ArticleJournal of molecular neuroscience : MN2018
In Silico Preliminary Association of Ammonia Metabolism Genes GLS, CPS1, and GLUL with Risk of Alzheimer's Disease, Major Depressive Disorder, and Type 2 Diabetes.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- CPS1: a multipurpose mitochondrial enzyme, bile protein, acute liver injury biomarker, and cytokine.Gut · 2026Review
- αB-crystallin elastin-like polypeptides for sustained ocular drug delivery.Drug delivery and translational research · 2026Article
- Controllability of morphometric network colocalize with underlying neurobiology in major depression.Psychological medicine · 2026Article
- Comprehensive Analysis to Reveal Nitrogen Metabolism-Associated Genes as a Prognostic Index in Head and Neck Squamous Cell Cancer.Current medicinal chemistry · 2026Article
- Complementary Strategies to Identify Differentially Expressed Genes in the Choroid Plexus of Patients with Progressive Multiple Sclerosis.Neuroinformatics · 2025Article
- The Effect of glna Loss on the Physiological and Pathological Phenotype of Parkinson's Disease C. elegans.Journal of clinical laboratory analysis · 2024Article
- Longitudinal Neuropathological Consequences of Extracranial Radiation Therapy in Mice.International journal of molecular sciences · 2024Article
- Metabolic phenotyping reveals an emerging role of ammonia abnormality in Alzheimer's disease.Nature communications · 2024Article
- Article
- Human neural stem cells restore spatial memory in a transgenic Alzheimer's disease mouse model by an immunomodulating mechanism.Frontiers in aging neuroscience · 2023Article
- Bioinformatics Analysis of Next Generation Sequencing Data Identifies Molecular Biomarkers Associated With Type 2 Diabetes Mellitus.Clinical medicine insights. Endocrinology and diabetes · 2023Article
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis.BMC cardiovascular disorders · 2021Article
- CPS1: Looking at an ancient enzyme in a modern light.Molecular genetics and metabolism · 2020Review
- A constitutive knockout of murine carbamoyl phosphate synthetase 1 results in death with marked hyperglutaminemia and hyperammonemia.Journal of inherited metabolic disease · 2019Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ammonia is a toxic by-product of protein catabolism and is involved in changes in glutamate metabolism. Therefore, ammonia metabolism genes may link a range of diseases involving glutamate signaling such as Alzheimer's disease (AD), major depressive disorder (MDD), and type 2 diabetes (T2D). We analyzed data from a National Institute on Aging study with a family-based design to determine if 45 single nucleotide polymorphisms (SNPs) in glutaminase (GLS), carbamoyl phosphate synthetase 1 (CPS1), or glutamate-ammonia ligase (GLUL) genes were associated with AD, MDD, or T2D using PLINK software. HAPLOVIEW software was used to calculate linkage disequilibrium measures for the SNPs. Next, we analyzed the associated variations for potential effects on transcriptional control sites to identify possible functional effects of the SNPs. Of the SNPs that passed the quality control tests, four SNPs in the GLS gene were significantly associated with AD, two SNPs in the GLS gene were associated with T2D, and one SNP in the GLUL gene and three SNPs in the CPS1 gene were associated with MDD before Bonferroni correction. The in silico bioinformatic analysis suggested probable functional roles for six associated SNPs. Glutamate signaling pathways have been implicated in all these diseases, and other studies have detected similar brain pathologies such as cortical thinning in AD, MDD, and T2D. Taken together, these data potentially link GLS with AD, GLS with T2D, and CPS1 and GLUL with MDD and stimulate the generation of testable hypotheses that may help explain the molecular basis of pathologies shared by these disorders.
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