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Published in: Translational Neurodegeneration 1/2019

Open Access 01-12-2019 | Alzheimer's Disease | Research

Lower serum expression of miR-181c-5p is associated with increased plasma levels of amyloid-beta 1–40 and cerebral vulnerability in normal aging

Authors: Marta Manzano-Crespo, Mercedes Atienza, Jose L. Cantero

Published in: Translational Neurodegeneration | Issue 1/2019

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Abstract

Background

Previous studies have shown that expression levels of miR-181c are downregulated by amyloid-β (Aβ) deposition and chronic cerebral hypoperfusion, both factors largely associated with the development of AD. Moreover, reduced 2-[18F]fluoro-2-deoxy-D-glucose (FDG)-PET brain metabolism and volume loss of regions of the medial temporal lobe have been generally recognized as hallmarks of AD. Based on this evidence, we have here investigated potential associations between serum levels of miR-181c-5p and these AD signatures in asymptomatic elderly subjects.

Methods

Ninety-five normal elderly subjects underwent clinical, cognitive, structural MRI, and FDG-PET explorations. Serum expression levels of miR-181c-5p and plasma Aβ concentrations were further analyzed in this cohort. Regression analyses were performed to assess associations between serum miR-181c-5p levels and cognitive functioning, plasma Aβ, structural and metabolic brain changes.

Results

Decreased serum expression of miR-181c-5p was associated with increased plasma levels of Aβ1–40, deficits in cortical glucose metabolism, and volume reduction of the entorhinal cortex. No significant associations were found between lower miR-181c-5p levels and cognitive deficits or cortical thinning.

Conclusions

These findings suggest that deregulation of serum miR-181c-5p may indicate cerebral vulnerability in late life.
Appendix
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Metadata
Title
Lower serum expression of miR-181c-5p is associated with increased plasma levels of amyloid-beta 1–40 and cerebral vulnerability in normal aging
Authors
Marta Manzano-Crespo
Mercedes Atienza
Jose L. Cantero
Publication date
01-12-2019
Publisher
BioMed Central
Published in
Translational Neurodegeneration / Issue 1/2019
Electronic ISSN: 2047-9158
DOI
https://doi.org/10.1186/s40035-019-0174-8

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