Table 1.

AD-like pathology-related miRNAs identified in this study and previously associated with AD.

This study			Previous studies
miRNA	Sample	Lower/Higher	Sample	Lower/Higher	References	Target
miR-132	Plasma of 3xTg-AD and WT mice of 2–3 and 14–15 months	−	AD brain	−	Cogswell et al., 2008	p250-GAP
			AD neocortex	−	Hébert et al., 2013
			AD CSF	−	Burgos et al., 2014
miR-138		−	AD CSF	−	Burgos et al., 2014	APT1
miR-139		−	AD CSF	−	Burgos et al., 2014
miR-146a		−	AD CSF/plasma	−	Kiko et al., 2014	IRAK-1 TRAF6
			AD CFS	−	Müller et al., 2014
			AD hippocampus	±
miR-146b		−	AD CSF	−	Cogswell et al., 2008
			AD brain	−
miR-29a		−	AD cortex	−	Hébert et al., 2008	BACE1
			AD serum	−	Geekiyanage et al., 2011
			AD CSF	+	Kiko et al., 2014
miR-29c		−	AD cortex	−	Hébert et al., 2008

The table contains data obtained from this study (left) and collected from others (right). It indicates the miRNA, the sample used for determination, the abundance respect to the control cases and the reference of the other studies. It also contains the mRNA-target for the miRNA: p250-GAP, a brain-enriched GTPase-activating protein for Rho Family GTPases involved in the N-Methyl-d-aspartate receptor (NMDAR) signaling; APT1, acyl protein thioesterase 1, an enzyme regulating the palmitoylation status of proteins that are known to function at the synapse; IRAK1, interleukin-1 receptor-associated kinase 1, a kinase that associates with the interleukin-1 receptor upon stimulation which is responsible for interleukin-1 transcription of NFkB; TRAF6, TNF receptor associated factor 6 involved in the regulation of inflammation response and apoptosis; BACE1, β-secretase, a protease that cleaves the APP in the β site to produce the Aβ peptide in the amyloidogenic APP processing.