Evidence map›Paper›PMID 34625606›Full record

ArticleScientific reports2021

Hypermethylation of Mest promoter causes aberrant Wnt signaling in patients with Alzheimer's disease.

Renuka Prasad, Hwajin Jung, Anderson Tan, Yonghee Song, Sungho Moon, Mohammed R Shaker, Woong Sun, Junghee Lee, Hoon Ryu, Hyun Kook Lim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Cell-Free DNA Hypermethylation in Patients with Acute Pancreatitis.International journal of molecular sciences · 2025
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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

11 authors at 4 institutions in 2 countries.

Renuka Prasad *Department of Life Science, University of Seoul, Seoul, 02504, Republic of Korea.
Hwajin Jung *Department of Life Science, University of Seoul, Seoul, 02504, Republic of Korea.
Anderson TanDepartment of Life Science, University of Seoul, Seoul, 02504, Republic of Korea.
Yonghee SongDepartment of Life Science, University of Seoul, Seoul, 02504, Republic of Korea.
Sungho MoonDepartment of Life Science, University of Seoul, Seoul, 02504, Republic of Korea.
Mohammed R ShakerDepartment of Anatomy, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Woong SunDepartment of Anatomy, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Junghee LeeBoston University Alzheimer's Disease Center and Department of Neurology, Boston University School of Medicine, Boston, MA, 02118, USA.
Hoon RyuBoston University Alzheimer's Disease Center and Department of Neurology, Boston University School of Medicine, Boston, MA, 02118, USA. hoonryu@bu.edu.
Hyun Kook LimDepartment of Psychiatry, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. drblues@catholic.ac.kr.
Eek-Hoon JhoDepartment of Life Science, University of Seoul, Seoul, 02504, Republic of Korea. ej70@uos.ac.kr.
University of Seoul · KRBoston University · USKorea University · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that leads to dementia and behavioral changes. Extracellular deposition of amyloid plaques (Aβ) and intracellular deposition of neurofibrillary tangles in neurons are the major pathogenicities of AD. However, drugs targeting these therapeutic targets are not effective. Therefore, novel targets for the treatment of AD urgently need to be identified. Expression of the mesoderm-specific transcript (Mest) is regulated by genomic imprinting, where only the paternal allele is active for transcription. We identified hypermethylation on the Mest promoter, which led to a reduction in Mest mRNA levels and activation of Wnt signaling in brain tissues of AD patients. Mest knockout (KO) using the CRIPSR/Cas9 system in mouse embryonic stem cells and P19 embryonic carcinoma cells leads to neuronal differentiation arrest. Depletion of Mest in primary hippocampal neurons via lentivirus expressing shMest or inducible KO system causes neurodegeneration. Notably, depletion of Mest in primary cortical neurons of rats leads to tau phosphorylation at the S199 and T231 sites. Overall, our data suggest that hypermethylation of the Mest promoter may cause or facilitate the progression of AD.

Indexed as

DNA MethylationPromoter Regions, GeneticWnt Signaling PathwayAlzheimer DiseaseAnimalsEmbryonal Carcinoma Stem CellsEmbryonic Stem CellsHippocampusHumansMiceNeuronsPhosphorylationProteinstau Proteinsmesoderm specific transcript proteinProteinstau Proteins

Identifiers

PMID34625606
PMCPMC8501037
OpenAlexW3163756553

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LicenceCC BY
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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.