore dopamine cell function. The rate of clinicalprogression of Parkinson’s disease is highly variable andcurrently unpredictable.

Genetics loads the gun but environment pulls thetrigger Carly Tanner, NSF 14 Jun 2008






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A major goal of Parkinson's disease research is todevelop therapies which slow or stop disease progression

and/or restore dopamine cell function. The rate of clinicalprogression of Parkinson’s disease is highly variable andcurrently unpredictable.





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Parkinson's cure in the nose 30 Jun 2008

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FDA approves Requip®XL 30 Jun 2008


Azilect slows Parkinson's Disease Progression 30 Jun 2008


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Sick Transplants and the health of cell replacementtherapies 30 Jun 2008

esearch News

Reprogrammed Cells Reduce Parkinson's Symptons inRats 30 Jun 2008

Neurons derived from reprogrammed adult skin cellssuccessfully integrated into foetal mouse brains and reducedsymptoms in a Parkinson’s disease rat model, according to astudy published on April 7 in the online Early Edition of ...

A major goal of Parkinson's disease research is to developtherapies which slow or stop disease progression and/or restore dopamine cell function.The rate of clinical progresionof Parkinson’s disease is variable and currently unpredictable.

Drafts: Neuroimaging progresion markers...

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ll the content on this site can be found organized by subject area by browsing the PD Guide, MJFF’somprehensive outline of current areas of research in basic and clinical PD science.

ach PD Guide Term has a short opinionated description and bibliography, and Terms associated withach piece of PD Online content will be displayed in the PD Guide tree in the upper right of each page.























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Welcome Chris Scientist ProfilePD Online Research The Michael J. Fox Foundation for Parkinson’s Research


EtiopathogenesisRisk Factors

Genetic factorsCausative Genetic Factors

Autosomal Inheritance of PDAutosomal 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 FactorsNon-genetic/Environmental Factors

• Environmental toxins• Biological pathogenic agents• Recreational/Pharmacological drug use• Dietary Factors• Metabolites

• Cancer • Brain Injury• Occupation• Physical activity

Pathogenic pathwaysDopamine metabolism/toxicityProtein handling

Translation/transcription• Promoter haplotype• REP1 allele

Misfolding• Chaperones• α-synuclein

Post-translational modification• Phosphorylation and Nitration

Trafficking• Lipid membranes• Microtubules

Protein/protein interactionsAggregation

• Oligomerization• Fibril formation

DegradationProteosome (ubiquitin)Lysosomal function

Implicated Genes/Proteins• α-synuclein• Parkin• Uchl1

The PD Guide is a comprehensive outline of the current basic scienceand clinical understanding of PD

D GuideEdit

See Also


Cannabinoids and neuroprotection inbasal ganglia disordersJ. Fernandez-Ruiz, Ciuidad Universitaria,Madrid 6 May 2008

Existing anti-inflammatory agents are

ineffective or dangerousJ. McGeer, USC 8 Mar 2008

Research Questions

Are there any already-approved anti-inflammatory drugs that should be

tested for PD? 9 Feb 2008

News

Researchers To Simulate And AnalyzeBrain, Immune System Activity ...Science Daily 17 Jun 2008

Study shows coffee lowers risk of

Parkinson's disease but not cancerdeathsUSA Today 16 Jun 2008

Grant opportunities worldwide

Parkinson's Disease Foundation, Inc.Grant program to support research inneuroinflammation, genetics, programmedcell death/GDNF in development of DA

neurons

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EtiopathogenesisRisk Factors

Genetic factorsCausative Genetic Factors

Autosomal Inheritance of PDAutosomal 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 FactorsNon-genetic/Environmental Factors

• Environmental toxins• Biological pathogenic agents• Recreational/Pharmacological drug use• Dietary Factors• Metabolites

• Cancer • Brain Injury• Occupation• Physical activity

Pathogenic pathwaysDopamine metabolism/toxicityProtein handling

Translation/transcriptionMisfoldingPost-translational modificationTraffickingProtein/protein interactionsDegradationImplicated Genes/ProteinsAnimal ModelsTherapeutic Strategies

Mitochondrial dysfunctionImplicated Genes/ProteinsAnimal ModelsTherapeutic Strategies

