Evidence map›Paper›PMID 30486438›Full record

ReviewInternational journal of molecular sciences2018

Genomics: New Light on Alzheimer's Disease Research.

Yeong Ju Jung, Yoon Ha Kim, Mridula Bhalla, Sung Bae Lee, Jinsoo Seo

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The APOE ε4 exerts differential effects on familial and other subtypes of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Article
  10. Article
  11. Review
  12. 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

5 authors.

Yeong Ju JungDepartment of Brain & Cognitive Sciences, DGIST, Daegu 42988, Korea. jyj5028@naver.com.
Yoon Ha KimDepartment of Brain & Cognitive Sciences, DGIST, Daegu 42988, Korea. dbsgk1005@dgist.ac.kr.
Mridula BhallaInstitute of Bioinformatics and Biotechnology, Savitribai Phule Pune University, Pune 411007, India. bmridula158@gmail.com.
Sung Bae LeeDepartment of Brain & Cognitive Sciences, DGIST, Daegu 42988, Korea. sblee@dgist.ac.kr.ORCID 0000-0002-8980-6769
Jinsoo SeoDepartment of Brain & Cognitive Sciences, DGIST, Daegu 42988, Korea. jsseo@dgist.ac.kr.

Funding

Daegu Gyeongbuk Institute of Science and Technology MIREBraiN programDaegu Gyeongbuk Institute of Science and Technology R&D programNational Research Foundation of Korea 18-BD-0402National Research Foundation of Korea 18-BT-02National Research Foundation of Korea 2018R1A2B6001607National Research Foundation of Korea 2018R1D1A1B07046356
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease that represents a major cause of death in many countries. AD is characterized by profound memory loss, disruptions in thinking and reasoning, and changes in personality and behavior followed by malfunctions in various bodily systems. Although AD was first identified over 100 years ago, and tremendous efforts have been made to cure the disease, the precise mechanisms underlying the onset of AD remain unclear. The recent development of next-generation sequencing tools and bioinformatics has enabled us to investigate the role of genetics in the pathogenesis of AD. In this review, we discuss novel discoveries in this area, including the results of genome-wide association studies (GWAS) that have implicated a number of novel genes as risk factors, as well as the identification of epigenetic regulators strongly associated with the onset and progression of AD. We also review how genetic risk factors may interact with age-associated, progressive decreases in cognitive function in patients with AD.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyGenomicsAge FactorsAlzheimer DiseaseAnimalsEpigenesis, GeneticGene Expression RegulationGenetic VariationHumansResearchRisk Factorsagingalzheimer’s diseaseepigenetic modificationgenetic risk factorsgenomicsGWAS

Identifiers

PMID30486438
PMCPMC6321384

What OpenQuestion holds

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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.