Cited by 16Alzheimer's disease research and treatmentsBioinformatics and Genomic NetworksDementia and Cognitive Impairment Research

ADAS-viewer: web-based application for integrative analysis of multi-omics data in Alzheimer’s disease

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Han, Seonggyun, Shin, Jaehang, Jung, Hyeim, Ryu, Jane, Minassie, Habtamu, Nho, Kwangsik, Koh, Insong, Lee, Younghee·2021·npj Systems Biology and Applications

Abstract

Abstracts: Alzheimer’s disease (AD) is a neurodegenerative disorder and is represented by complicated biological mechanisms and complexity of brain tissue. Our understanding of the complicated molecular architecture that contributes to AD progression benefits from performing comprehensive and systemic investigations with multi-layered molecular and biological data from different brain regions. Since recently different independent studies generated various omics data in different brain regions of AD patients, multi-omics data integration can be a useful resource for better comprehensive understanding of AD. Here we present a web platform, ADAS-viewer, that provides researchers with the ability to comprehensively investigate and visualize multi-omics data from multiple brain regions of AD patients. ADAS-viewer offers means to identify functional changes in transcript and exon expression (i.e., alternative splicing) along with associated genetic or epigenetic regulatory effects. Specifically, it integrates genomic, transcriptomic, methylation, and miRNA data collected from seven different brain regions (cerebellum, temporal cortex, dorsolateral prefrontal cortex, frontal pole, inferior frontal gyrus, parahippocampal gyrus, and superior temporal gyrus) across three independent cohort datasets. ADAS-viewer is particularly useful as a web-based application for analyzing and visualizing multi-omics data across multiple brain regions at both transcript and exon level, allowing the identification of candidate biomarkers of Alzheimer’s disease.

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  • ADAS-Viewer enables the identification of region-specific transcriptomic and epigenetic alterations associated with AD onset and progression.

    “Platforms such as ADAS-Viewer exemplify the potential of spatially resolved omics analysis, enabling the identification of region-specific transcriptomic and epigenetic alterations associated with AD onset and progression330.”

    From Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions (2025) · cites this paper as [330]

    The Results (Fig. 1 caption; page not supplied) describe region-specific transcript expression in normal and AD groups, and the Results and Discussion describe analyses of methylation and disease severity. However, the Methods > Data section (page not supplied) says epigenetic data came only from the dorsolateral prefrontal cortex. The paper does not establish that ADAS-viewer identifies epigenetic alterations across regions or alterations associated specifically with AD onset; its regional comparisons are not spatially resolved omics measurements. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 34