Oxidative StressImplicated Genes/ProteinsAnimal ModelsTherapeutic Strategies

NeuroinflammationImplicated Genes/ProteinsAnimal ModelsTherapeutic Strategies

The PD Guide is a comprehensive outline of the current basic scienceand clinical understanding of PD

D GuideEdit

See Also


Cannabinoids and neuroprotection inbasal ganglia disordersJ. Fernandez-Ruiz, Ciuidad Universitaria,Madrid 6 May 2008

Existing anti-inflammatory agents are

ineffective or dangerousJ. McGeer, USC 8 Mar 2008

Research Questions

Are there any already-approved anti-inflammatory drugs that should be

tested for PD? 9 Feb 2008

News

Researchers To Simulate And AnalyzeBrain, Immune System Activity ...Science Daily 17 Jun 2008




Parkinson's Disease Foundation, Inc.Grant program to support research inneuroinflammation, genetics, programmedcell death/GDNF in development of DA

neurons

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Search

LoginAbout



The brain has generally been considered to be immune privileged and thus largely protectedfrom immune factors. However, it is now recognized that the brain can initiate injuryresponses including neuroinflammation as a means to reduce injury and clean up injuredbrain tissue. The main cellular responders to brain injury are microglia, which produce anumber of factors to regulate the injury response including cytokines and protective factors.Although neuroinflammation may have initial protective effects, prolonged and chronic

uroinflammation may lead to prolonged neurodegeneration such as that seen in PD. Whether uroinflammation acts as an initial trigger of PD pathogenesis or is a downstream result of another ggering pathogenic event is unclear. Neuroinflammation may lead to increased oxidative stress. Evidencer neuroinflammation in PD includes presence of activated microglia, increased expression of cytokines ando-inflammatory signaling cascades (e.g., NF-kB). Furthermore, epidemiological data supports a reduce riskPD in users of anti-inflammatory drugs (e.g., NSAIDS).

eferences

nsey MG, Frank-Cannon TC, McCoy MK, Lee JK, Martinez TN, McAlpine FE, Ruhn KA, Tran TA.Neuroinflammation inrkinson's disease: is there sufficient evidence for mechanism-based interventional therapy?Front Biosci. 2008n 1;13:709-17. PubMed

lms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R.Inflammation in Parkinson's diseases and other urodegenerative diseases: cause and therapeutic implications.Curr Pharm Des. 2007;13(18):1925-8. PubMed

ontributions

annabinoids and neuroprotection in basal ganglia disorders 6 May 2008J. Fernandez-Ruiz, Ciudad Universitaria, Madrid

xisting anti-inflammatory agents are ineffective or dangerous 8 Mar 2008J. McGeer, USC

esearch Questions

e there any already-approved anti-inflammatory drugs that should 9 Feb 2008tested for PD?

By Chris Scientist, Clinician, Washington University

D Guide TERMS

Neuroinflammation

PD GuideEtiopathogenesis

Risk FactorsPathogenic Pathways

Neuron health/death processes

NeuroinflammationClinical and Biological Signs

Clinical SymptomsBiological Signs

NeuroimagingTherapeutic Approaches

Symptomatic Relief Disease Modification

Mechanisms of neuroprotection

For full context go to PD Guide

See Also

News

Researchers To Simulate And Analyze

Brain, Immune System Activity ...Science Daily 17 Jun 2008




Parkinson's Disease Foundation, Inc.Grant program to support research inneuroinflammation, genetics, programmed

cell death/GDNF in development of DAneurons



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By Chris Scientist, Clinician, Washington University

D Guide TERMS

Neuroinflammation

PD GuideEtiopathogenesis


Neuron health/death processes

NeuroinflammationClinical and Biological Signs

Clinical SymptomsBiological Signs

NeuroimagingTherapeutic Approaches

Symptomatic Relief Disease Modification


For full context go to PD Guide

Create ResponseRequest ResponseEdit

The brain has generally been considered to be immune privileged and thus largely protectedfrom immune factors. However, it is now recognized that the brain can initiate injuryresponses including neuroinflammation as a means to reduce injury and clean up injuredbrain tissue. The main cellular responders to brain injury are microglia, which produce anumber of factors to regulate the injury response including cytokines and protective factors.Although neuroinflammation may have initial protective effects, prolonged and chronic

uroinflammation may lead to prolonged neurodegeneration such as that seen in PD. Whether uroinflammation acts as an initial trigger of PD pathogenesis or is a downstream result of another ggering pathogenic event is unclear. Neuroinflammation may lead to increased oxidative stress. Evidencer neuroinflammation in PD includes presence of activated microglia, increased expression of cytokines ando-inflammatory signaling cascades (e.g., NF-kB). Furthermore, epidemiological data supports a reduce riskPD in users of anti-inflammatory drugs (e.g., NSAIDS).

