ReviewCell and tissue research2013
Transgenic mouse models for ADHD.
Review in Cell and tissue research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Brain imaging genetics in ADHD and beyond - Mapping pathways from gene to disorder at different levels of complexity.Neuroscience and biobehavioral reviews · 2017Pooled it
- Article
- Increased expression of ATase1/NAT8B or ATase2/NAT8 in the mouse results in an autistic-like phenotype with altered dendritic branching and spine formation.Molecular psychiatry · 2026Article
- QnAs with Anne K. Churchland.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A Comprehensive 4-layeredCurrent pharmaceutical biotechnology · 2025Article
- Dopamine Transporter andJournal of child and adolescent psychopharmacology · 2024Article
- Neurobiology of attention-deficit hyperactivity disorder: historical challenges and emerging frontiers.Nature reviews. Neuroscience · 2024Review
- Patterns of ethanol intake in male rats with partial dopamine transporter deficiency.Genes, brain, and behavior · 2023Article
- Perinatal oxycodone exposure causes long-term sex-dependent changes in weight trajectory and sensory processing in adult mice.Psychopharmacology · 2022Article
- Slitrk2 deficiency causes hyperactivity with altered vestibular function and serotonergic dysregulation.iScience · 2022Article
- Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.Brain : a journal of neurology · 2022Article
- SLC13A5/sodium-citrate co-transporter overexpression causes disrupted white matter integrity and an autistic-like phenotype.Brain communications · 2022Article
- Promising Developments in the Use of Induced Pluripotent Stem Cells in Research of ADHD.Current topics in behavioral neurosciences · 2022Article
- Article
- Haloperidol rescues the schizophrenia-like phenotype in adulthood after rotenone administration in neonatal rats.Psychopharmacology · 2021Article
- Dysfunction of ventral tegmental area GABA neurons causes mania-like behavior.Molecular psychiatry · 2021Article
- Review
- Neonatal Rotenone Administration Induces Psychiatric Disorder-Like Behavior and Changes in Mitochondrial Biogenesis and Synaptic Proteins in Adulthood.Molecular neurobiology · 2021Article
- Animal Models of Depression: What Can They Teach Us about the Human Disease?Diagnostics (Basel, Switzerland) · 2021Review
- Hyperactive and impulsive behaviors of LMTK1 knockout mice.Scientific reports · 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
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Attention-deficit hyperactivity disorder (ADHD) is a developmental disorder characterized by symptoms of inattention, impulsivity and hyperactivity that adversely affect many aspects of life. Whereas the etiology of ADHD remains unknown, growing evidence indicates a genetic involvement in the development of this disorder. The brain circuits associated with ADHD are rich in monoamines, which are involved in the mechanism of action of psychostimulants and other medications used to treat this disorder. Dopamine (DA) is believed to play a major role in ADHD but other neurotransmitters are certainly also involved. Genetically modified mice have become an indispensable tool used to analyze the contribution of genetic factors in the pathogenesis of human disorders. Although rodent models cannot fully recapitulate complex human psychiatric disorders such as ADHD, transgenic mice offer an opportunity to directly investigate in vivo the specific roles of novel candidate genes identified in ADHD patients. Several knock-out and transgenic mouse models have been proposed as ADHD models, mostly based on targeting genes involved in DA transmission, including the gene encoding the dopamine transporter (DAT1). These mutant models provided an opportunity to evaluate the contribution of dopamine-related processes to brain pathology, to dissect the neuronal circuitry and molecular mechanisms involved in the antihyperkinetic action of psychostimulants and to evaluate novel treatments for ADHD. New transgenic models mouse models targeting other genes have recently been proposed for ADHD. Here, we discuss the recent advances and pitfalls in modeling ADHD endophenotypes in genetically altered animals.
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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.