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Long non-coding RNAs in Huntington's disease neurodegeneration
Johnson R.. Neurobiology of disease, 2011-12-14
Topic: Genetics and APOE
Neurodegeneration in the brains of Huntington's disease patients is accompanied by widespread changes in gene regulatory networks. Recent studies have found that these changes are not restricted to protein-coding genes, but also include non-coding RNAs (ncRNAs). One particularly abundant but poorly understood class of ncRNAs is the long non-coding RNAs (lncRNAs), of which at least ten thousand have been identified in the human genome. Although we presently know little about their function, lncRNAs are widely expressed in the mammalian nervous system, and many are likely to play critical roles in neuronal development and activity. LncRNAs are now being implicated in neurodegenerative processes, including Alzheimer's (AD) and Huntington's disease (HD). In the present study, I discuss the potential significance of lncRNAs in HD. To support this, I have mined existing microarray data to discover seven new lncRNAs that are dysregulated in HD brains. Interestingly, several of these contain genomic binding sites for the transcriptional repressor REST, a key mediator of transcriptional changes in HD, including the known REST target lncRNA, DGCR5. Previously described lncRNAs TUG1 (necessary for retinal development) and NEAT1 (a structural component of nuclear paraspeckles) are upregulated in HD caudate, while the brain-specific tumour-suppressor MEG3 is downregulated. Three other lncRNAs of unknown function are also significantly changed in HD brains. Many lncRNAs regulate gene expression through formation of epigenetic ribonucleoprotein complexes, including TUG1 and MEG3. These findings lead me to propose that lncRNA expression changes in HD are widespread, that many of these result in altered epigenetic gene regulation in diseased neurons, and that contributes to neurodegeneration. Therefore, elucidating lncRNA network changes in HD may be important in understanding and treating this and other neurodegenerative processes.
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APA 7th
Johnson, R. (2012). Long non-coding RNAs in Huntington's disease neurodegeneration. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2011.12.006
Vancouver
Johnson R. Long non-coding RNAs in Huntington's disease neurodegeneration. Neurobiology of disease. 2012. doi:10.1016/j.nbd.2011.12.006. PMID: 22202438.
BibTeX
@article{johnson2012-22202438,
author = {Johnson, R.},
title = {{Long non-coding RNAs in Huntington's disease neurodegeneration}},
journal = {Neurobiology of disease},
year = {2012},
doi = {10.1016/j.nbd.2011.12.006},
pmid = {22202438},
url = {https://doi.org/10.1016/j.nbd.2011.12.006}
}
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Key findings
- Three other lncRNAs of unknown function are also significantly changed in HD brains.
- These findings lead me to propose that lncRNA expression changes in HD are widespread, that many of these result in altered epigenetic gene regulation in diseased neurons, and that contributes to neurodegeneration.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of disease) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22202438) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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