Evidence map›Paper›PMID 34884940›Full record

ArticleInternational journal of molecular sciences2021

Targeting MicroRNA-485-3p Blocks Alzheimer's Disease Progression.

Han Seok Koh, SangJoon Lee, Hyo Jin Lee, Jae-Woong Min, Takeshi Iwatsubo, Charlotte E Teunissen, Hyun-Jeong Cho, Jin-Hyeob Ryu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. The Role of miRNAs in Parkinson's Disease: A Systematic Review.International journal of molecular sciences · 2025
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Han Seok KohBIORCHESTRA Co., Ltd., 17, Techno 4-ro, Yuseong-gu, Daejeon 34013, Korea.
SangJoon LeeDepartment of Infection Biology, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8577, Japan.ORCID 0000-0001-7500-782X
Hyo Jin LeeBIORCHESTRA Co., Ltd., 17, Techno 4-ro, Yuseong-gu, Daejeon 34013, Korea.
Jae-Woong MinBIORCHESTRA Co., Ltd., 17, Techno 4-ro, Yuseong-gu, Daejeon 34013, Korea.
Takeshi IwatsuboDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Charlotte E TeunissenNeurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam University Medical Centers, 1081 Amsterdam, The Netherlands.
Hyun-Jeong ChoDepartment of Biomedical Laboratory Science, College of Medical Science, Konyang University, Daejeon 35365, Korea.ORCID 0000-0003-2331-1306
Jin-Hyeob RyuBIORCHESTRA Co., Ltd., 17, Techno 4-ro, Yuseong-gu, Daejeon 34013, Korea.
Amsterdam Neuroscience · NLKonyang University · KRThe University of Tokyo · JPUniversity of Tsukuba · JP

Funding

Ministry of Education, Culture, Sports, Science, and Technology of Japan 19K16665National Research Foundation of Korea 2017M3A9G2094069
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a form of dementia characterized by progressive memory decline and cognitive dysfunction. With only one FDA-approved therapy, effective treatment strategies for AD are urgently needed. In this study, we found that microRNA-485-3p (miR-485-3p) was overexpressed in the brain tissues, cerebrospinal fluid, and plasma of patients with AD, and its antisense oligonucleotide (ASO) reduced Aβ plaque accumulation, tau pathology development, neuroinflammation, and cognitive decline in a transgenic mouse model of AD. Mechanistically, miR-485-3p ASO enhanced Aβ clearance via CD36-mediated phagocytosis of Aβ in vitro and in vivo. Furthermore, miR-485-3p ASO administration reduced apoptosis, thereby effectively decreasing truncated tau levels. Moreover, miR-485-3p ASO treatment reduced secretion of proinflammatory cytokines, including IL-1β and TNF-α, and eventually relieved cognitive impairment. Collectively, our findings suggest that miR-485-3p is a useful biomarker of the inflammatory pathophysiology of AD and that miR-485-3p ASO represents a potential therapeutic candidate for managing AD pathology and cognitive decline.

Indexed as

Alzheimer DiseaseAnimalsCase-Control StudiesCognitive DysfunctionCytokinesDisease Models, AnimalDisks Large Homolog 4 ProteinHumansMiceMice, Inbred C57BLMice, TransgenicMicroRNAsMolecular Targeted TherapyMotor NeuronsOligonucleotides, AntisensePhagocytosisCytokinesDisks Large Homolog 4 ProteinDlg4 protein, mouseMicroRNAsMIRN485 microRNA, humanOligonucleotides, Antisensetau ProteinsAlzheimer’s diseaseantisense oligonucleotidecognitive functionIL-1βmicroRNAmiR-485-3pneuroinflammationtauTNF-αβ-amyloid

Identifiers

PMID34884940
PMCPMC8658496
OpenAlexW4200086146

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.