
Uxue BalantzategiUniversity of the Basque Country | UPV/EHU · Departamento de Neurociencias
Uxue Balantzategi
PhD in Neuroscience | Master's degree in Neuroscience | Biochemist and Molecular Biologist
Postdoctoral researcher at the University of the Basque Country (EHU/UPV) and Achucarro Basque Center for Neuroscience
About
6
Publications
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Introduction
Postdoctoral researcher at the University of the Basque Country and Achucarro Basque Center for Neuroscience.
My study focuses on elucidating oligodendrocyte and myelin alterations in the early stages of Alzheimer's disease, aiming to uncover their potential role in disease progression and therapeutic strategies.
Skills and Expertise
Additional affiliations
Education
September 2018 - July 2019
September 2014 - July 2018
Publications
Publications (6)
Amyloid β oligomers (Aβo) 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 Aβo affect OL differentiation and myelination in vivo , and the underlying molecular mechanisms. In this study, we explored the effects of a...
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. Here, transc...
Glial cells participate actively in the early cognitive decline in Alzheimer’s disease (AD) pathology. In fact, recent studies have found molecular and functional abnormalities in astrocytes and microglia in both animal models and brains of patients suffering from this pathology. In this regard, reactive gliosis intimately associated with amyloid p...
Amyloid beta (Aβ)-mediated synapse dysfunction is an early event in Alzheimer’s disease (AD) pathogenesis and previous studies suggest that NMDA receptor (NMDAR) dysregulation may contribute to these pathological effects. Although Aβ peptides impair NMDAR expression and activity, the mechanisms mediating these alterations in the early stages of AD...
Background
Amyloid beta (Aβ)-mediated synapse dysfunction is an early event in Alzheimer's disease (AD) pathogenesis and previous studies suggest that NMDA receptor (NMDAR) dysregulation may contribute to these pathological effects. Although Aβ peptides impair NMDAR expression and activity, the mechanisms mediating these alterations in early stages...