Evidence map›Paper›PMID 28092081›Full record

ReviewMolecular neurobiology2018

Epigenetics in Alzheimer's Disease: Perspective of DNA Methylation.

Talal Jamil Qazi, Zhenzhen Quan, Asif Mir, Hong Qing

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% 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

84 citing papers in PubMed, 3 syntheses or guidelines pooled it, 152 citations in OpenAlex.

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  19. Generation and characterization of two acid-resistant macrocinComputational and structural biotechnology journal · 2024
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24 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Talal Jamil QaziBeijing Key Laboratory of Separation and Analysis in Biomedical and Pharmaceuticals, Department of Biomedical Engineering, School of Life Sciences, Beijing Institute of Technology, Beijing, People's Republic of China.
Zhenzhen QuanBeijing Key Laboratory of Separation and Analysis in Biomedical and Pharmaceuticals, Department of Biomedical Engineering, School of Life Sciences, Beijing Institute of Technology, Beijing, People's Republic of China.
Asif MirDepartment of Bioinformatics and Biotechnology, International Islamic University Islamabad, Islamabad, Pakistan.
Hong QingBeijing Key Laboratory of Separation and Analysis in Biomedical and Pharmaceuticals, Department of Biomedical Engineering, School of Life Sciences, Beijing Institute of Technology, Beijing, People's Republic of China. hqing@bit.edu.cn.
Beijing Institute of Technology · CNInternational Islamic University, Islamabad · PK

Funding

Ministry of Science and Technology of the People's Republic of China No. 2013YQ03059514National Natural Science Foundation of China 81671268
6 · The paper itself

Abstract

Research over the years has shown that causes of Alzheimer's disease are not well understood, but over the past years, the involvement of epigenetic mechanisms in the developing memory formation either under pathological or physiological conditions has become clear. The term epigenetics represents the heredity of changes in phenotype that are independent of altered DNA sequences. Different studies validated that cytosine methylation of genomic DNA decreases with age in different tissues of mammals, and therefore, the role of epigenetic factors in developing neurological disorders in aging has been under focus. In this review, we summarized and reviewed the involvement of different epigenetic mechanisms especially the DNA methylation in Alzheimer's disease (AD), late-onset Alzheimer's disease (LOAD), familial Alzheimer's disease (FAD), and autosomal dominant Alzheimer's disease (ADAD). Down to the minutest of details, we tried to discuss the methylation patterns like mitochondrial DNA methylation and ribosomal DNA (rDNA) methylation. Additionally, we mentioned some therapeutic approaches related to epigenetics, which could provide a potential cure for AD. Moreover, we reviewed some recent studies that validate DNA methylation as a potential biomarker and its role in AD. We hope that this review will provide new insights into the understanding of AD pathogenesis from the epigenetic perspective especially from the perspective of DNA methylation.

Indexed as

DNA MethylationAlzheimer DiseaseDNA, MitochondrialEpigenesis, GeneticHumansMitochondriaDNA, MitochondrialAlzheimer’s diseaseDNA methylationEpigenetic factorsHistone modificationsmtDNA methylationncRNAs

Identifiers

PMID28092081
OpenAlexW2572342044

What OpenQuestion holds

Textmetadata
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.