Topic: DCX

Introduction: Early life stress (ELS) might produce long lasting changes in hippocampal neurogenesis and increase the vulnerability to stress-related disorders later in adulthood. Objective: The analysis of immature granule cell densities in the hippocampal dentate gyrus (DG) between male and female mice subjected to ELS. Methods: Female and male C57BL/6J mice were subjected to 3h daily maternal separation (MS) for 21 days since birth. In day 60, mice underwent a single 2h restriction stress (RS) and sacrificed 24 hours after. The experimental groups were: Control, RS, MS, MS+RS. The DG was an

Development of the cerebral cortex involves many phases, including neural stem cell proliferation, neuronal migration, and differentiation. Defects in these phases lead to malformations in cortical development (MCDs). For example, disruption in neuronal migration causes lissencephaly, a form of MCD characterized by a smooth brain surface. Mutations in a number of genes, such as PAFAH1B1 (aka LIS1), DCX, TUBA1A, ARX, and DYNC1H1, are common causes behind lissencephaly. Many of those genes are involved in microtubule assembly and stabilization during neuronal migration. Recently, mutations in MA

In the adult mammalian brain, there are dormant neuronal precursors located in various cortical and subcortical areas. Unlike progenitors of the canonical neurogenic niches, dormant precursors emerge prenatally and maintain a state of post-mitotic quiescence until they mature in response to yet unknown stimuli. Several reports indicated that the maturation of dormant precursors is rather slow and staggered across adulthood. Here, we directly compared the maturation rate of cortical dormant precursors to that of age-matched adult-born hippocampal neurons, derived from adult neurogenesis. To thi

Pathogenic variants in DCX on the X chromosome lead to lissencephaly and subcortical band heterotopia (SBH), brain malformations caused by neuronal migration defects. Doublecortin (DCX) binds to microtubules to modulate microtubule polymerization. How pathogenic DCX variants affect these activities remains not fully investigated. Our aim is to examine whether these variants affect microtubule binding and dynamics and develop a verification tool to apply on clinical research. DCX variants were identified using whole exome and Sanger sequencing from six families with lissencephaly/SBH. We examin