Publications by authors named "V D Bocchi"
Article Synopsis
- Huntington's disease (HD) leads to the degeneration of specific brain neurons, resulting in a mix of functional and dysfunctional cells, but the interactions between these cell types are not well understood.
- Researchers created brain organoids containing both healthy and HD cells, finding that HD organoids displayed neurodevelopmental issues and fewer GABAergic neurons compared to healthy ones.
- Healthy cells in mixed organoids helped to restore the identity and function of HD cells through direct interactions, suggesting that enhancing communication between different cell types could offer new treatment strategies for HD.
Outer radial glia (oRG) emerge as cortical progenitor cells that support the development of an enlarged outer subventricular zone (oSVZ) and the expansion of the neocortex. The in vitro generation of oRG is essential to investigate the underlying mechanisms of human neocortical development and expansion. By activating the STAT3 signaling pathway using leukemia inhibitory factor (LIF), which is not expressed in guided cortical organoids, we define a cortical organoid differentiation method from human pluripotent stem cells (hPSCs) that recapitulates the expansion of a progenitor pool into the oSVZ.
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- Researchers have developed a protocol for engineering striatal medium spiny neurons (MSNs) from human pluripotent stem cells (PSCs), which could be useful for understanding and treating neurological diseases, particularly Huntington's disease (HD).
- The protocol achieves high reproducibility and generates functional D1- and D2-MSNs in just 25 days by carefully modulating cell density and specific morphogens.
- Single-cell RNA sequencing confirms that these engineered cells resemble natural fetal MSNs in terms of gene expression and development, and adjustments to the midkine pathway can enhance MSN production.
Article Synopsis
- Researchers are creating human telencephalic organoids from stem cells to better understand developmental processes related to uniquely human behaviors and disorders.
- These organoids show complex organization with various types of neural cells, allowing for detailed study of excitatory and inhibitory neuron development.
- The study also reveals specific deficits in organoids with a deletion of the SHANK3 gene, which is linked to autism and intellectual disabilities, highlighting the usefulness of these organoids for investigating neurological issues.
Huntington's disease is caused by a pathologically long (>35) CAG repeat located in the first exon of the Huntingtin gene (HTT). While pathologically expanded CAG repeats are the focus of extensive investigations, non-pathogenic CAG tracts in protein-coding genes are less well characterized. Here, we investigated the function and evolution of the physiological CAG tract in the HTT gene.
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