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The Expression of MicroRNA miR-107 Decreases Early in Alzheimer's Disease and May Accelerate Disease Progression through Regulation of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1

Wang, Wang-Xia, Rajeev, Bernard W., Stromberg, Arnold J., Ren, Na, Tang, Guiliang, Huang, Qingwei, Rigoutsos, Isidore, Nelson, Peter T.·2008·The Journal of Neuroscience
DOI 10.1523/jneurosci.5065-07.2008
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Abstract

MicroRNAs (miRNAs) are small regulatory RNAs that participate in posttranscriptional gene regulation in a sequence-specific manner. However, little is understood about the role(s) of miRNAs in Alzheimer's disease (AD). We used miRNA expression microarrays on RNA extracted from human brain tissue from the University of Kentucky Alzheimer's Disease Center Brain Bank with near-optimal clinicopathological correlation. Cases were separated into four groups: elderly nondemented with negligible AD-type pathology, nondemented with incipient AD pathology, mild cognitive impairment (MCI) with moderate AD pathology, and AD. Among the AD-related miRNA expression changes, miR-107 was exceptional because miR-107 levels decreased significantly even in patients with the earliest stages of pathology. In situ hybridization with cross-comparison to neuropathology demonstrated that particular cerebral cortical laminas involved by AD pathology exhibit diminished neuronal miR-107 expression. Computational analysis predicted that the 3′-untranslated region (UTR) of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) mRNA is targeted multiply by miR-107. From the same RNA material analyzed on miRNA microarrays, mRNA expression profiling was performed using Affymetrix Exon Array microarrays on nondemented, MCI, and AD patients. BACE1 mRNA levels tended to increase as miR-107 levels decreased in the progression of AD. Cell culture reporter assays performed with a subset of the predicted miR-107 binding sites indicate the presence of at least one physiological miR-107 miRNA recognition sequence in the 3′-UTR of BACE1 mRNA. Together, the coordinated application of miRNA profiling, Affymetrix microarrays, new bioinformatics predictions, in situ hybridization, and biochemical validation indicate that miR-107 may be involved in accelerated disease progression through regulation of BACE1.

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  • miR-107 is downregulated in AD and MCI compared to nondemented with no/negligible AD-type pathology.

    “Among the four groups, miR-107 was downregulated in AD and MCI compared to nondemented with no/negligible AD-type pathology [61]”

    From MicroRNAs in Extracellular Vesicles of Alzheimer’s Disease (2023) · cites this paper as [61]

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Metadata

Authors
Wang, W.-X., Rajeev, B. W., Stromberg, A. J., Ren, N., Tang, G., Huang, Q., Rigoutsos, I., & Nelson, P. T.
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
2008-01-30
Volume
28
Issue
5
Pages
1213-1223
ISSN
  • 0270-6474
  • 1529-2401
DOI
10.1523/jneurosci.5065-07.2008
Cited by
701
References
8
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 182 d)

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