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ASTROCYTE-MEDIATED REGULATION OF CEREBRAL VASCULATURE IN A MOUSE MODEL OF FAMILIAL ALZHEIMER’S DISEASE
Nicole Tonesiand 4 co-authors
University of Padua
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-091
Presentation
Date TBA
Board: PS03-08AM-091
Event Information
Poster Board
PS03-08AM-091
Poster
View posterAbstract
Cerebrovascular dysfunction is often associated to Alzheimer’s disease (AD) and cerebral amyloid angiopathy is frequently observed in familial AD subjects. Vascular pathology contributes to neuronal degeneration, neuroinflammation and amyloid accumulation, and all these phenomena mutually amplify in AD. Here, we aim to characterize cerebrovascular features in the B6.152H mouse model of familial AD, carrying the APPswe mutation in neurons and the PSEN2 N141I mutation in neurons and astrocytes. Since astrocytes play a fundamental role in the neurovascular unit, we are investigating intracellular Ca²⁺ activity in astrocyte endfeet, specialized processes mediating astrocyte–vascular communication. We previously demonstrated weakened astrocytic Ca²⁺ dynamics in the somatosensory cortex of B6.152H mice and showed that restoration of astrocyte Ca²⁺ signaling is sufficient to fully rescue impaired long-term potentiation in 6-month-old AD mice. The goal of this project is to test whether this rescue strategy can be beneficial also in dampening vascular dysfunction. By combining two-photon Ca²⁺ imaging of astrocytic endfeet, intraluminal labelling with TRITC-dextran and immunohistochemical analysis, we are assessing possible alterations in the cerebrovascular system and in astrocyte signaling at the gliovascular interface. Our analysis reveals local cortical hypoperfusion in B6.152H mice at 8 months of age, despite comparable vessel density. Moreover, preliminary data indicate an altered Aquaporin-4 polarization between endfeet and cerebral parenchyma. We are now investigating astrocyte Ca2+ signal at endfeet and developing a protocol to probe neurovascular coupling, to gain fundamental information on functional impairment of the gliovascular unit.
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