ReviewMolecular psychiatry2025
An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.
Review in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Elevated synaptic PKA activity and abnormal striatal dopamine signaling in Akap11 mutant mice, a genetic model of schizophrenia and bipolar disorder.Nature communications · 2025Article
- Elevated synaptic PKA activity and abnormal striatal dopamine signaling inbioRxiv : the preprint server for biology · 2025Article
- The acoustic startle response in 22q11 deletion syndrome: from animal models to humans.Frontiers in neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
In applying model organisms to study the neurobiology of mental disorders, rodents offer unique potential for probing, with high spatiotemporal resolution, the neural and molecular mechanisms underlying behavior in a mammalian system. Furthermore, investigators can wield exceptional power to manipulate genes, molecules, and circuits in mice to pin down causal relationships. While these advantages have allowed us to understand much more deeply than ever before the brain mechanisms regulating complex behaviors, the impact of rodent models on developing therapeutic strategies for psychiatric disorders has remained thus far limited. Herein, we will discuss the opportunities and limits of using mouse models in the context of schizophrenia, a complex psychiatric disorder with strong genetic basis that poses various unmet clinical needs calling out for basic science research. We review approaches for employing behavioral, genetic, and circuit-based methods in rodents to inform schizophrenia symptomatology, pathophysiology, and, ultimately, treatment.
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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.