iNtoPoreAge SIGNED
Assessing transcriptional and nuclear pore aging in age-equivalent and rejuvenated induced neurons from Alzheimer patients
Total Cost €
0EC-Contrib. €
0Partnership
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0iNtoPoreAge project word cloud
Explore the words cloud of the iNtoPoreAge project. It provides you a very rough idea of what is the project "iNtoPoreAge" about.
Project "iNtoPoreAge" data sheet
The following table provides information about the project.
| Coordinator |
UNIVERSITAET INNSBRUCK
Organization address contact info |
| Coordinator Country | Austria [AT] |
| Total cost | 178˙156 € |
| EC max contribution | 178˙156 € (100%) |
| Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
| Code Call | H2020-MSCA-IF-2017 |
| Funding Scheme | MSCA-IF-EF-RI |
| Starting year | 2019 |
| Duration (year-month-day) | from 2019-08-01 to 2021-07-31 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | UNIVERSITAET INNSBRUCK | AT (INNSBRUCK) | coordinator | 178˙156.00 |
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Project objective
I am a stem cell biologist specialized on modeling human neurodegenerative diseases. During my PhD with Dr. O. Brüstle (University of Bonn), I was trained in human stem cell and reprogramming technologies working on human models for Alzheimer’s Disease (AD). As a postdoc at the Salk Institute with Dr. F. H. Gage, I acquired and strong foundation in functional neuroscience, nuclear pore biology and systems biology/bioinformatics. My work helped to better understand complex neuropsychiatric disorders, as well as the process of neuronal aging. I could show that direct conversion of human fibroblasts into induced neurons (iN) preserves signatures of cell aging, while iPSC reprogramming erases them. To start my own independent lab, I have accepted a tenure track position at the University of Innsbruck. As an independent scientist, I seek to bring together my recent findings on reprogramming and aging, my permanent interest in AD, and powerful systems biology and bioinformatics to unravel the age-dependent disease-initiating mechanisms of sporadic AD. In this proposal, I, together with my supervisor Prof. Dr. Frank Edenhofer, designed a dedicated research and training plan. In the first aim of the project, I will generate phenotypically old (iN) and rejuvenated (iPSC) neurons from an established set of well-characterized AD patients and controls. Using unbiased transcriptome approaches, the data will help to better understand the impact of neuronal aging on sporadic AD pathogenesis. In a second aim, I will use live-cell imaging approaches to study the age-related dysregulation of nucleo-cytoplasmic transport. The goal is to better understand how cellular aging affects pathogenesis, in order to pinpoint the earliest and potentially most treatable mechanisms involved in AD. This award will enable my research in Innsbruck and give me protected time to successfully complete the proposed research, which is vital for establishing myself as an independent researcher in Europe.
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