Publications by authors named "I-Ting J Wang"
CDKL5 deficiency disorder (CDD) is characterized by epilepsy, intellectual disability, and autistic features, and CDKL5-deficient mice exhibit a constellation of behavioral phenotypes reminiscent of the human disorder. We previously found that CDKL5 dysfunction in forebrain glutamatergic neurons results in deficits in learning and memory. However, the pathogenic origin of the autistic features of CDD remains unknown.
View Article and Find Full Text PDFCyclin-dependent kinase-like 5 (CDKL5) deficiency is a neurodevelopmental disorder characterized by epileptic seizures, severe intellectual disability, and autistic features. Mice lacking CDKL5 display multiple behavioral abnormalities reminiscent of the disorder, but the cellular origins of these phenotypes remain unclear. Here, we find that ablating CDKL5 expression specifically from forebrain glutamatergic neurons impairs hippocampal-dependent memory in male conditional knock-out mice.
View Article and Find Full Text PDFArticle Synopsis
- Rett Syndrome (RTT) is a neurological disorder caused by mutations in the MECP2 gene, leading to loss of motor and language skills, with observable changes in neuronal structure.
- Researchers studied three Mecp2 mouse models (loss-of-function, partial loss-of-function, and gain-of-function) to assess the relationship between neuronal morphology and RTT-like behaviors at different developmental stages.
- Findings indicate that dendritic complexity varies across age and brain regions in loss-of-function models but remains consistent in gain-of-function models, suggesting soma size is a more reliable marker for evaluating MeCP2 function in RTT research.