16th International Congress Themed Courses

Streaming Content

 

Pricing:
MDS Members: Free
Non-Members: $125 USD


The 16th International Congress Themed Sessions Streaming Content includes the following sessions:

Session 2103: Is it time to change how we define Parkinson’s disease?

Chairs:
Anthony Lang
Toronto, ON, Canada
Matthew Stern
Philadelphia, PA, USA

A clinical diagnoses based on bradykinesia, tremor and rigidity: Pathology and genetics are irrelevant
Baastian Bloem
Nijmegen, Netherlands

Parkinson's disease is a synucleinopathy: The clinical syndrome and genetics are irrelevant
Glenda Halliday
Randwick, Australia

Parkinson's disease is a genetic disorder and should be defined as such: The clinical syndrome and pathology are irrelevant
Matthew Farrer
Vancouver, BC, Canada

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe the different pathological changes associated with genetic Parkinson’s disease
  2. Identify the clinical features associated with Lewy body pathology
  3. Recognize the various genetic factors that are associated with Parkinson’s disease

Recorded: June 18, 2012 (8:00-10:00)

Session 2207: Whatever happened to environmental factors in the etiology of Parkinson’s disease? Are they still important?

Chairs:
Francesca Cicchetti
Guebec, PQ, Canada
Riona Mulcahy
Waterford, Ireland

Environmental toxins and parkinsonism
Alberto Ascherio
Boston, MA, USA

Environmental factors: What have we learned from animal models?
Francesca Cicchetti
Quebec, PQ, Canada

Epigenetics of psychiatric and neurological diseases
Art Petronis
Toronto, ON, Canada

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe the role of environmental factors and toxins in causing parkinsonism
  2. Understand how animal models inform our understanding of the pathophysiology of Parkinson's disease
  3. Explain epigenetic mechanisms and their possible relevance to the pathogenesis of Parkinson’s disease

Recorded: June 18, 2012 (15:45-17:45)

Session 3103: Lost in translation: Has genetics informed our knowledge of nonparkinsonian movement disorders?

Chairs:
Michael Hutchinson
Dublin, Ireland
Christine Klein
Luebeck, Germany

What is more important: DYT phyenotype or genotype?
Christine Klein
Luebeck, Germany

Getting the balance right: Can we make sense of the SCAs?
Bart van de Warrenburg
Nijmegen, Netherlands

Has identification of the Huntington’s disease gene mutation been the most over-hyped scientific news in the last twenty years?
M. Flint Beal
New York, NY, USA

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe how gene status affect the management of dystonia
  2. Express the genotype-phenotype relationship (if any) of spinocerebellar ataxias
  3. Understand the relevance of finding the gene for Huntington’s disease to neurological practice

Recorded: June 19, 2012 (8:00-10:00)

Session 3208: Imaging genetics in movement disorders

Chairs:
Jose Obeso
Pamplona, Spain
Antonio Strafella
Toronto, ON, Canada

Imaging genomics: Mapping preclinical changes in Parkinson’s disease
A. Jon Stoessl
Vancouver, BC, Canada

Functional neural networks linking dopaminergic gene polymorphisms to behavioral cognition in Parkinson’s disease
Antonio Strafella
Toronto, ON, Canada

Structural abnormalities in hereditary dystonia and other movement disorders
Stephane Lehericy
Paris, France

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe functional imaging changes underlying preclinical Parkinson’s disease asymptomatic carriers
  2. Identify abnormal connectivity and receptor changes in hereditary movement disorders
  3. Explain how dopaminergic gene polymorhisms influence neural networks affecting behavior and cognition in Parkinson’s disease.

Recorded: June 19, 2012 (15:15-17:15)

Session 3404: How to critically read and interpret genetic and molecular biological literature in movement disorders (e.g. GWAS studies) (Skills Workshop)

Vincenzo Bonifati
Rotterdam, Netherlands
Jeffery Vance
Miami, FL, USA

 

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Understand the strengths and limitations of genetic models of movement disorders
  2. Understand how GWAS studies should be designed
  3. Know the common shortcomings of GWAS studies of movement disorders

Recorded: June 19, 2012 (17:45-19:15)

Session 4208: What is essential tremor?

Chairs:
Guenther Deuschl
Kiel, Germany
Rodger Elble
Springfield, IL USA

A clinical perspective
Rodger Elble
Springfield, IL, USA

A neurophysiological perspective
Alfons Schnitzler
Dusseldorf, Germany

 

A biological perspective
Alexander Rajput
Saskatoon, SK, Canada

 

Learning Objectives
At the conclusion of this session, participants should be better able to:

Recorded: June 20, 2012 (15:00-17:00)

  1. Identify the controversies related to what constitutes essential tremor and its association with other movement disorders
  2. Recognize the genetic heterogeneity of essential tremor and the challenges to defining its genetic basis
  3. Discuss the various pathological findings that have been associated with essential tremor and controversies related to these
Session 4507: Clinical clues and pearls in the recognition of genetic forms of parkinsonism (Video Session)

