Evidence map›Paper›PMID 29858092›Full record

ArticleMolecular therapy. Nucleic acids2018

Supplemental Treatment for Huntington's Disease with miR-132 that Is Deficient in Huntington's Disease Brain.

Masashi Fukuoka, Masaki Takahashi, Hiromi Fujita, Tomoko Chiyo, H Akiko Popiel, Shoko Watanabe, Hirokazu Furuya, Miho Murata, Keiji Wada, Takashi Okada and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  10. Non-coding RNAs and neuroinflammation: implications for neurological disorders.Experimental biology and medicine (Maywood, N.J.) · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Masashi FukuokaDepartment of Molecular Pharmacology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Masaki TakahashiDepartment of Molecular Pharmacology, National Institute of Neuroscience, NCNP, Tokyo, Japan; Division of RNA Medical Science, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiromi FujitaDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Tomoko ChiyoDepartment of Molecular Therapy, National Institute of Neuroscience, NCNP, Tokyo, Japan.
H Akiko PopielDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Shoko WatanabeNational Center Hospital, NCNP, Tokyo, Japan.
Hirokazu FuruyaOomuta Hospital, Fukuoka, Japan.
Miho MurataNational Center Hospital, NCNP, Tokyo, Japan.
Keiji WadaDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Takashi OkadaDepartment of Molecular Therapy, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Yoshitaka NagaiDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Hirohiko HohjohDepartment of Molecular Pharmacology, National Institute of Neuroscience, NCNP, Tokyo, Japan. Electronic address: hohjohh@ncnp.go.jp.
National Center of Neurology and Psychiatry · JPTokyo National Hospital · JPOmuta hospital · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is an intractable neurodegenerative disorder caused by mutant Huntingtin (HTT) proteins that adversely affect various biomolecules and genes. MicroRNAs (miRNAs), which are functional small non-coding RNAs, are also affected by mutant HTT proteins. Here, we show amelioration in motor function and lifespan of HD-model mice, R6/2 mice, by supplying miR-132 to HD brains using a recombinant adeno-associated virus (rAAV) miRNA expression system. miR-132 is an miRNA related to neuronal maturation and function, but the level of miR-132 in the brain of R6/2 mice was significantly lower than that of wild-type mice. Our miR-132 supplemental treatment, i.e., supplying miR-132 to the brain, produced symptomatic improvement or retarded disease progression in R6/2 mice; interestingly, it had little effect on disease-causing mutant HTT mRNA expression and its products. Therefore, the findings suggest that there may be a therapeutic way to treat HD without inhibiting and/or repairing disease-causing HTT genes and gene products. Although miR-132 supplement may not be a definitive treatment for HD, it may become a therapeutic method for relieving HD symptoms and delaying HD progression.

Indexed as

adeno-associated virusHuntington’s diseasemicroRNAmiR-132 supplementationR6/2 mice

Identifiers

PMID29858092
PMCPMC5852323
OpenAlexW2788972437

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.