Do astrocytes store more fat when our brain gets older: a new target for dementia?

Award Number
216646/Z/19/Z
Status / Stage
Completed
Dates
8 July 2019 -
7 September 2019
Duration (calculated)
00 years 01 months
Funder(s)
Wellcome Trust
Funding Amount
£0.00
Contracted Centre
University of Nottingham
Principal Investigator
Mr Obinna Aniaku
WHO Catergories
Models of Disease
Understanding Underlying Disease
Disease Type
Vascular Dementia (VD)

CPEC Review Info
Reference ID293
ResearcherReside Team
Published12/06/2023

Data

Award Number216646/Z/19/Z
Status / StageCompleted
Start Date20190708
End Date20190907
Duration (calculated) 00 years 01 months
Contracted CentreUniversity of Nottingham
Funding Amount£0.00

Abstract

In this project, I will investigate the fate of lipid metabolism in astrocytes, the most abundant brain cells that form a physical bridge between neurons and blood vessels. Astrocytes are keys components of the brain as they control neurovascular coupling that serves to match local cerebral blood flow to regional neuronal energy use and ensures the normal functioning of the brain. When astrocytes react to pathological changes in vascular dementia (VD), they become reactive and form a scar that takes place without any obvious clinical symptoms. Recent studies suggested that both reactive astrocytes and lipid metabolism can be induced by hypoxia, a key feature of brain VD. However, no molecular links have been found between both processes. In this context, primary rat astrocyte will be incubated in either normoxia or hypoxia oxygen environment induce reactive astrocytes and changes in lipid metabolism. We will use immunocytochemistry and BODIPY fluorophore to detect changes in astrocytes as well as lipid droplet (LD) formation. 13C magnetic resonance spectroscopy (13C-MRS) will be applied to measure fat oxidation in the same conditions. 13C-NMR will be quantitatively correlated to LD formation and reactive astrocytes.