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iMIND SIGNED

iPS-derived MIcroglia and Neuroinflammation in Dementia

Total Cost €

EC-Contrib. €

Partnership

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iMIND project word cloud

Explore the words cloud of the iMIND project. It provides you a very rough idea of what is the project "iMIND" about.

worldwide cutting throughput transmembrane plcg2 microglia biochemical p522a ipsc generate million neuroinflammation pluripotent encodes irreversible rare date ad calcium phospholipase revolves alzheimer characterization disease patient human gene closer modifying array mutation protective preclinical interestingly provides molecular screening grounds signaling editing cell animal experimental edge cas9 pathological rna imaging seq gwas reprogramming coding gamma transcriptomic lines ipscs enzyme therapeutic brain edited model enriched crispr underpinnings limitations innovative mutated stem functional neurodegenerative models cells explores people line isogenic shortcomings subcellular assays bypasses therapy framework

Project "iMIND" data sheet

The following table provides information about the project.

Coordinator	UNIVERSITA DEGLI STUDI GABRIELE D'ANNUNZIO DI CHIETI-PESCARA Organization address address: Via dei Vestini 31 city: CHIETI postcode: 66013 website: www.unich.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	Italy [IT]
Total cost	269˙002 €
EC max contribution	269˙002 € (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-GF
Starting year	2020
Duration (year-month-day)	from 2020-02-20 to 2023-02-19

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	UNIVERSITA DEGLI STUDI GABRIELE D'ANNUNZIO DI CHIETI-PESCARA UNIVERSITA DEGLI STUDI GABRIELE D'ANNUNZIO DI CHIETI-PESCARA Organization address address: Via dei Vestini 31 city: CHIETI postcode: 66013 website: www.unich.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	IT (CHIETI)	coordinator	269˙002.00
2	THE REGENTS OF THE UNIVERSITY OF CALIFORNIA THE REGENTS OF THE UNIVERSITY OF CALIFORNIA Organization address address: FRANKLIN STREET 1111, 12 FLOOR city: OAKLAND CA postcode: 94607 website: http://www.universityofcalifornia.edu/ contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	US (OAKLAND CA)	partner	0.00

Map

Project objective

Alzheimer’s disease (AD) is an irreversible neurodegenerative condition affecting 50 million people worldwide. To date, no disease modifying therapy for AD is available. Neuroinflammation is emerging as an important component of the disease. A recent GWAS analysis identified a rare protective coding mutation (P522A) in the PLCG2 (Phospholipase C Gamma 2) gene that is associated with AD. Interestingly, the gene encodes a transmembrane signaling enzyme that is highly enriched in microglia. The major aim of the proposal revolves around the functional characterization of the P522A mutation in microglia. To that aim, using an array of biochemical, imaging, functional, and transcriptomic assays, we will investigate human microglia generated from control- and AD patient-derived induced pluripotent stem cells (iPSCs). iPSCs will be gene-edited to generate P522A mutated isogenic cell lines. The proposal aims at identifying novel therapeutic targets and, in line with the objectives of the H2020 Framework Programme, explores new grounds in the molecular underpinnings of AD. The use of cutting-edge and innovative approaches (CRISPR/Cas9 gene editing, iPSC reprogramming, RNA-Seq analysis, high-throughput screening, and subcellular calcium imaging) provides a novel experimental model that is closer to the pathological processes of the AD brain and bypasses the limitations and shortcomings of preclinical AD animal models.

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The information about "IMIND" are provided by the European Opendata Portal: CORDIS opendata.