eferences

nsey MG, Frank-Cannon TC, McCoy MK, Lee JK, Martinez TN, McAlpine FE, Ruhn KA, Tran TA.Neuroinflammation inrkinson's disease: is there sufficient evidence for mechanism-based interventional therapy?Front Biosci. 2008n 1;13:709-17. PubMed

lms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R.Inflammation in Parkinson's diseases and other urodegenerative diseases: cause and therapeutic implications.Curr Pharm Des. 2007;13(18):1925-8. PubMed

esponses

Be the first to create a response to this PD Guide Term

ontributions

annabinoids and neuroprotection in basal ganglia disorders 6 May 2008

J. Fernandez-Ruiz, Ciudad Universitaria, Madrid

sting anti-inflammatory agents are ineffective or dangerous 8 Mar 2008J. McGeer, USC

esearch Questions

e there any already-approved anti-inflammatory drugs that should 9 Feb 2008tested for PD?

Add ReferenceSee Also

News

Researchers To Simulate And Analyze

Brain, Immune System Activity ...Science Daily 17 Jun 2008




Parkinson's Disease Foundation, Inc.Grant program to support research inneuroinflammation, genetics, programmed

cell death/GDNF in development of DAneurons

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Research Questions

Which symptoms are most in need of new therapies?Which are the most troubling to quality of life, and which

eatment routes have specific blockages?

ow to develop pharmacological approaches to mimicffects of DBS?

Would continuous delivery of L-DOPA allow for

ymptomatic benefit without development of dyskinesia?

What is the mechanism of DBS?

s regulated gene therapy needed? What technologies

may be available?

ow can direct brain infusion of therapeutic agents bemade more controlled and predictable?

What is the impact on fetal tissue transplants in PD of

he recent findings of synuclein pathology?

What are the metrics used to assess efficacy ofehavioral therapies? What are the clinical criteria that

ndicate these therapies?

MJFF question: Is inflammation a primary or secondary

actor in PD pathogenesis?


herapeutics?

What is the pathological role of Alpha Synuclein in PD?

What are the best preclinical models to test

europrotection?

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PD Online Research


ESEARCH QUESTIONS


sfolding and abnormal aggregation of the neuronal protein alpha-synuclein has beenplicated in the pathogenesis of Parkinson's disease and related neurological disorders, such 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, thecurrent model is being challenged by a series of new observations that demonstrate the

presence of alpha-synuclein and its aggregated forms in the extracellular fluid both in vivo

and in vitro. Extracellular alpha-synuclein appears to be delivered by unconventionalexocytosis of intravesicular alpha-synuclein, although the exact mechanism has not been

characterized.

eferences

ndisch M, Wolf H, Hutter-Paier B, Wronski R. The role of alpha-synuclein in neurodegenerativeseases: a potential target for new treatment strategies? Neurodegener Dis. 2008;5(3-4):218-21. Epub08 Mar 6. PubMed

e SJ. Origins and effects of extracellular alpha-synuclein: implications in Parkinson's disease.Mol Neurosci. 2008;34(1):17-22. Epub 2007 Apr 17. PubMed

esponses

e alpha-synuclein burden hypothesis of Parkinson disease. 12 Jun 2008cGeer EG. Kinsmen Laboratory of Neurological Research

The identification of duplicate and triplicate gene copy mutations in familial PD providessignificant evidence for excess synuclein being sufficient for PD.