  1. [1]Perl DP Neuropathology of Alzheimer’s disease Mt Sinai J. Med 2010 77 32 42 10.1002/msj.20157 20101720 PMC2918894 · DOI · Paper page
  2. [2]Bassett DS Gazzaniga MS Understanding complexity in the human brain Trends Cogn. Sci. 2011 15 200 209 10.1016/j.tics.2011.03.006 21497128 PMC3170818 · DOI · Paper page
  3. [3]Katsuki F Constantinidis C Unique and shared roles of the posterior parietal and dorsolateral prefrontal cortex in cognitive functions Front Integr. Neurosci. 2012 6 17 10.3389/fnint.2012.00017 22563310 PMC3342558 · DOI
  4. [4]Mills JD RNA-Seq analysis of the parietal cortex in Alzheimer’s disease reveals alternatively spliced isoforms related to lipid metabolism Neurosci. Lett. 2013 536 90 95 10.1016/j.neulet.2012.12.042 23305720 · DOI
  5. [5]Xu J Regional protein expression in human Alzheimer’s brain correlates with disease severity Commun. Biol. 2019 2 43 10.1038/s42003-018-0254-9 30729181 PMC6361956 · DOI
  6. [6]Freer R A protein homeostasis signature in healthy brains recapitulates tissue vulnerability to Alzheimer’s disease Sci. Adv. 2016 2 e1600947 10.1126/sciadv.1600947 27532054 PMC4980108 · DOI
  7. [7]Zanfardino M Bringing radiomics into a multi-omics framework for a comprehensive genotype-phenotype characterization of oncological diseases J. Transl. Med. 2019 17 337 10.1186/s12967-019-2073-2 31590671 PMC6778975 · DOI
  8. [8]Cuccurese M Russo G Russo A Pietropaolo C Alternative splicing and nonsense-mediated mRNA decay regulate mammalian ribosomal gene expression Nucleic Acids Res. 2005 33 5965 5977 10.1093/nar/gki905 16254077 PMC1270949 · DOI
  9. [9]Weyn-Vanhentenryck SM Precise temporal regulation of alternative splicing during neural development Nat. Commun. 2018 9 2189 10.1038/s41467-018-04559-0 29875359 PMC5989265 · DOI
  10. [10]Su CH D D Tarn WY Alternative splicing in neurogenesis and brain development Front Mol. Biosci. 2018 5 12 10.3389/fmolb.2018.00012 29484299 PMC5816070 · DOI
  11. [12]Shen L Jia J An overview of genome-wide association studies in Alzheimer’s disease Neurosci. Bull. 2016 32 183 190 10.1007/s12264-016-0011-3 26810783 PMC5563735 · DOI
  12. [15]Fransquet PD Ryan J Micro RNA as a potential blood-based epigenetic biomarker for Alzheimer’s disease Clin. Biochem 2018 58 5 14 10.1016/j.clinbiochem.2018.05.020 29885309 · DOI
  13. [16]Moore LD Le T Fan G DNA methylation and its basic function Neuropsychopharmacology 2013 38 23 38 10.1038/npp.2012.112 22781841 PMC3521964 · DOI · Paper page
  14. [17]Lev Maor G Yearim A Ast G The alternative role of DNA methylation in splicing regulation Trends Genet. 2015 31 274 280 10.1016/j.tig.2015.03.002 25837375 · DOI
  15. [18]Allen M Human whole genome genotype and transcriptome data for Alzheimer’s and other neurodegenerative diseases Sci. Data 2016 3 160089 10.1038/sdata.2016.89 27727239 PMC5058336 · DOI · Paper page
  16. [19]De Jager PL A multi-omic atlas of the human frontal cortex for aging and Alzheimer’s disease research Sci. Data 2018 5 180142 10.1038/sdata.2018.142 30084846 PMC6080491 · DOI · Paper page
  17. [20]Wang M The Mount Sinai cohort of large-scale genomic, transcriptomic and proteomic data in Alzheimer’s disease Sci. Data 2018 5 180185 10.1038/sdata.2018.185 30204156 PMC6132187 · DOI · Paper page
  18. [21]Han, S. J. et al. Association of thigh muscle mass with insulin resistance and incident type 2 diabetes mellitus in Japanese Americans. Diabetes Metab. J., 10.4093/dmj.2018.0022 (2018). PMC6300439 30302961 · DOI
  19. [22]Erten-Lyons D Jacobson A Kramer P Grupe A Kaye J The FAS gene, brain volume, and disease progression in Alzheimer’s disease Alzheimers Dement. 2010 6 118 124 10.1016/j.jalz.2009.05.663 19766542 PMC3100774 · DOI
  20. [23]Su JH Fas and Fas ligand are associated with neuritic degeneration in the AD brain and participate in beta-amyloid-induced neuronal death Neurobiol. Dis. 2003 12 182 193 10.1016/S0969-9961(02)00019-0 12742739 · DOI
  21. [24]Colangelo V Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: transcription and neurotrophic factor down-regulation and up-regulation of apoptotic and pro-inflammatory signaling J. Neurosci. Res. 2002 70 462 473 10.1002/jnr.10351 12391607 · DOI · Paper page
  22. [25]Hensel A Wolf H Busse A Arendt T Gertz HJ Association between global brain volume and the rate of cognitive change in elderly humans without dementia Dement Geriatr. Cogn. Disord. 2005 19 213 221 10.1159/000083501 15677869 · DOI
  23. [26]Jia L Genetic association between polymorphisms of Pen2 gene and late onset Alzheimer’s disease in the North Chinese population Brain Res. 2007 1141 10 14 10.1016/j.brainres.2007.01.005 17280645 · DOI
  24. [27]Andreoli V Presenilin enhancer-2 gene: identification of a novel promoter mutation in a patient with early-onset familial Alzheimer’s disease Alzheimers Dement. 2011 7 574 578 10.1016/j.jalz.2011.02.010 22055974 · DOI
  25. [29]Ng B An xQTL map integrates the genetic architecture of the human brain’s transcriptome and epigenome Nat. Neurosci. 2017 20 1418 1426 10.1038/nn.4632 28869584 PMC5785926 · DOI · Paper page
  26. [30]Miller, J. A. et al. Neuropathological and transcriptomic characteristics of the aged brain. Elife6, 10.7554/eLife.31126 (2017). PMC5679757 29120328 · DOI · Paper page
  27. [31]Li H The sequence alignment/map format and SAMtools Bioinformatics 2009 25 2078 2079 10.1093/bioinformatics/btp352 19505943 PMC2723002 · DOI · Paper page
  28. [32]Dobin A STAR: ultrafast universal RNA-seq aligner Bioinformatics 2013 29 15 21 10.1093/bioinformatics/bts635 23104886 PMC3530905 · DOI · Paper page
  29. [33]Li B Dewey CN RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome BMC Bioinformatics 2011 12 323 10.1186/1471-2105-12-323 21816040 PMC3163565 · DOI · Paper page
  30. [34]Zheng Z Genetic diversity, population structure, and botanical variety of 320 global peanut accessions revealed through tunable genotyping-by-sequencing Sci. Rep. 2018 8 14500 10.1038/s41598-018-32800-9 30266974 PMC6162295 · DOI
  31. [35]Chou CH miRTarBase 2016: updates to the experimentally validated miRNA-target interactions database Nucleic Acids Res. 2016 44 D239 D247 10.1093/nar/gkv1258 26590260 PMC4702890 · DOI
  32. [36]Lewis BP Burge CB Bartel DP Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets Cell 2005 120 15 20 10.1016/j.cell.2004.12.035 15652477 · DOI · Paper page
  33. [37]Betel D Wilson M Gabow A Marks DS Sander C The microRNA.org resource: targets and expression Nucleic Acids Res. 2008 36 D149 D153 10.1093/nar/gkm995 18158296 PMC2238905 · DOI
  34. [38]Han S Jung H Lee K Kim H Kim S Genome wide discovery of genetic variants affecting alternative splicing patterns in human using bioinformatics method Genes Genomics 2017 39 453 459 10.1007/s13258-016-0466-7 · DOI

