Publications by authors named "B Barak"
Article Synopsis
- Autism spectrum disorder (ASD) is associated with social and cognitive difficulties, and certain genetic mutations, particularly in the Shank3 gene, are linked to specific cases of monogenic ASD.
- Research using the InsG3680 mouse model shows that Shank3 plays an important role in the functioning of oligodendrocytes (cells that support myelin in the brain) and affects their development negatively when mutated.
- The study found that InsG3680 mice had significant issues with myelin formation and motor skills, showing that problems with Shank3 and oligodendrocytes may contribute to the neurological aspects of ASD.
Williams syndrome (WS) is a genetic neurodevelopmental disorder caused by a heterozygous microdeletion, characterized by hypersociability and unique neurocognitive abnormalities. Of the deleted genes, GTF2I has been linked to hypersociability in WS. We have recently shown that Gtf2i deletion from forebrain excitatory neurons, referred to as Gtf2i conditional knockout (cKO) mice leads to multi-faceted myelination deficits associated with the social behaviors affected in WS.
View Article and Find Full Text PDFInterest in myelin and its roles in almost all brain functions has been greatly increasing in recent years, leading to countless new studies on myelination, as a dominant process in the development of cognitive functions. Here, we explore the unique role myelin plays in the central nervous system and specifically discuss the results of altered myelination in neurodevelopmental disorders. We present parallel developmental trajectories involving myelination that correlate with the onset of cognitive impairment in neurodevelopmental disorders and discuss the key challenges in the treatment of these chronic disorders.
View Article and Find Full Text PDFArticle Synopsis
- Gtf2i is crucial for brain development, particularly in excitatory neurons, influencing mitochondrial function during critical growth periods.
- Deleting Gtf2i leads to abnormal mitochondrial structure, disrupted gene expression related to mitochondrial dynamics, and increased oxidative stress in neurons.
- These findings highlight the role of Gtf2i in mitochondrial regulation and may contribute to understanding conditions like Williams syndrome and related disorders.