ArticleFrontiers in genetics2020
Identification of
Article in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The aging epigenome: integrative analyses reveal intersection with Alzheimer's disease.GeroScience · 2026Pooled it
- Cognitive Deficits in Female GPR158 Knockout Mice Revealed by Automated Home-Cage Testing.Genes, brain, and behavior · 2026Article
- Whole genome sequencing analysis of over 3500 individuals dementia-free over 85 years old.Journal of Alzheimer's disease : JAD · 2026Article
- GABRD as an Emerging Oncogene: Exploring Functions and Therapeutic Implications Across Cancers.Life (Basel, Switzerland) · 2026Review
- Rare and novel genetic variants in sporadic and familial Alzheimer's disease: insights from the first Saudi cohort.Frontiers in aging · 2026Article
- Cell type-specific inference from bulk RNA-sequencing data by integrating single-cell reference profiles via EPIC-unmix.Genome biology · 2025Article
- Osteocalcin and GPR158: linking bone and brain function.Frontiers in cell and developmental biology · 2025Review
- Genome-Wide Association Study of Body Weight Traits in Texel and Kazakh Crossbred Sheep.Genes · 2024Article
- Maternal regulation of the vertebrate oocyte-to-embryo transition.PLoS genetics · 2024Article
- Longitudinal Neuropathological Consequences of Extracranial Radiation Therapy in Mice.International journal of molecular sciences · 2024Article
- A novel imprinted locus on bovine chromosome 18 homologous with human chromosome 16q24.1.Molecular genetics and genomics : MGG · 2024Article
- A review and analysis of key biomarkers in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Unveiling Immune-related feature genes for Alzheimer's disease based on machine learning.Frontiers in immunology · 2024Article
- Construction and validation of a novel lysosomal signature for hepatocellular carcinoma prognosis, diagnosis, and therapeutic decision-making.Scientific reports · 2023Article
- Identification of key lipid metabolism-related genes in Alzheimer's disease.Lipids in health and disease · 2023Article
- Identification of metabolism-related subtypes and feature genes in Alzheimer's disease.Journal of translational medicine · 2023Article
- Expression Mapping and Functional Analysis of Orphan G-Protein-Coupled Receptor GPR158 in the Adult Mouse Brain Using a GPR158 Transgenic Mouse.Biomolecules · 2023Article
- Review
- Establishment and Analysis of a Combined Diagnostic Model of Alzheimer's Disease With Random Forest and Artificial Neural Network.Frontiers in aging neuroscience · 2022Article
- Posterior cingulate cortex reveals an expression profile of resilience in cognitively intact elders.Brain communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer disease (AD) is the most common cause of dementia and creates a significant burden on society. As a result, the investigation of hub genes for the discovery of potential therapeutic targets and candidate biomarkers is warranted. In this study, we used the ComBat method to merge three gene expression datasets of AD from the Gene Expression Omnibus (GEO). During combined analysis, we identified 850 differentially expressed genes (DEGs) from the temporal cortex of AD and cognitively normal (CN) samples. We performed weighted gene coexpression network analysis to build gene coexpression networks incorporating these DEGs to identify key modules and hub genes. We found one module most strongly correlated with AD onset as the key module and 19 hub genes in the key module that were down-regulated in AD brains. According to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, DEGs were mostly enriched in synapse function, and genes in the key module were mostly related to learning and memory. We selected five little-studied genes,
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Registered trials
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.