See Also

News

Green tea compound may help prevent

PD 31 May 2008

Alpha Synuclein aggreation inhibited by

siRNA 2 Feb 2008

Grant opportunities

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

Parkinson patient fibroblasts showincreased alpha-synuclein expressionG. Aurberger, USC, Frankfurt 22 Mar 2008

Casein kinase-mediated

phosphorylation of alpha-synuclein EWaxman, U Penn 12 Feb 2008

Events

Webcast: Protein aggregation in

Alzheimer's and Parkinson'sAlzForum 12 Jul 2008

Posed by MJFF

Terms: Park1 (SNCA/Alpha Synuclein mutations, alpha-Synuclein, Anatomical Distribution of pathology,Llewy bodies, PD as proteinopathy

Contents & NavigationEtiopathogenesis

Risk Factors• PARK1 (SNCA/Alpha-

Synuclein mutations)Pathogenic pathways• α-synuclein

Clinical and Biological SignsClinical symptomsBiological signs

• Anatomical Distribution of pathology• Llewy bodies

Therapeutic ApproachesSymptomatic relief Disease modification

• PD as proteinopathy

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The Michael J. Fox Foundation for Parkinson’s Research



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ESEARCH QUESTIONS


sfolding and abnormal aggregation of the neuronal protein alpha-synuclein has beenplicated in the pathogenesis of Parkinson's disease and related neurological disorders, such dementia with Lewy bodies.

alpha-synuclein is a conventional cytosolic protein and is thought to exert its pathogenicfunction 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 fluid both in vivoand in vitro. Extracellular alpha-synuclein appears to be delivered by unconventional

exocytosis of intravesicular alpha-synuclein, although the exact mechanism has not been

characterized.

eferences

ndisch M, Wolf H, Hutter-Paier B, Wronski R. The role of alpha-synuclein in neurodegenerativeseases: a potential target for new treatment strategies? Neurodegener Dis. 2008;5(3-4):218-21. Epub08 Mar 6. PubMed

e SJ. Origins and effects of extracellular alpha-synuclein: implications in Parkinson's disease.Mol Neurosci. 2008;34(1):17-22. Epub 2007 Apr 17. PubMed

esponses

e alpha-synuclein burden hypothesis of Parkinson disease. 12 Jun 2008cGeer EG. Kinsmen Laboratory of Neurological Research

The identification of duplicate and triplicate gene copy mutations in familial PD providessignificant evidence for excess synuclein being sufficient for PD.

Create ResponseRequest ResponseEdit

Add Reference

Create ResponseRequest Response

See Also

News

Green tea compound may help prevent

PD 31 May 2008

Alpha Synuclein aggreation inhibited by

siRNA 2 Feb 2008

Grant opportunities

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

Parkinson patient fibroblasts showincreased alpha-synuclein expressionG. Aurberger, USC, Frankfurt 22 Mar 2008

Casein kinase-mediated

phosphorylation of alpha-synuclein EWaxman, U Penn 12 Feb 2008

Events

Webcast: Protein aggregation in

Alzheimer's and Parkinson'sAlzForum 12 Jul 2008

Posed by MJFF

Terms: Park1 (SNCA/Alpha Synuclein mutations, alpha-Synuclein, Anatomical Distribution of pathology,Llewy bodies, PD as proteinopathy

Contents & NavigationEtiopathogenesis

Risk Factors• PARK1 (SNCA/Alpha-

Synuclein mutations)Pathogenic pathways• α-synuclein

Clinical and Biological SignsClinical symptomsBiological signs

• Anatomical Distribution of pathology• Llewy bodies

Therapeutic ApproachesSymptomatic relief Disease modification

• PD as proteinopathy

Browse full contents



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Kurt Danzer Lead Editor Michael J Fox Foundation 99

Michael Gerlach Lead Editor Michael J Fox Foundation 99

Frank Gillardon Lead Editor Michael J Fox Foundation 99

Allan Hendrich Lead Editor Michael J Fox Foundation 99

Bob Hengerer Lead Editor Michael J Fox Foundation 99

Robert Hueber Lead Editor Michael J Fox Foundation 99

Bill Hutter-Paier Lead Editor Michael J Fox Foundation 99

Walter Jost Lead Editor Michael J Fox Foundation 99

Jeffrey Kordower Lead Editor Michael J Fox Foundation 99

Anne Persona Lead Editor Michael J Fox Foundation 99

Paul Riederer Lead Editor Michael J Fox Foundation 99

Colin Schnack Lead Editor Michael J Fox Foundation 99

Chris Scientist Lead Editor Michael J Fox Foundation 99

Todd Sherer Lead Editor Michael J Fox Foundation 99

David Sulzer Lead Editor Michael J Fox Foundation 99

Mark Windisch Lead Editor Michael J Fox Foundation 99

Joshua Winkler Lead Editor Michael J Fox Foundation 99



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Chris Scientist

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Published Contributions Contributions Authored PublishedNeuroimaging progression markers are required to validate ... [Edit] DRAFT (15 Jan 2008)

