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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 €


EC-Contrib. €






 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.

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Project "SweetBrain" data sheet

The following table provides information about the project.


Organization address
address: RAMAT AVIV
city: TEL AVIV
postcode: 69978

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


Take a look of project's partnership.

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


 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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