Daniel Healy
Dublin, Ireland
Ebba Lohmann
Kavacik, Turkey

Learning Objectives
At the conclusion of this session, participants should be better able to:

Recorded: June 20, 2012 (17:30-19:00)

  1. Identify red flags pointing towards genetic forms of parkinsonism
  2. Distinguish between clinically typical and clinically atypical genetic forms of parkinsonism
  3. Describe the pertinent clinical findings of the different forms of genetic parkinsonism and appreciate the broad spectrum of these disorders
Session 2206: Molecular methodology for dummies: New investigative tools to shake up our understanding of Parkinson’s disease

Chairs:
Thomas Gasser
Tubingen, Germany
Dolores Cahill
Dublin, Ireland

What have genome wide association studies taught us that is new in Parkinson's disease?
Thomas Gasser
Tubingen, Germany

Transcriptomics: Does it contribute to our understanding of Parkinson's disease?
Ron Shamir
Tel Aviv, Israel

Proteomic approach to Parkinson's disease: What does this mean?
Mauro Fasano
Busto Arsizio, Italy

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Understand the value of GWAS in the genetic basis for Parkinson's disease
  2. Identify the nature and use of "-omic" approaches as tools for studying Parkinson's disease
  3. Understand what these "-omic" approaches have revealed that is new in Parkinson’s disease

Recorded: June 18, 2012 (15:45-17:45)

Session 2403: Is my movement disorder genetic and what does that mean for me and my family? (Skills Workshop)

Rachel Saunders-Pullman
New York, NY, USA

Katja Lohmann
Luebeck, Germany

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe how to take a detailed family history and draw an appropriate pedigree
  2. Interpret pedigrees with respect to different possible modes of inheritance
  3. Appreciate the important ethical issues and principles involved in genetic counseling

Recorded: June 18, 2012 (18:15-19:45)

Session 3207: Is Parkinson’s disease a mitochondrial or proteostatic disorder?

Chairs:
Gavin Davey
Dublin, Ireland
D. James Surmeier
Chicago, IL, USA

Oxidative stress and mitochondrial dysfunction in Parkinson’s disease
D. James Surmeier
Chicago, IL, USA

Proteostatic dysfunction in Parkinson’s disease
David Sulzer
New York, NY, USA

Crosstalk between mitochondria and the proteasome
J. Timothy Greenamyre
Pittsburgh, PA, USA

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe the origins of mitochondrial oxidant stress in Parkinson’s disease and how it might be mitigated
  2. Describe the role of proteostatic dysfunction in neuronal vulnerability in Parkinson's disease
  3. Describe how a combination of mitochondrial and proteostatic deficits might accelerate neuronal pathogenesis in Parkinson's disease

Recorded: June 19, 2012 (15:15-17:15)

Session 3309: Frontotemporal dementias and parkinsonism*

Chairs:
Hugh Harrington
Cork, Ireland
Ian Mackenzie
Vancouver, BC, Canada

New advances in FTD genetics
Bryan Traynor
Bethesda, MD, SUA

The molecular basis of FTD
Ian Mackenzie
Vancouver, BC, Canada

 

Clinical overlap of FTD and parkinsonism
Zbigniew Wszolek
Jacksonville, FL, USA

 

Learning Objectives
At the conclusion of this session, participants should be better able to:

  1. Describe the relation of mutation in the C90RF72 gene on chromosome 9 with the FTD, ALS and parkinsonian phenotypic presentations
  2. Describe the heterogeneous molecular basis of FTD
  3. Discuss the overlap between FTD and parkinsonian syndromes

Recorded: June 19, 2012 (15:15-17:15) | *Also available on the 16th International Congress Teaching Course DVD

Session 3508: Clinical clues and pearls in the recognition of the primary dystonias and dystonia plus syndromes: Genotype-Phenotype correlation (Video Session)

Chairs:
Marie Vidailhet
Paris, France
Susan Bressman
New York, NY, USA

Learning Objectives
At the conclusion of this session, participants should be better able to:

Recorded: June 19, 2012 (17:45-19:15)

  1. Understand the classification and genotype/phenotype of the primary dystonias and their classical presentations
  2. Describe the spectrum of movement disorders associated with dystonia-plus syndromes
  3. Discuss the most relevant differential diagnoses and initiate adequate genetic testing
Session 4404: How to interpret the mysteries of RNA and mitochondrial-mediated pathophysiology in movement disorders (Skills Workshop)

Peter Todd
Ann Arbor, MI, USA
Carolyn Sue
Sydney, Australia

Learning Objectives
At the conclusion of this session, participants should be better able to:

Recorded: June 20, 2012 (17:30-19:00)

  1. Describe the mechanisms and techniques used to elucidate the role of RNA in neurodegeneration
  2. Understand the range of movement disorders associated with mitochondrial disease
  3. Explain the techniques involved to determine mitochondrial dysfunction
 

 

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