Lorem ipsum dolor sit amet consectateur nonummy lorenzino... 23 Feb 2008

Research Questions Authored PublishedHow do you Design clinical trials to test neuroprotective ... 3 Jun 2008

Participated Interviews PublishedHow do you Design clinical trials to test neuroprotective ... 12 Jul 2008

Workgroups Lorem ipsum dolor sit amet

Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendissetristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. Donec lectus turpis,

tempor id, cursus vitae, eleifend in, risus. Aenean turpis. Mauris ultricies quam malesuada ligula.Vivamus neque. Maecenas arcu lacus, bibendum in, pretium ut, imperdiet a, augue. Vivamuslorem velit, placerat non, porta sit amet, iaculis nec, est. Proin scelerisque lectus quis lectus.Integer felis. Duis sagittis auctor eros. Vivamus porta lacus id pede. Nulla scelerisque lorem utquam.

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Michael J Fox Foundation100 Madison AveNew York, NY55555800-555-1212www.michaeljfox.org

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Requests Received Requests for Research Questions Sent to me Accepted Last ModifiedLorem ipsum dolor sit amet [Edit] 3 Feb 2008 23 Feb 2008 23 Feb 2008

Requests Sent Requests Sent for Contributions Sent to Request sent StatusWhat is the pathological role of Alpha-... Anne Persona 23 Feb 2008 accepted

Neuroimaging progression markers are . .. Anne Persona 16 Mar 2008 accepted

Neuroimaging progression markers are . .. David Sulzer 16 Mar 2008 complete

Drafts Pending Contributions Last ModifiedNeuroimaging progression markers are required to validate ... [Edit] DRAFT (15 Jan 2008)

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Contributions Contribution Title Notification Dateedit subscriptions] What is the pathological role of Alpha-... New comment by Anne Persona 15 Mar 2008

What is the pathological role of Alpha-... New comment by David Sulzer 17 Mar 2008Neuroimaging progression markers... New comment by Anne Persona 18 Mar 2008

Framework Terms Term Name Notification Dateedit subscriptions] Neuroinflammation New article: Lorem ipsum 12 Mar 2008

Other Members Member Name Notification Dateedit subscriptions] Mark Cookson New article: Lorem ipsum 17 Mar 2008

David Sulzer New comment: Ipsum Lorem 20 Mar 2008

Requests Received Request Type From Status Dateedit subscriptions] Commentary on What is the pathological... Pat Editor Received 16 Mar 2008

Requests Sent Request Type To Status Dateedit subscriptions] Commentary on What is the pathological... Anne Persona Almost Due 14 Mar 2008

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Anne Persona

Published Contributions Contributions Authored PublishedNeuroimaging progression markers are required to validate ... 23 Feb 2008Lorem ipsum dolor sit amet consectateur nonummy lorenzino... 15 Mar 2008

Research Questions Authored PublishedHow do you Design clinical trials to test neuroprotective ... 3 Jun 2008

Participated Interviews PublishedHow do you Design clinical trials to test neuroprotective ... 12 Jul 2008

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Contributions

Lorem ipsum dolor sit amet, consectetuer adipiscing elit. Suspendisse ut purus. Suspendissetristique. Cras et sem at odio porttitor mattis. Donec dignissim ornare tortor. Donec lectus turpis,tempor id, cursus vitae, eleifend in, risus. Aenean turpis. Mauris ultricies quam malesuada ligula.

Vivamus neque. Maecenas arcu lacus, bibendum in, pretium ut, imperdiet a, augue. Vivamuslorem velit, placerat non, porta sit amet, iaculis nec, est. Proin scelerisque lectus quis lectus.Integer felis. Duis sagittis auctor eros. Vivamus porta lacus id pede. Nulla scelerisque lorem utquam.

