Authors
Chang Liu, Kimia Sakha, Jaime Anton, Alfredo Cardenas-Rivera, Mohammad A Yaseen
Published in
bioRxiv : the preprint server for biology. Oct 20, 2025. Epub Oct 20, 2025.
Abstract
Chronic neuroinflammation in Alzheimer's disease (AD) activates astrocytes-key regulators of both brain immunity and neurovascular coupling. The primed immune environment in AD brain also renders it highly susceptible to secondary systemic inflammatory challenges. Inflammatory activation drives phenotypic shifts in astrocytes that may compromise their ability to regulate cerebral blood flow. The capacity for inflammation-activated astrocytes to retain this regulatory function, however, remains unknown. To investigate astrocyte regulation of cerebral blood flow in AD brain and under systemic inflammation, we investigated astrocytic Ca2+ dynamics and functional hyperemia at rest and during brief and prolonged sensory stimulation in 12-month-old female APP/PS1dE9 mice. We further examined how a secondary systemic inflammatory challenge induced by low-dose, repeated injection of LPS modulates astrocytic signaling and neurovascular function. AD mice exhibited elevated spontaneous but diminished stimulation-evoked astrocytic Ca2+ activity, accompanied by impaired sustained functional hyperemia, particularly within the capillary network. LPS-induced systemic inflammation further suppressed both spontaneous and evoked astrocytic Ca2+ responses and attenuated functional hyperemia. Together, these findings reveal that inflammation disrupts astrocyte-dependent regulation of sustained neurovascular responses in the AD brain.
PMID:
40950061
Bibliographic data and abstract were imported from PubMed on 26 Oct 2026.
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