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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.

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

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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