RTTOPHAGY SIGNED
"""Investigating autophagy enhancement as a therapeutic approach for the treatment of Rett syndrome."""
Total Cost €
0EC-Contrib. €
0Partnership
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0RTTOPHAGY project word cloud
Explore the words cloud of the RTTOPHAGY project. It provides you a very rough idea of what is the project "RTTOPHAGY" about.
Project "RTTOPHAGY" data sheet
The following table provides information about the project.
| Coordinator |
OSPEDALE SAN RAFFAELE SRL
Organization address contact info |
| Coordinator Country | Italy [IT] |
| Total cost | 171˙473 € |
| EC max contribution | 171˙473 € (100%) |
| Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
| Code Call | H2020-MSCA-IF-2018 |
| Funding Scheme | MSCA-IF-EF-SE |
| Starting year | 2019 |
| Duration (year-month-day) | from 2019-06-03 to 2021-06-16 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | OSPEDALE SAN RAFFAELE SRL | IT (MILANO) | coordinator | 171˙473.00 |
Map
Project objective
Intellectual disability (ID) is a generalized neurodevelopmental disorder characterized by deficits in mental abilities, social and motor skills. ID affects about 2-3% of the general population and it is mostly caused by a genetic lesion. Accordingly, mutations in the X-linked MECP2 cause Rett syndrome (RTT), a devastating neurological disorder that, because of its incidence (1:10000), represents the most common form of severe ID in girls worldwide with no approved cure. RTT profoundly affect the lives of affected individuals and their families and represent a considerable burden for health care providers across Europe. While the molecular pathways causing RTT remain mainly unknown, it is recognized that they ultimately lead to prominent alterations of synaptic transmission and neuronal activity. Autophagy is a catabolic process that sequesters aberrant organelles and macromolecules into autophagosomes and delivers it to lysosomes for degradation. Autophagy participates in a variety of events in neuronal cells including synaptic growth and neuronal activity, however, its possible involvement in neurodevelopmental disorders is still mainly neglected. In accordance with a recent study applied to human samples, my preliminary data suggest that autophagy is altered in RTT. By using cellular models of the disease, this project aim at characterize the therapeutic potential of restoring the autophagy pathway in RTT. (i) I will dissect the defective autophagy signaling cascade; (ii) identify target molecules that restore the neuronal dysfunction and synapses transmission; (iii) provide therapeutic targets to treat RTT and other nerudevepmental disorders with impaired autophagy function. My results have the potential to be translated into therapeutics. This research will contribute to provide new clinical targets against RTT. The Experienced Researcher will emerge from the project with new skills, and the capability to lead her own research group.
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