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NeuroFreezing SIGNED

Biophysical Properties of the Neuronal Cytosol and their Dynamics upon Nutrient Starvation, Aging, and in Neurodegenerative Diseases.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 NeuroFreezing project word cloud

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

neurodegenerative    h1    influence    biochemistry    cytosolic    polyq    discovered    protein    density    glucose    homogeneous    environmental    poorly    huntington    induce    stable    diseases    regulate    diffusive    alter    differences    mouse    inducing    fundamentally    sufficient    despite    ultimately    therapeutic    proteins    cytosol    aged    critical    first    aging    polyglutamine    nutrient    cell    investigation    actively    types    crowding    strategies    yeast    material    trigger    model    deprived    regulated    biophysics    techniques    regulating    separations    aggregation    biophysical    expertise    disease    viscosity    disorders    cells    intracellular    dynamic    potentially    rates    hd    description    combining    metabolism    neurobiology    mammalian    h2    starvation    shifting    neurons    neuronal    inherited    molecular    reveal    stress    exhibit    hypotheses    stresses    decrease    interactions    transport    unclear    paradigm    hallmark    volume   

Project "NeuroFreezing" data sheet

The following table provides information about the project.

Coordinator
EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH 

Organization address
address: Raemistrasse 101
city: ZUERICH
postcode: 8092
website: https://www.ethz.ch/de.html

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 Switzerland [CH]
 Total cost 203˙149 €
 EC max contribution 203˙149 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-06-01   to  2021-11-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH CH (ZUERICH) coordinator 203˙149.00

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 Project objective

The material properties of the cytosol control the biochemistry of the cell and influence all molecular interactions by regulating rates of intracellular diffusive transport. Despite this critical role, these properties remain poorly understood, and it is unclear to what extent the cytosol is homogeneous, whether there are differences between cell types, and if these properties are stable or dynamic. It has recently been discovered that yeast cells regulate their cytosolic properties in response to stress, namely glucose-starvation and aging. These stresses result in a decrease in cell volume and an increase in cytosolic crowding, inducing widespread phase separations and aggregation of polyglutamine (polyQ)-proteins. This type of polyQ-protein aggregation is the molecular hallmark of neurodegenerative diseases like Huntington's Disease (HD), and is very poorly understood. In this project, I will produce the first description of the biophysical properties of the neuronal cytosol, and I will directly test whether aged or nutrient-deprived neurons, or neurons from an HD mouse model exhibit changes in these properties. I propose that viscosity and density of mammalian cells, and in particular neuronal cells, are dynamic properties that can be actively regulated in response to environmental changes. In particular, I will test two hypotheses: - H1: Nutrient starvation and aging induce changes to the material properties of the neuronal cytosol. - H2: A neuronal stress-response upon starvation or aging is sufficient to trigger aggregation of polyQ-proteins. Combining state-of-the-art techniques and expertise in the fields of neurobiology, metabolism, and biophysics, my investigation of these novel and potentially paradigm shifting hypotheses could fundamentally alter our understanding of the material properties of the neuronal cytosol, and ultimately reveal new therapeutic strategies for the most common inherited neurodegenerative disorders.

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The information about "NEUROFREEZING" are provided by the European Opendata Portal: CORDIS opendata.

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