Imperial College London
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ProfessorMagdalenaSastre

Faculty of Medicine, Department of Brain Sciences

Professor in Molecular Neuroscience
 
 
 
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Contact

 

+44 (0)20 7594 6673m.sastre

 
 
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Location

 

406Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Naseer:2022:10.3390/biom12101457,
author = {Naseer, S and Abelleira, Hervas L and Savani, D and De, Burgh R and Aleksynas, R and Donat, C and Syed, N and Sastre, M},
doi = {10.3390/biom12101457},
journal = {Biomolecules},
title = {Traumatic brain injury leads to alterations in contusional cortical miRNAs involved in dementia},
url = {http://dx.doi.org/10.3390/biom12101457},
volume = {12},
year = {2022}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - There is compelling evidence that head injury is a significant environmental risk factor for Alzheimer's disease (AD) and that a history of traumatic brain injury (TBI) accelerates the onset of AD. Amyloid-β plaques and tau aggregates have been observed in the post-mortem brains of TBI patients; however, the mechanisms leading to AD neuropathology in TBI are still unknown. In this study, we hypothesized that focal TBI induces changes in miRNA expression in and around affected areas, resulting in the altered expression of genes involved in neurodegeneration and AD pathology. For this purpose, we performed a miRNA array in extracts from rats subjected to experimental TBI, using the controlled cortical impact (CCI) model. In and around the contusion, we observed alterations of miRNAs associated with dementia/AD, compared to the contralateral side. Specifically, the expression of miR-9 was significantly upregulated, while miR-29b, miR-34a, miR-106b, miR-181a and miR-107 were downregulated. Via qPCR, we confirmed these results in an additional group of injured rats when compared to naïve animals. Interestingly, the changes in those miRNAs were concomitant with alterations in the gene expression of mRNAs involved in amyloid generation and tau pathology, such as β-APP cleaving enzyme (BACE1) and Glycogen synthase-3-β (GSK3β). In addition increased levels of neuroinflammatory markers (TNF-α), glial activation, neuronal loss, and tau phosphorylation were observed in pericontusional areas. Therefore, our results suggest that the secondary injury cascade in TBI affects miRNAs regulating the expression of genes involved in AD dementia.
AU  - Naseer,S
AU  - Abelleira,Hervas L
AU  - Savani,D
AU  - De,Burgh R
AU  - Aleksynas,R
AU  - Donat,C
AU  - Syed,N
AU  - Sastre,M
DO  - 10.3390/biom12101457
PY  - 2022///
SN  - 2218-273X
TI  - Traumatic brain injury leads to alterations in contusional cortical miRNAs involved in dementia
T2  - Biomolecules
UR  - http://dx.doi.org/10.3390/biom12101457
UR  - http://hdl.handle.net/10044/1/100793
VL  - 12
ER  -
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