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CTS-TEs-ADprogress

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Cell type specific molecular analysis of epigenetic changes and transposable ele...

Cell type specific molecular analysis of epigenetic changes and transposable element derepression in Alzheimer s disease progression 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... ver más

24/08/2023

BUNDESMINISTERIUM...

175K€

Presupuesto del proyecto: 175K€

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BUNDESMINISTERIUM FUER GESUNDHEIT No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2023-08-24

MSCA-IF-2019: Individual Fellowships Objective:The goal of the Individual Fellowships is to enhance the creative and innovative potential...

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BUNDESMINISTERIUM FUER GESUN...

174.81K€ | Lider

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Duración del proyecto: 42 meses Fecha Inicio: 2020-02-24
Fecha Fin: 2023-08-24

Líder del proyecto

BUNDESMINISTERIUM FUER GESUNDHEIT No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 175K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto 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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