ArticleScientific reports2018
Guanosine monophosphate reductase 1 is a potential therapeutic target for Alzheimer's disease.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Sensogenomics of music and Alzheimer's disease: An interdisciplinary view from neuroscience, transcriptomics, and epigenomics.Frontiers in aging neuroscience · 2023Pooled it
- Characterization of Recombinant GMPR fromBiology · 2026Article
- A Graph Neural Network Framework with Equivariance and Heterogeneity for Drug Repositioning.Interdisciplinary sciences, computational life sciences · 2026Article
- Single-nucleus multiome analysis in the human prefrontal cortex identifies gene expression and cis-regulatory elements associated with aging.Cell reports · 2026Article
- Integrating imaging and omics for enhanced subtyping of mild cognitive impairment associated with Alzheimer's disease.Journal of translational medicine · 2025Article
- Characterizing the expression profile of 3R tau pathology in Pick's disease.Science advances · 2025Article
- Microscopy assessment of a fluorescence [Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Article
- Corrigendum to "Binge ethanol exposure in advanced age elevates neuroinflammation and early indicators of neurodegeneration and cognitive impairment in female mice" [Brain Behav. Immun. 116 (2024) 303-316].Brain, behavior, and immunity · 2024Article
- Potential shared gene signatures and molecular mechanisms between recurrent pregnancy loss and ovarian cancer.Frontiers in oncology · 2024Article
- Targeting of wnt signalling pathway by small bioactive molecules for the treatment of Alzheimer's disease.In silico pharmacology · 2024Article
- Identification of key proteins in early-onset Alzheimer's disease based on WGCNA.Frontiers in aging neuroscience · 2024Article
- Treatment of Alzheimer's Disease: Beyond Symptomatic Therapies.International journal of molecular sciences · 2023Review
- Longitudinal APOE4- and amyloid-dependent changes in the blood transcriptome in cognitively intact older adults.Alzheimer's research & therapy · 2023Article
- Molecular crosstalk between COVID-19 and Alzheimer's disease using microarray and RNA-seq datasets: A system biology approach.Frontiers in medicine · 2023Article
- Integrated analyses of brain and platelet omics reveal their common altered and driven molecules in Alzheimer's disease.MedComm · 2022Article
- Molecular dynamics and structure-based virtual screening and identification of natural compounds as Wnt signaling modulators: possible therapeutics for Alzheimer's disease.Molecular diversity · 2022Article
- Phosphorylation of guanosine monophosphate reductase triggers a GTP-dependent switch from pro- to anti-oncogenic function of EPHA4.Cell chemical biology · 2022Article
- Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer's disease risk.Scientific reports · 2022Article
- Genome-wide association study identifies quantitative trait loci affecting cattle temperament.Zoological research · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a severe neurodegenerative disorder for which identification of differentially expressed genes is one way to find new therapeutic targets. Here, we conducted analysis to identify age-independent, AD-specific genes. We found that the MET, WIF1, and NPTX2 genes are downregulated in AD. WIF1 and MET are implicated in Wnt and MET signaling and regulate GSK3β activity and are thus linked with AD. Importantly, we found that the GMPR gene exhibited a gradual increase in AD progression. A logistic model based on GMPR has good ability to classify AD cases. GMPR's product GMPR1 is in the AMPK and adenosine receptor pathways and is thus associated with Tau phosphorylation in AD. This allows GMPR1 to be a therapeutic target. Therefore, we screened five possible inhibitors to GMPR1 by docking GMPR1 with 1,174 approved drugs. Among them, lumacaftor is ideal. We then tested the effects of lumacaftor on AD model mice. After 20 days of oral administration, we observed that β-Amyloid accumulation was slowed down, and phosphorylation of Tau was almost eliminated in the treated mice. We highlight the elevated expression level of GMPR in AD and propose a therapeutic strategy of inhibiting GMPR1 with lumacaftor.
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