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NEURINFDNA

Neuronal DNA double strand breaks as novel epigenetic actors: roles in cognition, health and neuro-inflammatory diseases

Total Cost €

0

EC-Contrib. €

0

Partnership

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 NEURINFDNA project word cloud

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

sometimes    chromatin    sensing    signals    function    mechanisms    epigenetic    perturbations    infection    involve    diseases    totally    dna    neurological    accompany    perspectives    toxoplasma    context    impairments    double    herpesviruses    modulation    persistent    expression    persist    cytokines    parasites    dysfunction    durable    innovative    unknown    opened    gene    proinflammatory    pathogen    constitute    alterations    epigenetics    course    deficits    host    central    strand    nervous    localization    repair    episomal    cns    breaks    genome    accumulating    date    cognitive    detecting    postulate    hijacking    infectious    showed    detection    always    structure    pathogens    epigenome    dsbs    prior    analyze    thereby    infections    secretion    impairment    manifested    generation    interaction    persistence    viral    whereby    immune    bornavirus    lasting    remodeling    apoptosis    neuronal    underlying    regulators    overt    neurodegenerative    cell    behavioral    underlie    alter   

Project "NEURINFDNA" data sheet

The following table provides information about the project.

Coordinator
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS 

Organization address
address: RUE MICHEL ANGE 3
city: PARIS
postcode: 75794
website: www.cnrs.fr

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 France [FR]
 Total cost 141˙848 €
 EC max contribution 141˙848 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2016
 Duration (year-month-day) from 2016-01-04   to  2018-01-03

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS FR (PARIS) coordinator 56˙032.00
2    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) participant 85˙816.00

Map

 Project objective

Cognitive deficits are manifested several years prior detecting any neuronal loss in neurodegenerative diseases or during persistent infections of the central nervous system (CNS). Accumulating evidence show that epigenetic alterations contribute to neuronal dysfunction, as they cause durable changes of the chromatin structure that affect gene expression. In this context, DNA double-strand breaks (DSBs) are now emerging as central regulators of neuronal epigenetics. My recent findings opened innovative perspectives of research. I showed that DSBs are not always associated with neuronal apoptosis, but rather constitute novel epigenetic signals that contribute to cognitive processes. To date, the role of DSBs in pathogen persistence and the mechanisms whereby DSBs affect neuronal function in the course of an infection are totally unknown. Here, we postulate that perturbations in sensing, production and/or repair of DSBs may underlie the behavioral impairment that is observed in many CNS infectious diseases. Persistent neuronal viral infections, such as Bornavirus or Herpesviruses alter neuronal function, sometimes without overt immune response. The underlying mechanisms may result from episomal persistence of the viral genome in interaction with neuronal chromatin, thereby hijacking the chromatin remodeling system of the host cell, or from the secretion of proinflammatory cytokines. Parasites such as Toxoplasma also persist in the CNS and cause behavioral impairment. Their long-lasting impact on neuronal function may involve the modulation of the epigenome. Here, we propose to analyze the role of DSBs in cognitive alterations that accompany neurological infectious diseases. In particular, we will: 1) characterize the role of pathogens and the associated immune response to neuronal localization of DSBs during CNS infections; 2) analyze which mechanisms of neuronal DSBs generation, detection and repair contribute to cognitive impairments in CNS infections.

 Publications

year authors and title journal last update
List of publications.
2018 Alexandre Bétourné, Marion Szelechowski, Anne Thouard, Erika Abrial, Arnaud Jean, Falek Zaidi, Charlotte Foret, Emilie M. Bonnaud, Caroline M. Charlier, Elsa Suberbielle, Cécile E. Malnou, Sylvie Granon, Claire Rampon, Daniel Gonzalez-Dunia
Hippocampal expression of a virus-derived protein impairs memory in mice
published pages: 1611-1616, ISSN: 0027-8424, DOI: 10.1073/pnas.1711977115
Proceedings of the National Academy of Sciences 115/7 2019-09-17

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