MicroRNAs, small non-coding RNAs that regulate gene expression post-transcriptionally, have been shown to be deregulated in the development of Alzheimer's disease (AD), the major cause of dementia in the elderly. Nowadays implies a large health, social and economic burden with no effective disease-modifying therapy available. A deeper understanding of the events involved in early synaptic dysfunction in AD would provide the necessary insight to eventually identify new targets and develop novel therapeutic strategies.Transcriptomic analyses revealed that a factor involved in these deficits is the alteration of a gene transcriptional program dependent on the CREB-regulated transcription coactivator-1. Among the genes altered are the Nr4a nuclear orphan receptor family that has been linked to hippocampal synaptic plasticity. We observed that Nr4a2 levels are reduced in AD mice and in human brain at intermediate Braak pathological stages. We have recently identified alterations in miRNAs related to synaptic protein in AD brain and plasma samples that constitute a putative molecular signature that could be used as an early AD biomarker. Several miRNAs (miR-93-5p, miR132-3p and miR-204-5p) have been predicted to regulate Nr4a2 protein levels and we believe that changes in those miRNAs levels could be related to Nr4a2-mediated dysfunction of synaptic activity in AD.We analyzed levels of those miRNAs in different human AD brain areas (entorhinal cortex, hippocampus, prefrontal cortex, and cerebellum) and plasma samples. We only observed a decrease in miR-132-3p levels, indicating that those other are not involved in Nr4a2 deregulation observed both in AD mice and human brain samples.