ReviewNeurobiology of disease2012
Better understanding of mechanisms of schizophrenia and bipolar disorder: from human gene expression profiles to mouse models.
Review in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed.
- Shared Genetic Networks in Schizophrenia and Bipolar Disorder: Hippocampal Volume-Mediated Neurobiological Mechanisms.Schizophrenia bulletin · 2026Article
- Brain banking in the United States and Europe: Importance, challenges, and future trends.Journal of neuropathology and experimental neurology · 2024Article
- An Overview of Animal Models Related to Schizophrenia.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- An Integrative Computational Approach to Evaluate Genetic Markers for Bipolar Disorder.Scientific reports · 2017Article
- miRNAs in NMDA receptor-dependent synaptic plasticity and psychiatric disorders.Clinical science (London, England : 1979) · 2016Review
- Molecular substrates of schizophrenia: homeostatic signaling to connectivity.Molecular psychiatry · 2016Review
- Matrix Metalloproteinase-9 as a Novel Player in Synaptic Plasticity and Schizophrenia.Schizophrenia bulletin · 2015Review
- BrainNet Europe's Code of Conduct for brain banking.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
- Psychiatric risk factor ANK3/ankyrin-G nanodomains regulate the structure and function of glutamatergic synapses.Neuron · 2014Article
- What causes aberrant salience in schizophrenia? A role for impaired short-term habituation and the GRIA1 (GluA1) AMPA receptor subunit.Molecular psychiatry · 2014Review
- Chronic treatment with mood-stabilizers attenuates abnormal hyperlocomotion of GluA1-subunit deficient mice.PloS one · 2014Article
- MicroRNA-382 expression is elevated in the olfactory neuroepithelium of schizophrenia patients.Neurobiology of disease · 2013Article
- Genes, behavior and next-generation RNA sequencing.Genes, brain, and behavior · 2013Review
- Ankyrin 3: genetic association with bipolar disorder and relevance to disease pathophysiology.Biology of mood & anxiety disorders · 2012Article
- Systematic approaches to central nervous system myelin.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The molecular mechanisms of major mental illnesses, such as schizophrenia and bipolar disorder, are unclear. To address this fundamental question, many groups have studied molecular expression profiles in postmortem brains and other tissues from patients compared with those from normal controls. Development of unbiased high-throughput approaches, such as microarray, RNA-seq, and proteomics, have supported and facilitated this endeavor. In addition to genes directly involved in neuron/glia signaling, especially those encoding for synaptic proteins, genes for metabolic cascades are differentially expressed in the brains of patients with schizophrenia and bipolar disorder, compared with those from normal controls in DNA microarray studies. Here we propose the importance and usefulness of genetic mouse models in which such differentially expressed molecules are modulated. These animal models allow us to dissect the mechanisms of how such molecular changes in patient brains may play a role in neuronal circuitries and overall behavioral phenotypes. We also point out that models in which the metabolic genes are modified are obviously untested from mental illness viewpoints, suggesting the potential to re-address these models with behavioral assays and neurochemical assessments.
Indexed as
Identifiers
What OpenQuestion holds
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.