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Cited by 339MicroRNA in disease regulationAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Patterns of microRNA expression in normal and early Alzheimer's disease human temporal cortex: white matter versus gray matter

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Wang, Wang-Xia, Huang, Qingwei, Hu, Yanling, Stromberg, Arnold J., Nelson, Peter T.·2011·Acta Neuropathologica
DOI 10.1007/s00401-010-0756-0PMC PMC3073518
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Abstract

MicroRNA (miRNA) expression was assessed in human cerebral cortical gray matter (GM) and white matter (WM) in order to provide the first insights into the difference between GM and WM miRNA repertoires across a range of Alzheimer's disease (AD) pathology. RNA was isolated separately from GM and WM portions of superior and middle temporal cerebral cortex (N = 10 elderly females, postmortem interval < 4 h). miRNA profiling experiments were performed using state-of-the-art Exiqon(©) LNA-microarrays. A subset of miRNAs that appeared to be strongly expressed according to the microarrays did not appear to be conventional miRNAs according to Northern blot analyses. Some well-characterized miRNAs were substantially enriched in WM as expected. However, most of the miRNA expression variability that correlated with the presence of early AD-related pathology was seen in GM. We confirm that downregulation of a set of miRNAs in GM (including several miR-15/107 genes and miR-29 paralogs) correlated strongly with the density of diffuse amyloid plaques detected in adjacent tissue. A few miRNAs were differentially expressed in WM, including miR-212 that is downregulated in AD and miR-424 which is upregulated in AD. The expression of certain miRNAs correlates with other miRNAs across different cases, and particular subsets of miRNAs are coordinately expressed in relation to AD-related pathology. These data support the hypothesis that patterns of miRNA expression in cortical GM may contribute to AD pathogenetically, because the aggregate change in miRNA expression observed early in the disease would be predicted to cause profound changes in gene expression.

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  • Multiple miRNAs are dysregulated in the affected regions of AD brains.

    “Recent miRNA profiling studies showed that multiple miRNAs are dysregulated in the affected regions of AD brains (Lau et al. 2013, Hebert et al. 2008, Wang et al. 2011, Delay et al. 2012, Cogswell et al. 2008, Lukiw 2007).”

    From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Wang et al. 2011

  • miR-186 level is decreased in the white matter of the temporal cortex in AD brain.

    “Interestingly, one report showed that miR-186 level is decreased in the white matter of the temporal cortex in AD brain (Wang et al. 2011).”

    From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Wang et al. 2011

    The Abstract reports that miR-212 is downregulated in AD white matter, but does not identify miR-186. Searches of the indexed Results and Discussion for miR-186 and decreased expression in white matter found no passage establishing the claimed change. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

  • miR-106b levels were significantly decreased in brains of AD cases and AD mouse model.

    “Interestingly, miR-106b levels were significantly decreased in brains of AD cases and AD mouse model (Hebert et al., 2009; Wang et al., 2011; Wang et al., 2009).”

    From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Wang et al., 2011

    The Results and Discussion describe downregulation of other miRNAs in human AD gray matter, but the passages found do not report decreased miR-106b. Searches for miR-106b and for decreased levels in an AD mouse model found no passage addressing either part of the claim. (LLM, conf=0.76)

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Research works printed but not linked: 32

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Authors
Wang, W.-X., Huang, Q., Hu, Y., Stromberg, A. J., & Nelson, P. T.
Affiliations
University of Kentucky (US)
Corresponding author
Nelson, Peter T.
ORCID
Venue
Acta Neuropathologica
Publisher
Springer Science and Business Media LLC
Published
2010-10-10
Volume
121
Issue
2
Pages
193-205
ISSN
  • 0001-6322 (ISSN-L)
  • 1432-0533
DOI
10.1007/s00401-010-0756-0
PMC
PMC3073518
OpenAlex
W2017129209
Cited by
339
References
6
Citations by year
2026: 3 · 2025: 12 · 2024: 11 · 2023: 10 · 2022: 16 · 2021: 34 · 2020: 30 · 2019: 23 · 2018: 24 · 2017: 27 · 2016: 33 · 2015: 26 · 2014: 28 · 2013: 32 · 2012: 16
FWCI
6.25
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Acta Neuropathologica (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • UKnowledge (University of Kentucky) (submittedVersion)
Funders
  • University of Kentucky
  • National Institute on Aging (P30AG028383, R21AG036875)
  • National Institute of Neurological Disorders and Stroke (R01NS061933, P01NS058484)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
microRNA expression, Alzheimer's disease, temporal cortex, gray matter, white matter, amyloid plaques, miR-212, miR-424, microRNA downregulation, postmortem brain, disease pathology
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Female, Humans, Nerve Fibers, Myelinated, Nerve Tissue, Postmortem Changes, Statistics as Topic, Temporal Lobe, Amyloid beta-Peptides, Neurofibrillary Tangles, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, MicroRNAs

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