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EVALUATING THE OXYSTEROL-DEPENDENT PATHWAYS INVOLVED IN ALZHEIMER’S DISEASE ASTROCYTE REACTIVITY
Gianni Vinayand 11 co-authors
University of Turin
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-142
Presentation
Date TBA
Board: PS01-07AM-142
Event Information
Poster Board
PS01-07AM-142
Poster
View posterAbstract
Astrocyte reactivity is a hallmark of neuroinflammation that arises with Alzheimer's disease (AD) and correlates with neuronal loss. Although astrocyte mechanisms that influence neuronal health are not clear, one possibility is the increased release of lipocalin-2 (Lcn2). Lcn2 affects neurite complexity and dendritic spine density in co-culture experiments. Cholesterol dysmetabolism is involved in AD. Excess cholesterol in the brain is oxidized into oxysterols which are involved in several regulatory functions (cholesterol metabolism, inflammation, immune response) and whose accumulation correlates with AD progression. Challenging astrocytes with an oxysterol mixture, in a proportion that reflects the composition observed in cortices of advanced AD brains, triggered astrocyte reactivity and Lcn2 upregulation. The aim is to unveil the pathways responsible for Lcn2 increase in primary astrocytes following exposure to oxysterols. Primary astrocytes were harvested from CD1 mouse pups at the 2nd day of life, then plated and treated with the oxysterol mixture (33.2% 24-OHC, 5.8% 27-OHC, 12.6% 7-KC, 5.3% 7alpha-OHC, 23.5% 7beta-OHC, 4.8% alpha-EPOX, 13,9% beta-EPOX, 0,9% 25-OHC) for different time-frames, in the presence or not of ERK1/2 and STAT3 inhibitors. Lcn2 protein levels as well as ERK1/2 and STAT3 phosphorylation levels were analysed by Western blotting. We demonstrated a time-dependent activation of ERK1/2 and STAT3 and confirmed the oxysterol ability to upregulate Lcn2 synthesis. The results highlight the involvement of ERK1/2- and STAT3-dependend pathways in the activation of Lcn2 transcription by oxysterols. The Project will deepen the pathways underlying neuroinflammation in AD, contributing to the development of preventive strategies and new targeted therapies.
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