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Michael J Fox Foundation100 Madison AveNew York, NY55555800-555-1212www.michaeljfox.org

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Etiology & PathogenisisRisk Factors

Pathogenic PathwaysPD as proteinopathy

Neuron health/death processesMitochondrial dysfunctionOxidative StressImmune response• Neuroinflamation

Clinical & Biological SignsBiological signs

Biomarkers• Neuroimaging

Therapeutic ApproachesDisease Modification

Mechanisms of neuroprotectionRelated Resources

Articles [more]

Ken Marek, INDD 30 Mar 2008

Imaging is certainly developing as adiagnostic tool for Parkinson disease

Thomas Jovin, Max Planck 21 Feb 2008

Learning from NMR of alpha synuclein

aggregation

Clinical Trials [more]

Avid Pharmaceuticals 14 Feb 2008

Phase 1: PET imaging compound for

PD

Inst. Neurodegenerative

Disorders 23 Jan 2008

Impact on behavior of disclosingimaging data to trial participants

Grant OpportunitiesWorldwide [more]

NIH NINDS, USA

Neuroimaging, Depression, Cognitivefunction

MJFF, USATherapeutics Development Initiative

Welcome Trust, UK EU 23 Jan 2008

Stem Cells: measures of success

Seeking Research Partners [more]

Robert Burke, Columbia U 14 Feb 2008 Bioinformatics infrastructure

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Etiology & PathogenisisRisk Factors

Pathogenic PathwaysPD as proteinopathy

Neuron health/death processesMitochondrial dysfunctionOxidative StressImmune response• Neuroinflamation




Mechanisms of neuroprotectionRelated Resources

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Etiology & PathogenisisRisk FactorsPathogenic Pathways

PD as proteinopathy Neuron health/death processes

Mitochondrial dysfunctionOxidative StressImmune response• Neuroinflamation

Clinical & Biological Signs

Biological signsBiomarkers• Neuroimaging



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Reprogrammed cells reduce Parkinson's symptoms ... David Sulzer Article 23 Feb 2008 6Lorem ipsum dolor sit amet consectateur nonummy lorenzino

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Misfolding and abnormal aggregation of the neuronal protein Questionalpha-synuclein has been implicated in the pathogenesis of Parkinson's

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Human Interleukin-10 Gene Transfer Is Protective in a

Rat Model of Parkinson's Disease.by Johnston LC, Su X, Maguire-Zeiss K, Horovitz K,Ankoudinova I, Guschin D, Hadaczek P, Federoff HJ,Bankiewicz K, Forsayeth J.

Estrogen anti-inflammatory activity in brain: Atherapeutic opportunity for menopause andneurodegenerative diseases.by Vegeto E, Benedusi V, Maggi A.

Neuroinflammation and peripheral immune infiltrationin Parkinson's disease: an autoimmune hypothesis.by Monahan AJ, Warren M, Carvey PM

Triptolide protects against 1-methyl-4-phenylpyridinium-induced dopaminergic neurotoxicity in rats:Implication for immunosuppressive therapy inParkinson's disease.by Gao JP, Sun S, Li WW, Chen YP, Cai DF.

Neuroimaging progression markers are required tovalidate new clinical scalesby Anne Persona

Glucagon-like peptide 1 receptor stimulation reverseskey deficits in distinct rodent models of Parkinson'sdisease.by Harkavyi A, Abuirmeileh A, Lever R, Kingsbury AE,

Biggs CS, Whitton PS.

The synthetic triterpenoid CDDO-methyl estermodulates microglial activities, inhibits TNF production,and provides dopaminergic neuroprotection.by Tran TA, McCoy MK, Sporn MB, Tansey MG.

A new road to neuroinflammation in Parkinson'sdisease?by Fuxe KG, Tarakanov AO, Goncharova LB, AgnatiLF.

BV-2 stimulation by lactacystin results in a stronginflammatory reaction and apoptotic neuronal death in

SH-SY5Y cells.by Kwon SJ, Ahn TB, Yoon MY, Jeon BS

New developments in understanding and treatingneuroinflammation.by Infante-Duarte C, Waiczies S, Wuerfel J, Zipp F.

