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Adhara Gaminde-Blasco on Muck Rack

Adhara Gaminde-Blasco

As seen in: Wiley Online Library, BioRxiv
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Articles

Amyloid‐β Dysregulates Oligodendroglial Lineage Cell Dynamics and Myelination via PKC in the Zebrafish Spinal Cord

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By Uxue Balantzategi, Adhara Gaminde-Blasco, Christina A Kearns, Laura Bayon-Cordero
| Wiley Online Library Verified
1 Introduction Oligodendrocytes (OLs) are specialized glial cells responsible for forming myelin sheaths around axons in the central nervous system (CNS). This myelination is essential for the rapid propagation of electrical signals and overall neuronal connectivity (Baumann and Pham-Dinh 2001).
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Amyloid beta oligomers dysregulate oligodendrocyte differentiation and myelination via PKC in the zebrafish spinal cord

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By Uxue Balantzategi, Adhara Gaminde-Blasco, Laura Bayon-Cordero, Maria Victoria Sanchez-Gomez
| BioRxiv
Abstract Amyloid beta oligomers (Abetao) have been proposed as candidates to induce oligodendrocyte (OL) and myelin dysfunctions in early stages of Alzheimer's disease (AD) pathology. Nevertheless, little is known about how Abetao affect OL differentiation and myelination in vivo, and the underlying molecular mechanisms. In this study, we explored the effects of a brain intraventricular injection of Abetao on OLs and myelin in the developing spinal cord of zebrafish larvae.
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Amyloid-beta increases MBP and MOBP translation in oligodendrocytes through dysregulation of hnRNP A2 dependent RNA dynamics

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By Adhara Gaminde-Blasco, Rodrigo Senovilla-Ganzo, Fernando Garcia-Moreno, Uxue Balantzategi
| BioRxiv
Abstract Oligodendrocyte dysfunction, myelin degeneration, and white matter structural alterations are critical events in Alzheimer's disease (AD) that contribute to cognitive decline. A key hallmark of AD, Abeta oligomers, disrupt oligodendrocyte and myelin homeostasis, but a comprehensive global analysis of the mechanisms involved is lacking.
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