Publications by authors named "Yuto Kubota"

Alexander disease (AxD) is an intractable neurodegenerative disease caused by mutations in (), which is predominantly expressed in astrocytes. Thus, AxD is a primary astrocyte disease. However, it remains unclear how mutations affect astrocytes and cause AxD pathology.

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Peripheral infection induces inflammation in peripheral tissues and the brain, impacting brain function. Glial cells are key players in this process. However, the effects of peripheral infection on glial activation and brain function remain unknown.

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Alexander disease (AxD) is an intractable neurodegenerative disorder caused by GFAP mutations. It is a primary astrocyte disease with a pathological hallmark of Rosenthal fibres within astrocytes. AxD astrocytes show several abnormal phenotypes.

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Purpose: Because the importance of glia in regulating brain functions has been demonstrated, genetic technologies that manipulate glial cell-specific gene expression in the brain have become essential and have made great progress. However, it is unknown whether the same strategy that is used in the brain can be applied to the retina because retinal glia differs from glia in the brain. Here, we aimed to find a method for selective gene expression in Müller cells (characteristic glial cells in the retina) and identified Mlc1 as a specific promoter of Müller cells.

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Article Synopsis
  • Metabotropic glutamate receptor 5 (mGluR5) is essential for synapse remodeling in astrocytes, being abundant in neonates but declining in adults; however, it may reappear in adults during certain diseases, leading to uncontrolled synapse formation.
  • Recent research indicates that ATP and adenosine signaling can down-regulate mGluR5 expression in astrocytes, with calcium responses decreasing as development progresses, while mGluR5 gene expression also declines.
  • The adenosine A receptor (Adora2b) plays a key role in this down-regulation; deleting this receptor leads to more excitatory synapses, suggesting it helps prevent excessive synapse formation during development.
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