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Bill Clinician, Clinician, Washington Universityrms: Neuron health/death processes, Neuroinflammation, Neuroimaging, Mechanisms of neuroprotection

euroimaging progression markers are requiredo validate new clinical scales

PD TreeEtiology & Pathogenisis


PD as proteinopathy

Neuron health/death processesMitochondrial dysfunctionOxidative StressImmune response• Neuroinflammation





Related Resources

esponses

nctional Neuroimaging has unique potential 22 Aug 2007

hn Doe, Director, BioBlahe complexities and hazards of PET make it unusable for large scale studies, especially with the protracted

ngitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, itessential to develop this technology as a non-invasive method to track PD progression.


hn Doe, Director, BioBlah

e complexities and hazards of PET make it unusable for large scale studies, especially with the protracted

ngitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it

major goal of Parkinson’s disease research is to develop therapies which slow or stop diseaseogression and/or restore dopamine cell function. The rate of clinical progression of Parkinson’ssease is highly variable and currently unpredictable. Several clinical studies have followedrge cohorts of patients with Parkinson’s disease for several years, but these studies lack anbjective measure of disease progression and are frequently confounded by changes ineatment. Imaging studies provide the opportunity to evaluate patients longitudinally from earlylate disease using an objective biomarker for dopamine nerve cell degeneration.

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Robert Burke, Columbia U 14 Feb 2008

Bioinformatics infrastructure

In studies evaluating sequential [123I] ß-CIT and SPECT imaging in patients with Parkinson’sdisease, there was an approximately 7% reduction in [123I] ß-CIT and SPECT activity eachyear. This rate of nerve cell loss is similar to that found in another imaging study using PETand [18F]DOPA. Evidence from studies of hemi-Parkinson’s disease subjects providesfurther insight into the rate of progression of disease. In early hemi-Parkinson’s disease,there is a reduction in the [123I] ß-CIT activity of about 50% in the brain hemisphere opposite

e symptomatic side, but also a 25-30% reduction in the brain hemisphere opposite to the ‘presymptomatic’

de. Since most patients will progress clinically from unilateral to bilateral symtoms in a 3-6 year period, it iserefore likely that the loss of [123I] ß-CIT activity in the brain hemisphere reflected in the previouslyesymptomatic’ side will progress at about 5-10% per year.

ogression studies have begun to provide important new insights into the onset and natural history of arkinson’s disease. For example, given the assumption that progression is linear, it is possible totrapolate back in time from sequential imaging data and reported symptom duration to estimate when thepamine neuron loss began and at what level of dopamine neuron loss symptoms began. Theselculations are fraught with many assumptions, but likely provide an estimate for the duration of timetween the start of the disease process and the start of disease symptoms, called the preclincial phase of e illness. Our data from longitudinal imaging studies suggest that disease symptoms start at 70-75% of rmal dopamine cell function and it may take a period of 3-6 years from the start of nerve degeneration toe onset of symptoms. While the data available to calculate the estimates of the preclinical phase must beewed as preliminary, they are consistent with other imaging studies and with pathology studies. If correct,s has tremendous implications for understanding the cause of Parkinson’s disease and for developingategies for disease screening and treatment. For example, if preclinical disease is relatively short,petitive screening might be required to identify affected individuals in an ‘at risk’ population. Furthermore,

potential preventative or restorative therapies are developed, these treatments might be directed to theme period from onset of degeneration to onset of symptoms.

tations

owers KA, Robertson C: Perceptual abnormalities in Parkinson's disease: top-down or bottom-up processes? rception 1995, 24:1201-1221. PubMed

amgoz MB, Hankins MW, Hirano J, Archer SN:Neurobiology of retinal dopamine in relation to degenerative states of e tissue. Vision Res 1997, 37:3509-3529. PubMed | Publisher Full Text

nk B, Harris J: A model of the Parkinsonian visual system: support for the dark adaptation hypothesis.Vision Res00, 40:1937-1946. PubMed | Publisher Full Text

