Trial reportMolecular psychiatry2005
GAD1 (2q31.1), which encodes glutamic acid decarboxylase (GAD67), is associated with childhood-onset schizophrenia and cortical gray matter volume loss.
Trial report in Molecular psychiatry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
What it found
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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
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.
- Childhood-Onset Schizophrenia: A Systematic Overview of Its Genetic Heterogeneity From Classical Studies to the Genomic Era.Frontiers in genetics · 2019Pooled it
- Excitatory neurons and oligodendrocyte precursor cells are vulnerable to focal cortical dysplasia type IIIa as suggested by single-nucleus multiomics.Clinical and translational medicine · 2024Article
- Integrative metabolomics-genomics analysis identifies key networks in a stem cell-based model of schizophrenia.Molecular psychiatry · 2024Article
- Beyond the γ-aminobutyric acid hypothesis of schizophrenia.Frontiers in cellular neuroscience · 2023Review
- Regulation of the E/I-balance by the neural matrisome.Frontiers in molecular neuroscience · 2023Review
- A preliminary genetic association study of GAD1 and GABAB receptor genes in patients with treatment-resistant schizophrenia.Molecular biology reports · 2022Article
- Interdisciplinary Approach to Biological and Health Implications in Selected Professional Competences.Brain sciences · 2022Review
- Exploration of Mutated Genes and Prediction of Potential Biomarkers for Childhood-Onset Schizophrenia Using an Integrated Bioinformatic Analysis.Frontiers in aging neuroscience · 2022Article
- Cellular Models in Schizophrenia Research.International journal of molecular sciences · 2021Review
- Association of lncRNA with regulatory molecular factors in brain and their role in the pathophysiology of schizophrenia.Metabolic brain disease · 2021Review
- Genome wide association study identifies four loci for early onset schizophrenia.Translational psychiatry · 2021Article
- CRISPR/Cas: a Nobel Prize award-winning precise genome editing technology for gene therapy and crop improvement.Journal of Zhejiang University. Science. B · 2021Review
- Weak Association Between the Glutamate Decarboxylase 1 Gene (GAD1) and Schizophrenia in Han Chinese Population.Frontiers in neuroscience · 2021Article
- Behavioral Consequences of a Combination ofFrontiers in pharmacology · 2021Article
- CRISPR/Cas9-engineered Gad1 elimination in rats leads to complex behavioral changes: implications for schizophrenia.Translational psychiatry · 2020Article
- Bi-allelic GAD1 variants cause a neonatal onset syndromic developmental and epileptic encephalopathy.Brain : a journal of neurology · 2020Article
- GABAergic Abnormalities Associated with Sensorimotor Cortico-striatal Community Structural Deficits in ErbB4 Knockout Mice and First-Episode Treatment-Naïve Patients with Schizophrenia.Neuroscience bulletin · 2020Article
- Bypassing Glutamic Acid Decarboxylase 1 (Gad1) Induced Craniofacial Defects with a Photoactivatable Translation Blocker Morpholino.ACS chemical neuroscience · 2019Article
- Association of rs4680Frontiers in psychiatry · 2019Article
- A novel homozygous mutation in GAD1 gene described in a schizophrenic patient impairs activity and dimerization of GAD67 enzyme.Scientific reports · 2018Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Postmortem brain studies have shown deficits in the cortical gamma-aminobutyric acid (GABA) system in schizophrenic individuals. Expression studies have shown a decrease in the major GABA-synthesizing enzyme (glutamic acid decarboxylase (GAD67) mRNA levels in neurons in dorsolateral prefrontal cortex in schizophrenics relative to controls. In the present study, SNPs in and around the GAD1 gene, which encodes the protein GAD67, were tested on a rare, severely ill group of children and adolescents with childhood-onset schizophrenia (COS) (n=72), in a family-based association analysis. Compared to adult-onset samples, the COS sample has evidence for more salient familial, and perhaps genetic, risk factors for schizophrenia, as well as evidence for frontal cortical hypofunction, and greater decline in cortical gray matter volume on anatomic brain MRI scans during adolescence. We performed family-based TDT and haplotype association analyses of the clinical phenotype, as well as association analyses with endophenotypes using the QTDT program. Three adjacent SNPs in the 5' upstream region of GAD1 showed a positive pairwise association with illness in these families (P=0.022-0.057). Significant transmission distortion of 4-SNP haplotypes was also observed (P=0.003-0.008). Quantitative trait TDT analyses showed an intriguing association between several SNPs and increased rate of frontal gray matter loss. These observations, when taken together with the positive results reported recently in two independent adult-onset schizophrenia pedigree samples, suggest that the gene encoding GAD67 may be a common risk factor for schizophrenia.
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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.