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Editor’s summary Structured Abstract Abstract Supplementary Materials References and Notes Information & Authors Metrics & Citations Check Access References Figures Tables Media Share This article has 0 eLetter . Editor’s summary The mechanisms underlying the formation of cortical layers during cerebral cortex development (corticogenesis) remain to be fully elucidated. Nguyen et al.
Keywords: neural circuits cellular neuroscience neural stem cells epilepsy brain organoids disease modeling hippocampal assembloids Research topic(s) CP: Neuroscience Introduction Human neurodevelopmental disorders are often characterized by complex phenotypes involving neural network dysfunction across multiple brain regions. Despite this, our understanding of how a single perturbation can uniquely impact brain development and network function in different regions remains limited.
Abstract Repeat-associated non-AUG-initiated translation of expanded CGG repeats (CGG RAN) from the FMR1 5′-leader produces toxic proteins that contribute to neurodegeneration in fragile X-associated tremor/ataxia syndrome. Here we describe how unexpanded CGG repeats and their translation play conserved roles in regulating fragile X protein (FMRP) synthesis. In neurons, CGG RAN acts as an inhibitory upstream open reading frame to suppress basal FMRP production.
Many neuropsychiatric disorders are thought to result from subtle changes in neural circuit formation. We used human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) to model mature, postmitotic excitatory neurons and examine effects of FGF2. FGF2 gene expression is known to be altered in brain regions of major depressive disorder (MDD) patients and FGF2 has anti-depressive effects in animal models of depression.
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