ArticleNeuroImage. Clinical2012
Age dependent forebrain structural changes in mice deficient in the autism associated gene Met tyrosine kinase.
Article in NeuroImage. Clinical, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Translational Magnetic Resonance Imaging in Autism Spectrum Disorder From the Mouse Model to Human.Frontiers in neuroscience · 2022Review
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020Review
- Morphological Alterations in the Thalamus, Striatum, and Pallidum in Autism Spectrum Disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Insulin-Independent GABAA Receptor-Mediated Response in the Barrel Cortex of Mice with Impaired Met Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Striatal Circuits as a Common Node for Autism Pathophysiology.Frontiers in neuroscience · 2016Review
- Behavioral and Neuroanatomical Phenotypes in Mouse Models of Autism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- HGF-Met Pathway in Regeneration and Drug Discovery.Biomedicines · 2014Review
- Altered Forebrain Functional Connectivity and Neurotransmission in a Kinase-Inactive Met Mouse Model of Autism.Molecular imagingArticle
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
The MET tyrosine kinase has been identified as a susceptibility gene in patients with autism spectrum disorders. MET is expressed in the forebrain during prenatal and postnatal development. After birth, MET participates in dendritic outgrowth and circuit formation. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Patients with autism can exhibit abnormal cortical volumes and head circumferences. We tested the hypothesis that impaired Met signaling during development alters forebrain structure. We have utilized a conditional mutant mouse line which expresses a kinase-dead Met restricted to the cerebral cortex and hippocampal structures. In these mice, we have used magnetic resonance imaging (MRI) to analyze the structure of the cerebral cortex and related structures across postnatal development. We found that the rostral cortex, caudal hippocampus, dorsal striatum, thalamus, and corpus callosum were all larger in adult, but not juvenile, mutant mice relative to control mice. The specificity of the changes suggests that aberrant expansion of the forebrain is consistent with continued axonal and dendritic growth, potentially leading to improper circuit formation and maintenance.
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.