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CTS-TEs-ADprogress SIGNED

Cell type-specific molecular analysis of epigenetic changes and transposable element derepression in Alzheimer's disease progression

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 CTS-TEs-ADprogress project word cloud

Explore the words cloud of the CTS-TEs-ADprogress project. It provides you a very rough idea of what is the project "CTS-TEs-ADprogress" about.

point    limited    recapitulates    burden    preclinical    run    epigenetic    rna    symptoms    hallmarks    thereby    plaques    pathology    molecular    patients    diagnosed    dysregulation    mouse    death    epigenome    atac    healthcare    imperative    mutations    heterochromatin    bulk    plays    expression    samples    environmental    linked    beta    translating    single    model    transposable    critical    seq    impairment    drivers    alterations    occurred    suggesting    once    survival    resolution    app    neurodegeneration    subtypes    contributor    memory    shown    stage    limitations    hippocampal    age    chromatin    influencing    pathological    cut    decades    cell    alzheimer    progression    lack    tissue    ps1    disease    inhibit    treatments    symptom    transposition    coverage    onset    stress    evident    human    neuronal    mice    te    underlying    mechanisms    chronic    signals    population    isolated    structure    regulatory    insertional    ad    neuron    either    few    correlating    cellular    usually    aging    worldwide    gene   

Project "CTS-TEs-ADprogress" data sheet

The following table provides information about the project.

Coordinator
DEUTSCHES ZENTRUM FUR NEURODEGENERATIVE ERKRANKUNGEN EV 

Organization address
address: SIGMUND FREUD STRASSE 27
city: BONN
postcode: 53127
website: www.dzne.de

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 Germany [DE]
 Total cost 174˙806 €
 EC max contribution 174˙806 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2022-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    DEUTSCHES ZENTRUM FUR NEURODEGENERATIVE ERKRANKUNGEN EV DE (BONN) coordinator 174˙806.00

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 Project objective

Alzheimer’s disease (AD) is a major contributor to disease burden and healthcare costs worldwide. AD is usually diagnosed once symptoms like memory impairment become evident. However, at this point typical AD pathology such as Aβ plaques and cell death is already widespread, suggesting that molecular changes have occurred decades before symptom onset. With an increasingly aging population and no available treatments, it has become imperative to identify the molecular mechanisms underlying onset and progression of AD. Chronic environmental stress and age-associated changes in stress response have been associated as drivers of AD pathology. The epigenome plays a critical role in translating stress signals into a cellular response by influencing gene expression, which can either promote or inhibit cell survival. Several studies have shown that alterations in chromatin structure, including heterochromatin loss, and associated changes in gene expression contribute to neurodegeneration. In addition, neuronal death was also linked to transposable element (TE) dysregulation due to epigenetic changes, which can lead to changes in gene expression and insertional mutations due to transposition. However, our understanding of epigenetic changes at onset and during progression of AD pathology is very limited, as current studies have two major limitations: 1) lack of cell type resolution due to use of bulk tissue samples and 2) coverage of only few or only one disease stage. Here, single-cell RNA-seq and ATAC-seq as well as CUT&RUN on isolated hippocampal neuron subtypes will be used to identify cell type-specific alterations of gene expression and gene regulatory mechanisms during onset and progression of AD pathology in the APP/PS1 mouse model. APP/PS1 mice are a well-established AD model, which recapitulates many characteristics of preclinical AD in human patients and thereby allows correlating the identified changes with the development of specific pathological hallmarks.

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