Cited by

Sorted by citations

Authors
Han, S., Shin, J., Jung, H., Ryu, J., Minassie, H., Nho, K., Koh, I., & Lee, Y.
Affiliations
  • University of Utah (US)
  • Indiana University Indianapolis (US)
  • Hanyang University (KR)
Corresponding author
Lee, Younghee
Venue
npj Systems Biology and Applications
Published
2021-03-19
Volume
7
Issue
1
Pages
18-18
ISSN
2056-7189 (ISSN-L)
OpenAlex
W3137114858
Cited by
16
References
3
Citations by year
2026: 1 · 2025: 5 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 1
FWCI
1.57
Type
journal article
Language
en
Open access
Locations
  • npj Systems Biology and Applications (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • IUScholarWorks (Indiana University) (submittedVersion, cc-by)
Funders
  • University of Utah
  • National Research Foundation
  • Iran Telecommunication Research Center
  • Ministry of Science and ICT, South Korea (IITP-2018-2018-0-01833, IITP-2018, NRF-2017M3C9A6047623)
  • School of Medicine
  • Institute for Information and Communications Technology Promotion
  • National Institute on Aging (R03AG063250, R03AG054936)
  • U.S. National Library of Medicine (R01LM012535)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, multi-omics integration, web-based data visualization, brain regions, transcript expression, exon expression, alternative splicing, DNA methylation, microRNA, epigenetic regulation, biomarkers, cerebellum, temporal cortex, prefrontal cortex, parahippocampal gyrus, superior temporal gyrus
MeSH terms
Dorsolateral Prefrontal Cortex, Alzheimer Disease, Brain, Humans, Internet, Genomics

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