Uxue Balantzategi

Uxue Balantzategi
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University of the Basque Country | UPV/EHU · Departamento de Neurociencias

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
422
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32
Citations
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.
Additional affiliations
Achucarro Basque Center for Neuroscience
Position
  • Postdoctoral researcher
Education
September 2018 - July 2019
University of Barcelona
Field of study
  • Neuroscience
September 2014 - July 2018
University of the Basque Country
Field of study
  • Biochemistry and Molecular Biology

Publications

Publications (6)
Preprint
Full-text available
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...
Preprint
Full-text available
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...
Article
Full-text available
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...
Article
Full-text available
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...
Preprint
Full-text available
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...

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