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Hui-Hsin Tsai

Researcher at University of California, San Francisco

Publications -  21
Citations -  3939

Hui-Hsin Tsai is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Oligodendrocyte & Astrocyte. The author has an hindex of 20, co-authored 21 publications receiving 3338 citations. Previous affiliations of Hui-Hsin Tsai include National Taiwan University & Case Western Reserve University.

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Corridors of migrating neurons in the human brain and their decline during infancy

TL;DR: It is found that the infant human subventricular zone and RMS contain an extensive corridor of migrating immature neurons before 18 months of age but, contrary to previous reports, this germinal activity subsides in older children and is nearly extinct by adulthood.
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Astrocytes and disease: a neurodevelopmental perspective

TL;DR: It is proposed here that a precise understanding of astrocyte development is critical to defining heterogeneity and could lead advances in understanding and treating a variety of neuropsychiatric diseases.
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Regional Astrocyte Allocation Regulates CNS Synaptogenesis and Repair

TL;DR: It is shown that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone, and these domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury.
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The Chemokine Receptor CXCR2 Controls Positioning of Oligodendrocyte Precursors in Developing Spinal Cord by Arresting Their Migration

TL;DR: It is suggested that population of presumptive white matter by oligodendrocyte precursors is dependent on localized expression of CXCL1, and the role for the chemokine C XCL1 and its receptor CXCR2 in patterning the developing spinal cord is demonstrated.
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A dramatic increase of C1q protein in the CNS during normal aging.

TL;DR: It is shown that C1q protein levels dramatically increase in the normal aging mouse and human brain, by as much as 300-fold, and this increase was predominantly localized in close proximity to synapses and occurred earliest and most dramatically in certain regions of the brain, including some but not all regions known to be selectively vulnerable in neurodegenerative diseases.