Understanding complex diseases such as sporadic Alzheimer disease (AD) has been 
a major challenge. Unlike the familial forms of AD, the genetic and 
environmental risks factors identified for sporadic AD are extensive. MicroRNAs 
are one of the major noncoding RNAs that function as negative regulators to 
silence or suppress gene expression via translational inhibition or message 
degradation. Their discovery has evoked great excitement in biomedical research 
for their promise as potential disease biomarkers and therapeutic targets. Key 
microRNAs have been identified as essential for a variety of cellular events 
including cell lineage determination, proliferation, apoptosis, DNA repair, and 
cytoskeletal organization; most, if not all, acting to fine-tune gene expression 
at the post-transcriptional level in a host of cellular signaling networks. 
Dysfunctional microRNA-mediated regulation has been implicated in the 
pathogenesis of many disease states. Here, the current understanding of the role 
of miRNAs in the central nervous system is reviewed with emphasis on their 
impact on the etiopathogenesis of sporadic AD.