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Wang WX, Rajeev BW, Stromberg AJ, Ren N, Tang G, Huang Q, Rigoutsos I, Nelson PT. The expression of microRNA miR-107 decreases early in Alzheimer's disease and may accelerate disease progression through regulation of beta-site amyloid precursor protein-cleaving enzyme 1. J Neurosci. 2008 Jan 30;28(5):1213-23. PubMed.
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Laval University
The role of miRNAs in fundamental biology and more recently in neurodegenerative disorders is gaining popularity (1). Now, Peter Nelson’s group provides the first evidence that changes in miRNA expression could contribute to Alzheimer disease development. These observations add to the recently published work on miRNAs in Parkinson disease (2).
Here, the authors performed miRNA microarray profiling and found miR-107 (and perhaps miR-103, which belongs to the same family) to be specifically decreased in “pre”-AD patients. For those who are not fully aware of miRNA literature, a decrease in miRNA levels would theoretically lead to increased protein expression. Interestingly, one of the candidate target genes for miR-107/103 is BACE1, and the authors show that, in vitro at least, miR-107 can indeed regulate BACE1 expression. While a follow-up study is now needed in a larger cohort of patients, these results support the hypothesis that changes in miRNA expression could be involved (perhaps early on) in sporadic AD development and that BACE1 can be regulated by miRNAs.
Overall, these results are in line with our own observations that we presented last year at the centennial meeting on AD in Tübingen, Germany, and the AD/PD conference in Salzburg, Austria. Now that an independent group has demonstrated similar findings, hopefully our work will soon be accepted for publication.
References:
Hébert SS, De Strooper B. Molecular biology. miRNAs in neurodegeneration. Science. 2007 Aug 31;317(5842):1179-80. PubMed.
Kim J, Inoue K, Ishii J, Vanti WB, Voronov SV, Murchison E, Hannon G, Abeliovich A. A MicroRNA feedback circuit in midbrain dopamine neurons. Science. 2007 Aug 31;317(5842):1220-4. PubMed.
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