Ardanaz, C.G. (Carlos G.)

Filtering

2021 - 20242

Settings

Author search.filters.isAuthorOfPublication.40133ce9-e419-473a-ab48-b29a8be0fcd8

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Astrocytic GLUT1 reduction paradoxically improves central and peripheral glucose homeostasis
    (AAAS, 2024) Ardanaz, C.G. (Carlos G.); Cruz, A. (Aida) de la; Minhas, P.S. (Paras S.); Hernández-Martí, N. (Nira); Pozo, M.A. (Miguel Ángel); Valdecantos, M.P. (Mª Pilar); Valverde, A.M. (Ángela M.); Villa-Valverde, P. (Palmira); Elizalde-Horcada, M. (Marcos); Puerta, E. (Elena); Ramirez, M.J. (María Javier); Ortega, J. (J.); Urbiola, A. (Ainhoa); Ederra, C. (Cristina); Ariz, M. (Mikel); Ortiz-de-Solorzano, C. (Carlos); Fernández-Irigoyen, J. (Joaquín); Santamaria, E. (Enrique); Karsenty, G. (Gerard); Brüning, J.C. (Jens C.); Solas, M. (Maite)
    Astrocytes are considered an essential source of blood-borne glucose or its metabolites to neurons. Nonetheless, the necessity of the main astrocyte glucose transporter, i.e., GLUT1, for brain glucose metabolism has not been defined. Unexpectedly, we found that brain glucose metabolism was paradoxically augmented in mice with astrocytic GLUT1 reduction (GLUT1ΔGFAP mice). These mice also exhibited improved peripheral glucose metabolism especially in obesity, rendering them metabolically healthier. Mechanistically, we observed that GLUT1-deficient astrocytes exhibited increased insulin receptor-dependent ATP release, and that both astrocyte insulin signaling and brain purinergic signaling are essential for improved brain function and systemic glucose metabolism. Collectively, we demonstrate that astrocytic GLUT1 is central to the regulation of brain energetics, yet its depletion triggers a reprogramming of brain metabolism sufficient to sustain energy requirements, peripheral glucose homeostasis, and cognitive function.
  • Thumbnail Image
    Biomarcadores en la enfermedad de Alzheimer
    (Gruyter, 2021) Janeiro-Arenas, M.H. (Manuel Humberto); Ardanaz, C.G. (Carlos G.); Sola-Sevilla; Dong, J. (Jinya); Cortés-Erice, M. (María); Solas-Zubiaurre, M. (Maite); Puerta, E. (Elena); Ramirez, M.J. (María Javier)
    Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disease. AD is the main cause of dementia worldwide and aging is the main risk factor for developing the illness. AD classical diagnostic criteria rely on clinical data. However, the development of a biological definition of AD using biomarkers that reflect the underling neuropathology is needed. Content: The aim of this review is to describe the main outcomes when measuring classical and novel biomarkers in biological fluids or neuroimaging. Summary: Nowadays, there are three classical biomarkers for the diagnosis of AD: Aβ42, t-Tau and p-Tau. The diagnostic use of cerebrospinal fluid biomarkers is limited due to invasive collection by lumbar puncture with potential side effects. Plasma/serum measurements are the gold standard in clinics, because they are minimally invasive and, in consequence, easily collected and processed. The two main proteins implicated in the pathological process, Aβ and Tau, can be visualized using neuroimaging techniques, such as positron emission tomography. Outlook: As it is currently accepted that AD starts decades before clinical symptoms could be diagnosed, the opportunity to detect biological alterations prior to clinical symptoms would allow early diagnosis or even perhaps change treatment possibilities.