Evidence map›Paper›PMID 33807010›Full record

ArticleInternational journal of molecular sciences2021

Utilizing an Animal Model to Identify Brain Neurodegeneration-Related Biomarkers in Aging.

Ming-Hui Yang, Yi-Ming Arthur Chen, Shan-Chen Tu, Pei-Ling Chi, Kuo-Pin Chuang, Chin-Chuan Chang, Chiang-Hsuan Lee, Yi-Ling Chen, Che-Hsin Lee, Cheng-Hui Yuan and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Trial
  2. Article
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 5 institutions in 2 countries.

Ming-Hui YangDepartment of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.ORCID 0000-0001-5856-0498
Yi-Ming Arthur ChenGraduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei City 242, Taiwan.
Shan-Chen TuDepartment of Medical Imaging and Radiological Sciences, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Pei-Ling ChiDepartment of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.
Kuo-Pin ChuangInternational Degree Program in Animal Vaccine Technology, International College, National Pingtung University of Science and Technology, Pingtung 912, Taiwan.
Chin-Chuan ChangSchool of Medicine, College of Medicine, Kaoshiung Medical University, Kaoshiung 807, Taiwan.ORCID 0000-0003-4618-0927
Chiang-Hsuan LeeDepartment of Nuclear Medicine, Chi Mei Medical Center, Tainan 710, Taiwan.ORCID 0000-0003-0090-1725
Yi-Ling ChenDepartment of Nuclear Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan.
Che-Hsin LeeDepartment of Biological Sciences, National Sun Yat-sen University, Kaohsiung 804, Taiwan.ORCID 0000-0002-8543-3862
Cheng-Hui YuanMass Spectrometry Laboratory, Department of Chemistry, National University of Singapore, Singapore 119077, Singapore.
Yu-Chang TyanDepartment of Medical Imaging and Radiological Sciences, Kaohsiung Medical University, Kaohsiung 807, Taiwan.ORCID 0000-0002-1917-5893
Kaohsiung Medical University · TWNational Sun Yat-sen University · TWFu Jen Catholic University · TWKaohsiung Veterans General Hospital · TWNational University of Singapore · SG

Funding

Kaohsiung Veterans General Hospital VGHKS109-181Ministry of Science and Technology MOST 108-2221-E-037-003
6 · The paper itself

Abstract

Glycine N-methyltransferase (GNMT) regulates S-adenosylmethionine (SAMe), a methyl donor in methylation. Over-expressed SAMe may cause neurogenic capacity reduction and memory impairment. GNMT knockout mice (GNMT-KO) was applied as an experimental model to evaluate its effect on neurons. In this study, proteins from brain tissues were studied using proteomic approaches, Haemotoxylin and Eosin staining, immunohistochemistry, Western blotting, and ingenuity pathway analysis. The expression of Receptor-interacting protein 1(RIPK1) and Caspase 3 were up-regulated and activity-dependent neuroprotective protein (ADNP) was down-regulated in GNMT-KO mice regardless of the age. Besides, proteins related to neuropathology, such as excitatory amino acid transporter 2, calcium/calmodulin-dependent protein kinase type II subunit alpha, and Cu-Zn superoxide dismutase were found only in the group of aged wild-type mice; 4-aminobutyrate amino transferase, limbic system-associated membrane protein, sodium- and chloride-dependent GABA transporter 3 and ProSAAS were found only in the group of young GNMT-KO mice and are related to function of neurons; serum albumin and Rho GDP dissociation inhibitor 1 were found only in the group of aged GNMT-KO mice and are connected to neurodegenerative disorders. With proteomic analyses, a pathway involving Gonadotropin-releasing hormone (GnRH) signal was found to be associated with aging. The GnRH pathway could provide additional information on the mechanism of aging and non-aging related neurodegeneration, and these protein markers may be served in developing future therapeutic treatments to ameliorate aging and prevent diseases.

Indexed as

BiomarkersAgingAnimalsBrainCellular SenescenceDisease Models, AnimalDisease SusceptibilityImmunohistochemistryMiceNerve Tissue ProteinsNeurodegenerative DiseasesNeuronsPrognosisProteomeProteomicsSignal TransductionBiomarkersNerve Tissue ProteinsProteomeagingbiomarkerGNMTneurons

Identifiers

PMID33807010
PMCPMC8004625
OpenAlexW3137092338

What Socratic 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 Socratic graph.