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Page 126 of 546-
Comparative studies on K -p-nitrophenylphosphatase, K -acylphosphatase and (Na + K)adenosinetriphosphatase in synaptosomes of rat brain.
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Founder cells shape brain evolution.
Humans have an extraordinarily expanded and complex cerebral cortex, relative to non-human primates. Yet the mechanisms underlying cortical differences across evolution are unclear. A new study by Benito-Kwiecinski et al. employs cerebral organoids derived across great apes to implicate neuroepithelial progenitor shape transitions in human cortical expansion.
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'Biocomputer' combines lab-grown brain tissue with electronic hardware.
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Should Cerebral Organoids be Used for Research if they Have the Capacity for Consciousness?
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MeCP2 regulates telencephalic development in human cerebral organoids.
Loss-of-function variants in the X-linked gene MeCP2 cause a severe form of syndromic autism spectrum disorder known as Rett syndrome (RTT). Although traditionally considered a postnatal disorder, increasing evidence suggests that MeCP2 plays a crucial role during prenatal brain development. Here, we used human pluripotent stem cell-derived cerebral organoids and human telencephalic assembloids to model early cortical development in the context of MeCP2 deficiency. Loss of MeCP2 led to widespread dysregulation of transcriptional programs associated with cortical excitatory neuron development, accompanied by delayed morphological and functional maturation, despite preserved neuroepithelial architecture, dorsal telencephalic identity, and laminar organization. MeCP2 deficiency also led to an overproduction of cortical interneurons (cINs), with these cINs exhibiting hypermotile tangential migration dynamics and contributing to persistent hypersynchronous network activity in assembloids. These findings highlight the critical role of MeCP2 in early telencephalic neurodevelopment and underscore the prenatal origin of RTT-related dysfunction.
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Spontaneous pineal body tumours (pinealomas) in Wistar rats; a histological and ultrastructural study.
The pathology of 5 cases of pinealomas in Wistar rats used in long-term toxicological studies is described both grossly, microscopically and ultrastructurally, together with a review of the related literature.
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Extracellular vesicle-mediated trafficking of molecular cues during human brain development.
Cellular crosstalk is an essential process influenced by numerous factors, including secreted vesicles that transfer nucleic acids, lipids, and proteins between cells. Extracellular vesicles (EVs) have been the center of many studies focusing on neurodegenerative disorders, but whether EVs display cell-type-specific features for cellular crosstalk during neurodevelopment is unknown. Here, using human-induced pluripotent stem cell-derived cerebral organoids, neural progenitors, neurons, and astrocytes, we identify heterogeneity in EV protein content and dynamics in a cell-type-specific and time-dependent manner. Our results support the trafficking of key molecules via EVs in neurodevelopment, such as the transcription factor YAP1, and their localization to differing cell compartments depending on the EV recipient cell type. This study sheds new light on the biology of EVs during human brain development.
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Expression of a novel brain specific isoform of C3G is regulated during development.
Mice lacking C3G (RapGEF1), a ubiquitously expressed protein essential for neuronal differentiation, show multiple defects in brain development. Function of C3G in neurogenesis is poorly defined. Here, we identify brain specific expression of a novel C3G isoform in mice and humans. This isoform has an insert in the Crk-binding region, generating a polypeptide of 175 kDa, unlike the previously known 140 kDa form expressed in all other tissues. In the adult mouse brain, C3G expression is seen in neurons, but was not detectable in GFAP-positive cells. C3G levels were high in the CA3 region of hippocampus and in mitral cells of olfactory bulb. Neural progenitor cells positive for Doublecortin and Nestin, show expression of C3G. During development, C3G is expressed in precursor cells prior to their differentiation into mature neurons or astrocytes. The 175 kDa as well as 140 kDa forms are seen in embryonic mouse brain, while only the 175 kDa variant is seen in post-natal brain. Human cerebral organoids generated from induced pluripotent stem cells predominantly expressed the 140 kDa polypeptides, and the 175 kDa isoform appeared upon maturation. This study describes developmental regulation and neuronal expression of a brain specific isoform of C3G, a molecule essential for normal development of the mammalian brain.
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Catecholamine uptake processes.
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Proceedings: Origin of brain macrophages - a new experimental model.