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Alterations of the microRNA network cause neurodegenerative disease
Abstract
Brain development crucially depends on the integrity of microRNA (miRNA) pathways, which function at the post-transcriptional level as a rheostat of the transcriptome and proteome of the cell. miRNAs are also involved in many other, more specific, aspects of neuronal function such as neurite outgrowth and synapse formation. Complete loss of miRNA expression in the brain leads to neurodegeneration in several animal models. Evidence from patient material is emerging that miRNA dysregulation could, indeed, contribute to neurodegenerative disorders. The translation of proteins previously implicated in familial forms of disease seems to be under control of miRNAs, and changes in miRNAs might explain how these proteins become affected in sporadic neurodegenerative disease. Thus, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributors to neurodegenerative disorder.
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“In previous study, miR-106b significantly decreased APP levels in HeLa cervical cancer cell line (Hebert et al., 2009).”
From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Hebert et al., 2009
In the citing paper
“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 Hebert et al., 2009
In the citing paper
“Most interestingly, APP is another miR-106b target gene.”
From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Hebert et al., 2009
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RetractedMisiorek, J. O., Schreiber, A. M., Urbanek-Trzeciak, M. O., Jazurek, M., Hauser, L. A., Lynch, D. R., Napierala, J. S., & Напиерала, М. (2020) · Molecular Neurobiology · doi:10.1007/s12035-020-01899-1 · Cited by 20
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Kurzyńska‐Kokorniak, A., Koralewska, N., Tyczewska, A., Twardowski, T., & Figlerowicz, M. (2013) · PLoS ONE · doi:10.1371/journal.pone.0077703 · Cited by 20
Metadata
- Authors
- Hébert, S. S., & De Strooper, B.
- Affiliations
- Vlaams Instituut voor Biotechnologie (BE)
- ORCID
- Hébert, Sébastien S.
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 32
- Issue
- 4
- Pages
- 199-206
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W2041945875
- Cited by
- 452
- References
- 94
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 10 · 2023: 16 · 2022: 18 · 2021: 17 · 2020: 26 · 2019: 26 · 2018: 26 · 2017: 19 · 2016: 37 · 2015: 38 · 2014: 26 · 2013: 39 · 2012: 33
- FWCI
- 2.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Lirias (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- microRNA, neurodegenerative diseases, microRNA dysregulation, post-transcriptional regulation, neuronal development, neurite outgrowth, synaptogenesis, familial neurodegenerative disease
- MeSH terms
- Animals, Humans, Models, Biological, Neurodegenerative Diseases, MicroRNAs, Gene Regulatory Networks
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