Imperial College London

ProfessorMagdalenaSastre

Faculty of MedicineDepartment of Brain Sciences

Professor in Molecular Neuroscience
 
 
 
//

Contact

 

+44 (0)20 7594 6673m.sastre

 
 
//

Location

 

406Burlington DanesHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Katsouri:2020:10.1002/glia.23759,
author = {Katsouri, L and Birch, A and Renziehausen, A and Zach, C and Aman, Y and Steeds, H and Bonsu, A and palmer, E and Mirzaei, N and Ries, M and Sastre, M},
doi = {10.1002/glia.23759},
journal = {Glia},
pages = {1017--1030},
title = {Ablation of reactive astrocytes exacerbates disease pathology in a model of Alzheimer’s disease},
url = {http://dx.doi.org/10.1002/glia.23759},
volume = {68},
year = {2020}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - The role of astrocytes in the progression of Alzheimer’s disease (AD) remains poorly understood. We assessed the consequences of ablating astrocytic proliferation in 9 months old double transgenic APP23/GFAP-TK mice. Treatment of these mice with the antiviral agent ganciclovir conditionally ablates proliferating reactive astrocytes. The loss of proliferating astrocytes resulted in significantly increased levels of monomeric amyloid-β (Aβ) in brain homogenates, associated with reduced enzymatic degradation and clearance mechanisms. In addition, our data revealed exacerbated memory deficits in mice lacking proliferating astrocytes concomitant with decreased levels of synaptic markers and higher expression of pro-inflammatory cytokines. Our data suggest that loss of reactive astrocytes in AD aggravates amyloid pathology and memory loss, possibly via disruption of amyloid clearance and enhanced neuroinflammation.
AU - Katsouri,L
AU - Birch,A
AU - Renziehausen,A
AU - Zach,C
AU - Aman,Y
AU - Steeds,H
AU - Bonsu,A
AU - palmer,E
AU - Mirzaei,N
AU - Ries,M
AU - Sastre,M
DO - 10.1002/glia.23759
EP - 1030
PY - 2020///
SN - 0894-1491
SP - 1017
TI - Ablation of reactive astrocytes exacerbates disease pathology in a model of Alzheimer’s disease
T2 - Glia
UR - http://dx.doi.org/10.1002/glia.23759
UR - https://onlinelibrary.wiley.com/doi/full/10.1002/glia.23759
UR - http://hdl.handle.net/10044/1/75381
VL - 68
ER -