Cause or effect: misregulation of microRNA pathways in neurodegeneration
- Department of Neurology, University of Massachusetts Medical School, Worcester, MA, USA
During normal aging or neurodegenerative diseases, neuronal survival and function depend on protein homeostasis, which is regulated by multiple mechanisms, including the microRNA (miRNA) pathway. In different cells types, the absence of Dicer, a key miRNA processing enzyme, leads to neurodegeneration through cell-autonomous and non-cell-autonomous mechanisms. Loss of certain miRNAs also causes neurodegeneration in some model organisms. On the other hand, miRNA expression is misregulated in patients with different neurodegenerative diseases. Thus, the miRNA pathway appears to be essential in the pathogenesis of several age-dependent neurodegenerative conditions; however, our understanding of the underlying mechanism remains rudimentary. The precise causal relationships between specific miRNAs and neurodegeneration in humans need to be further investigated.
Keywords: Alzheimer’s disease, ALS, FTD, microRNAs, neurodegeneration, C9ORF72, CHMP2B, TDP-43
Citation: Gascon E and Gao F-B (2012) Cause or effect: misregulation of microRNA pathways in neurodegeneration. Front. Neurosci. 6:48. doi: 10.3389/fnins.2012.00048
Received: 13 February 2012; Paper pending published: 29 February 2012;
Accepted: 23 March 2012; Published online: 09 April 2012.
, Medical Research Council Laboratory of Molecular Biology, UK
, Cornell University Weill Medical College, USA Philip Wong
, Johns Hopkins University School of Medicine, USA
Copyright: © 2012 Gascon and Gao. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
*Correspondence: Eduardo Gascon and Fen-Biao Gao, Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01605, USA. e-mail: email@example.com; firstname.lastname@example.org