Evidence map›Paper›PMID 35694866›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

Multi-Omics-Based Autophagy-Related Untypical Subtypes in Patients with Cerebral Amyloid Pathology.

Jong-Chan Park, Natalia Barahona-Torres, So-Yeong Jang, Kin Y Mok, Haeng Jun Kim, Sun-Ho Han, Kwang-Hyun Cho, Xiaopu Zhou, Amy K Y Fu, Nancy Y Ip and 10 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 24 citations in OpenAlex.

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  15. Autophagy and machine learning: Unanswered questions.Biochimica et biophysica acta. Molecular basis of disease · 2024
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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

20 authors at 8 institutions in 7 countries.

Jong-Chan ParkDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0001-7516-7292
Natalia Barahona-TorresDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
So-Yeong JangDepartment of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Kin Y MokDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Haeng Jun KimDepartment of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Sun-Ho HanDepartment of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Kwang-Hyun ChoDepartment of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Xiaopu ZhouDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, 999077, China.
Amy K Y FuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, 999077, China.
Nancy Y IpDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, 999077, China.
Jieun SeoDepartment of Laboratory Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
Murim ChoiDepartment of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Hyobin JeongEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, 69117, Germany.
Daehee HwangDepartment of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Dong Young LeeInstitute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, 03080, Republic of Korea.
Min Soo ByunDepartment of Psychiatry, Pusan National University Yangsan Hospital, Yangsan, 50612, Republic of Korea.
Dahyun YiBiomedical Research Institute, Seoul National University Hospital, Seoul, 03082, Republic of Korea.
Jong Won HanDepartment of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Inhee Mook-JungDepartment of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.ORCID 0000-0001-7085-4085
John HardyDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Seoul National University · KRHong Kong University of Science and Technology · HKMRC Prion Unit · GBKorea Advanced Institute of Science and Technology · KREuropean Molecular Biology Laboratory · DEPusan National University Yangsan Hospital · KRSeoul National University Hospital · KRYonsei University · KR

Funding

KBASE2: Korean Brain Aging Study, Longitudinal Endophenotypes and Systems BiologyU01AG072177 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LEE, DONG YOUNG, NHO, KWANGSIK TIMOTHY · 2021 to 2025
$11.2M
Medical Research Council G0701075Medical Research Council G0901254NIA NIH HHS U01 AG072177
6 · The paper itself

Abstract

Recent multi-omics analyses paved the way for a comprehensive understanding of pathological processes. However, only few studies have explored Alzheimer's disease (AD) despite the possibility of biological subtypes within these patients. For this study, unsupervised classification of four datasets (genetics, miRNA transcriptomics, proteomics, and blood-based biomarkers) using Multi-Omics Factor Analysis+ (MOFA+), along with systems-biological approaches following various downstream analyses are performed. New subgroups within 170 patients with cerebral amyloid pathology (Aβ+) are revealed and the features of them are identified based on the top-rated targets constructing multi-omics factors of both whole (M-TPAD) and immune-focused models (M-IPAD). The authors explored the characteristics of subtypes and possible key-drivers for AD pathogenesis. Further in-depth studies showed that these subtypes are associated with longitudinal brain changes and autophagy pathways are main contributors. The significance of autophagy or clustering tendency is validated in peripheral blood mononuclear cells (PBMCs; n = 120 including 30 Aβ- and 90 Aβ+), induced pluripotent stem cell-derived human brain organoids/microglia (n = 12 including 5 Aβ-, 5 Aβ+, and CRISPR-Cas9 apolipoprotein isogenic lines), and human brain transcriptome (n = 78). Collectively, this study provides a strategy for precision medicine therapy and drug development for AD using integrative multi-omics analysis and network modelling.

Indexed as

Alzheimer DiseaseAmyloidosisAmyloid beta-PeptidesAmyloidogenic ProteinsAutophagyHumansLeukocytes, MononuclearMicrogliaAmyloid beta-PeptidesAmyloidogenic ProteinsAlzheimer's diseaseautophagymulti-omicsperipheral bloodsubtypesystems biology

Identifiers

PMID35694866
PMCPMC9376815
OpenAlexW4282558611

What OpenQuestion 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 OpenQuestion graph.