MechAggrenamicsProject reference: 322034
Funded under :
Mechanisms of cell dysfunction by aggregation dynamics of polyQ-containing proteins
Total cost:EUR 100 000
EU contribution:EUR 100 000
Call for proposal:FP7-PEOPLE-2012-CIGSee other projects for this call
Funding scheme:MC-CIG - Support for training and career development of researcher (CIG)
Protein aggregation is a hallmark of several ageing-related neurodegenerative diseases, such as Huntington’s disease (HD), Alzheimer’s disease and prion-mediated diseases. Different cellular pathways influence the rate of aggregation, and clearance of intermediate protein species and aggregates in the cell (for example, autophagy or proteasomal degradation). Many signalling pathways regulate these processes. These signalling events, and the molecular pathways downstream are not completely understood. In HD there is an inverse correlation between the number of CAG triplets found in mutated huntingtin (htt) and the age-of-onset of the symptoms. However, there is a wide variation in the age-at-onset of the disease among carriers of short mutant glutamine tracts, suggesting that the genetic background strongly influences the severity of the disease. Hence the broad objective of this proposal is to find molecules that modulate protein aggregation.
We will use in vivo (C. elegans) and in vitro (mammalian cells) models of HD to find new molecules and pathways that modulate aggregation and toxicity induced by polyglutamines. The second objective of this proposal is to understand the mechanism by which mHtt toxic species alter cellular processes, with special focus on pre-synaptic function.
EU contribution: EUR 100 000
AVENIDA CAMPANAR 21