Evidence map›Paper›PMID 37386009›Full record

ArticleTranslational psychiatry2023

Classification and deep-learning-based prediction of Alzheimer disease subtypes by using genomic data.

Daichi Shigemizu, Shintaro Akiyama, Mutsumi Suganuma, Motoki Furutani, Akiko Yamakawa, Yukiko Nakano, Kouichi Ozaki, Shumpei Niida

Abstract read
In one paragraph

Article in Translational psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Genetic risk in Alzheimer's disease.NPJ systems biology and applications · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. LD-informed deep learning for Alzheimer's gene loci detection using WGS data.medRxiv : the preprint server for health sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

8 authors.

Daichi ShigemizuMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan. daichi@ncgg.go.jp.ORCID 0000-0002-4412-0552
Shintaro AkiyamaMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.
Mutsumi SuganumaMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.
Motoki FurutaniMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.
Akiko YamakawaMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.
Yukiko NakanoDepartment of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, 734-8553, Japan.
Kouichi OzakiMedical Genome Center, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.ORCID 0000-0003-0028-1570
Shumpei NiidaCore Facility Administration, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, 474-8511, Japan.

Funding

Japan Agency for Medical Research and Development (AMED) JP18kk0205009Japan Agency for Medical Research and Development (AMED) JP18kk0205012Japan Agency for Medical Research and Development (AMED) JP21de0107002Japan Agency for Medical Research and Development (AMED) JP21dk0207045Japan Agency for Medical Research and Development (AMED) JP21dk0207052Japan Agency for Medical Research and Development (AMED) JP21km0405501Japan Agency for Medical Research and Development (AMED) JP22dk0207060MEXT | Japan Society for the Promotion of Science (JSPS) JP21H02470
6 · The paper itself

Abstract

Late-onset Alzheimer's disease (LOAD) is the most common multifactorial neurodegenerative disease among elderly people. LOAD is heterogeneous, and the symptoms vary among patients. Genome-wide association studies (GWAS) have identified genetic risk factors for LOAD but not for LOAD subtypes. Here, we examined the genetic architecture of LOAD based on Japanese GWAS data from 1947 patients and 2192 cognitively normal controls in a discovery cohort and 847 patients and 2298 controls in an independent validation cohort. Two distinct groups of LOAD patients were identified. One was characterized by major risk genes for developing LOAD (APOC1 and APOC1P1) and immune-related genes (RELB and CBLC). The other was characterized by genes associated with kidney disorders (AXDND1, FBP1, and MIR2278). Subsequent analysis of albumin and hemoglobin values from routine blood test results suggested that impaired kidney function could lead to LOAD pathogenesis. We developed a prediction model for LOAD subtypes using a deep neural network, which achieved an accuracy of 0.694 (2870/4137) in the discovery cohort and 0.687 (2162/3145) in the validation cohort. These findings provide new insights into the pathogenic mechanisms of LOAD.

Indexed as

Alzheimer DiseaseDeep LearningNeurodegenerative DiseasesAgedGenome-Wide Association StudyGenomicsHumans

Identifiers

PMID37386009
PMCPMC10310810

What Socratic holds

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Registered trials

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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.