ReviewMolecular psychiatry2020
Turning strains into strengths for understanding psychiatric disorders.
Review in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 8 citations in OpenAlex.
- Sex Differences in Behavioral Responses to Chronic Unpredictable Mild Stress in Swiss Mice.The European journal of neuroscience · 2026Article
- Microbial Composition, Disease Trajectory and Genetic Background in a Slow Onset Model of Frontotemporal Lobar Degeneration.Biomolecules · 2025Article
- An in vitro neurogenetics platform for precision disease modeling in the mouse.Science advances · 2024Article
- Detecting the effect of genetic diversity on brain composition in an Alzheimer's disease mouse model.bioRxiv : the preprint server for biology · 2023Article
- CB2 cannabinoid receptor expression is increased in 129S1/SvImJ mice: behavioral consequences.Frontiers in pharmacology · 2022Article
- Pursuit of precision medicine: Systems biology approaches in Alzheimer's disease mouse models.Neurobiology of disease · 2021Review
- The Importance of Common Currency Tasks in Translational Psychiatry.Current behavioral neuroscience reports · 2021Review
- Deficits across multiple behavioral domains align with susceptibility to stress in 129S1/SvImJ mice.Neurobiology of stress · 2020Article
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 at 1 institution in 1 country.
Funding
Abstract
There is a paucity in the development of new mechanistic insights and therapeutic approaches for treating psychiatric disease. One of the major challenges is reflected in the growing consensus that risk for these diseases is not determined by a single gene, but rather is polygenic, arising from the action and interaction of multiple genes. Canonically, experimental models in mice have been designed to ascertain the relative contribution of a single gene to a disease by systematic manipulation (e.g., mutation or deletion) of a known candidate gene. Because these studies have been largely carried out using inbred isogenic mouse strains, in which there is no (or very little) genetic diversity among subjects, it is difficult to identify unique allelic variants, gene modifiers, and epigenetic factors that strongly affect the nature and severity of these diseases. Here, we review various methods that take advantage of existing genetic diversity or that increase genetic variance in mouse models to (1) strengthen conclusions of single-gene function; (2) model diversity among human populations; and (3) dissect complex phenotypes that arise from the actions of multiple genes.
Indexed as
Identifiers
What Socratic 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 Socratic graph.