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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.

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

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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lastchecktime (2022-05-23 21:30:36) correctly updated