Museu da Ci�ncia - Universidade de Coimbra


Protein aggregation is a hallmark of many late onset neurodegenerative disorders including Parkinson’s Disease (PD), Alzheimer’s Disease (AD), amylotrophic lateral sclerosis (ALS), prion diseases as well as the group of polyglutamine diseases (polyQ). The aim of this project was to create a network of European partners bridging important basic mechanisms involved in proteinopathies, research of model diseases and treatment approaches.

The “TreatPolyQ” european network focuses on two main representatives of the polyQ diseases: Huntington’s disease as the most common polyQ disease as well as spinocerebellar ataxia type 3 (SCA3) as the most frequent autosomal-dominantly inherited ataxia. Patients suffer from a multitude of neurological symptoms including movement abnormalities with late onset and in a progressive manner. Up to now, no treatment or cure is available.


Aaron Ciechanover | 11H30

Nobel Prize in Chemistry in 2004, Technion, Israel Institute of Technology

The Ubiquitin Proteolytic System – From Basic Mechanisms through Human Diseases and into Drug Targeting


Richard Morimoto| 11H30

Bill and Gayle Cook Professor of Biology, Department of Molecular Biosciences, Northwestern University, EUA

Proteostasis Networks and Stress Responses in Aging and Neurodegenerative Disease

Thorsten Schmidt | 14H15 

University of Tuebingen, Germany

Targeting the intracellular localization of Ataxin-3 as treatment strategy for SCA3 

Henry Paulson | 15H00

Department of Neurology, University of Michigan, EUA

Ubiquitin signaling pathways in neurodegeneration: insights from polyglutamine disorders


Nico Dantuma | 9H00

Karolinska Institut, Sweden

Critical roles for neurodegeneration-associated proteins in the DNA damage response

Ronald Melki | 9H30

Laboratory of Enzymology and Structural Biochemistry - CNRS, France

Prion-like propagation of protein assemblies in neurodegenerative diseases  

Angeleen Fleming | 10H00

Cambridge Institute for Medical Research, United Kingdom

Using zebrafish as a model to understand the role of autophagy in neurodegeneration

David Lowe | 11H00

The Interplay of Therapeutics and Diagnostics for Huntington’s Disease

Luís Pereira de Almeida | 11H30

CNC – Center for Neurosciences and Cell Biology, University of Coimbra, Portugal

Machado-Joseph disease: from gene silencing to protein clearance

Gillian Bates | 12H00

Kings College of London, UK

Insights into the molecular basis of Huntington’s disease and the validation of therapeutic targets

Hervé Tricoire | 14H30

Université Paris-Diderot

Time controlled and tissue specific Drosophila models of human neurodegenerative diseases

Angela Cenci-Nilsson | 15H00

Lund University, Sweden

Molecular and structural abnormalities of striatal projection neurons in Parkinson´s and Huntington´s disease

Karina Fog | 15H30

H. Lundbeck, Denmark

Immunotherapy with alpha-synuclein specific antibodies

End of the Meeting – Final Remarks | 16H00


- Entrada livre

- Conferências proferidas em inglês, sem tradução


ORGANIZAÇÃO                                             APOIO