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Bill Clinician, Clinician, Washington Universityrms: Neuron health/death processes, Neuroinflammation, Neuroimaging, Mechanisms of neuroprotection

euroimaging progression markers are requiredo validate new clinical scales

PD TreeEtiology & Pathogenisis


PD as proteinopathy

Neuron health/death processesMitochondrial dysfunctionOxidative StressImmune response• Neuroinflammation





Related Resources

esponses


hn Doe, Director, BioBlahe complexities and hazards of PET make it unusable for large scale studies, especially with the protracted

ngitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it

essential to develop this technology as a non-invasive method to track PD progression.


hn Doe, Director, BioBlah

e complexities and hazards of PET make it unusable for large scale studies, especially with the protractedngitudinal studies necessary for neuroprotection trials. Though fMRI related to PD is not well developed, it

major goal of Parkinson’s disease research is to develop therapies which slow or stop diseaseogression and/or restore dopamine cell function. The rate of clinical progression of Parkinson’ssease is highly variable and currently unpredictable. Several clinical studies have followedrge cohorts of patients with Parkinson’s disease for several years, but these studies lack anbjective measure of disease progression and are frequently confounded by changes ineatment. Imaging studies provide the opportunity to evaluate patients longitudinally from earlylate disease using an objective biomarker for dopamine nerve cell degeneration.

Articles [more]


Imaging is certainly developing as a

diagnostic tool for Parkinson disease


Learning from NMR of alpha synucleinaggregation




PD

Inst. NeurodegenerativeDisorders 23 Jan 2008



Grant Opportunities

Worldwide [more]

NIH NINDS, USA

Neuroimaging, Depression, Cognitive

function

MJFF, USA


Welcome Trust, UK EU 23 Jan 2008 Stem Cells: measures of success




In studies evaluating sequential [123I] ß-CIT and SPECT imaging in patients with Parkinson’sdisease, there was an approximately 7% reduction in [123I] ß-CIT and SPECT activity eachyear. This rate of nerve cell loss is similar to that found in another imaging study using PETand [18F]DOPA. Evidence from studies of hemi-Parkinson’s disease subjects providesfurther insight into the rate of progression of disease. In early hemi-Parkinson’s disease,there is a reduction in the [123I] ß-CIT activity of about 50% in the brain hemisphere opposite

e symptomatic side, but also a 25-30% reduction in the brain hemisphere opposite to the ‘presymptomatic’de. Since most patients will progress clinically from unilateral to bilateral symtoms in a 3-6 year period, it iserefore likely that the loss of [123I] ß-CIT activity in the brain hemisphere reflected in the previouslyesymptomatic’ side will progress at about 5-10% per year.

ogression studies have begun to provide important new insights into the onset and natural history of arkinson’s disease. For example, given the assumption that progression is linear, it is possible totrapolate back in time from sequential imaging data and reported symptom duration to estimate when thepamine neuron loss began and at what level of dopamine neuron loss symptoms began. Theselculations are fraught with many assumptions, but likely provide an estimate for the duration of timetween the start of the disease process and the start of disease symptoms, called the preclincial phase of e illness. Our data from longitudinal imaging studies suggest that disease symptoms start at 70-75% of rmal dopamine cell function and it may take a period of 3-6 years from the start of nerve degeneration toe onset of symptoms. While the data available to calculate the estimates of the preclinical phase must beewed as preliminary, they are consistent with other imaging studies and with pathology studies. If correct,s has tremendous implications for understanding the cause of Parkinson’s disease and for developingategies for disease screening and treatment. For example, if preclinical disease is relatively short,

petitive screening might be required to identify affected individuals in an ‘at risk’ population. Furthermore,potential preventative or restorative therapies are developed, these treatments might be directed to theme period from onset of degeneration to onset of symptoms.

tations

owers KA, Robertson C: Perceptual abnormalities in Parkinson's disease: top-down or bottom-up processes? rception 1995, 24:1201-1221. PubMed

amgoz MB, Hankins MW, Hirano J, Archer SN:Neurobiology of retinal dopamine in relation to degenerative states of e tissue. Vision Res 1997, 37:3509-3529. PubMed | Publisher Full Text

nk B, Harris J: A model of the Parkinsonian visual system: support for the dark adaptation hypothesis.Vision Res00, 40:1937-1946. PubMed | Publisher Full Text

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