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SweetBrain SIGNED

A new perspective on the metabolic pathway to neuronal dysfunction: Using organs on a chip to elucidate the role of the brain microvasculature

Total Cost €

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EC-Contrib. €

0

Partnership

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 SweetBrain project word cloud

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

function    drives    despite    hypothesis    mechanisms    regarding    unconsidered    communications    separately    perspective    central    revolutionize    disease    nervous    treatment    limitations    coupling    interactions    neurovascular    direct    diseases    grow    crosstalk    homeostasis    remaining    capacity    primarily    neurodegeneration    hyperglycemia    suggest    revealed    underpinnings    little    mainly    neuronal    physiology    endothelium    human    scarcity    functionally    thereby    overcomes    gatekeeper    hypothesize    elucidate    nvu    neurodegenerative    brain    chip    glucose    cns    cure    vein    coupled    observations    metabolic    metabolism    metabolites    drawing    decades    unexplored    previously    altering    clear    levels    fundamental    cell    illuminating    metabolically    populations    organ    subsequently    correlated    modeling    neurons    questions    pass    vasculature    diabetic    diminish    functional    relationship    edge    ignoring    types    pointing    model    cutting    dysfunction    elusive    models    ooc    astrocytes   

Project "SweetBrain" data sheet

The following table provides information about the project.

Coordinator
TEL AVIV UNIVERSITY 

Organization address
address: RAMAT AVIV
city: TEL AVIV
postcode: 69978
website: http://www.tau.ac.il/

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 Israel [IL]
 Total cost 1˙487˙438 €
 EC max contribution 1˙487˙438 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-STG
 Funding Scheme ERC-STG
 Starting year 2020
 Duration (year-month-day) from 2020-07-01   to  2025-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    TEL AVIV UNIVERSITY IL (TEL AVIV) coordinator 1˙487˙438.00

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 Project objective

Despite decades of research, the underpinnings of central nervous system (CNS) diseases and clear pathways to effective treatment remain elusive, mainly because of a scarcity of adequate models and methods with the capacity to elucidate human brain physiology. Recent studies suggest that high glucose levels are correlated with neuronal dysfunction and neurodegeneration, yet very little is known about the mechanisms of this relationship. Research in this vein has focused primarily on direct metabolic interactions between neurons and astrocytes, ignoring other cell populations in the neurovascular unit (NVU) that might have a meaningful role. My recent research revealed that the brain vasculature—the ‘gatekeeper’ through which all metabolites must pass to reach the neurons—has direct metabolic coupling with the neurons. Drawing from these observations, I adopt a previously unconsidered perspective and propose that the vasculature drives the neurodegenerative effects of hyperglycemia. Specifically, I hypothesize that high glucose levels change the metabolic function of the brain vasculature, thereby altering the direct endothelium-neuronal crosstalk and triggering neuronal dysfunction. To investigate this hypothesis, I will develop cutting-edge Organ-on-a-Chip (OoC) technology that overcomes the limitations of modeling NVU functionality and cell-cell interactions. Specifically, I will: (1) establish a human-relevant NVU-OoC model for metabolic and functional interactions, in which different cell types grow separately while remaining metabolically and functionally coupled; (2) identify the major metabolic and functional interactions in the human NVU at homeostasis and under diabetic conditions; and subsequently (3) target the vasculature communications to diminish neuronal dysfunction. This research has the potential to revolutionize the study of CNS disease, pointing to an unexplored pathway to a cure, and illuminating fundamental questions regarding brain metabolism.

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

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