Transcript The example of Parkinson disease

Research on Parkinson diseases in Europe
Parkinson’s disease (PD) is one of the most common chronic progressive
neurodegenerative diseases. PD has a prevalence of 1.2 million people in
Europe and an annual cost of 11 billion Euros, being one of the 12 most
costly brain diseases in Europe.
What do we ask to research?
A strong translational character:
Understanding the brain functioning at molecular, cellular and system
level is essential to unravel pathogenesis of brain diseases.
How to impact on disease onset and progression, to effectively
help those citizens leaving with PD
Consensus document on brain research,
J. Olesen, M Baker, T Freund, M Di Luca, J Mendlewicz, I Regan, M Westphal - EBC - J Neurol Neurosurg Psychiatry
2006
The needs
Key points still need to be addressed and require intense research effort.
REPLACES will handle the following issues:
1.Development of novel and appropriate chronic animal models for basic
research, where to address the study of brain plasticity in corticostriatal pathways.
2.Identification of changes in low abundance proteins and characterization of their
functions based on protein-protein interactions and the application of advanced
proteomic methodologies.
3.Identification of therapeutic proteins as well as targets for drug
intervention. In particular, the possible role of factors in the pathophysiology of
PD, and their potential role in its treatment, will be further explored.
REPLACES
will study a new aspect of pathogenesis of Parkinson Disease
that is the interplay between two transmitters in the brain:
dopamine and glutamate
Specific objectives are:
1.Characterization of the pathological
mechanisms underlying altered synaptic
function in experimental animal models
and in PD patients.
3. Restorative approaches for synaptic
alterations in PD animal models.
REPLACES
The study of the synaptic changes occurring in an experimental model of
Parkinson Disease is of critical importance in order to develop therapeutic
strategies to prevent neuronal death and to restore physiological
synaptic function at corticostriatal synapses where glutamate and dopamine
interplay.