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HIPPOCAMPAL IRF7 ELEVATION AND CORTICAL AND HIPPOCAMPAL CLDN5 LOSS MARK EARLY NEUROINFLAMMATORY CHANGES IN DIABETIC MICE
Lucía Martín Rodríguezand 6 co-authors
Centro de Biología Molecular Severo Ochoa (CBMSO)
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-041
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Date TBA
Board: PS04-08PM-041
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Poster Board
PS04-08PM-041
Poster
View posterAbstract
Type 2 diabetes mellitus (T2DM) is associated with an increased risk of cognitive dysfunction, including Alzheimer’s disease. Previous transcriptomic analyses performed in a mouse model of overt diabetes (high-fat diet (HFD)/streptozotocin) revealed cognitive deficits and increased expression of Interferon Regulatory Factor 7 (Irf7), along with decreased expression of the blood–brain barrier integrity molecule Claudin-5 (Cldn5).
In the present study, we aimed to determine whether cognitive deficits and region-specific molecular alterations also occur in a prediabetic/early T2DM model. Adult male and female mice fed an HFD for 16 weeks displayed impaired cognitive performance, characterized by reduced exploration of the target quadrant in the Barnes maze compared to control animals, indicating deficits in spatial memory.
IRF7 protein expression was significantly increased in the hippocampus of HFD-fed mice, whereas CLDN5 levels were reduced in both the hippocampus and cerebral cortex. These results support the notion that region-specific inflammatory responses are early events in the course of T2DM.
Future studies will focus on: a) determining the degree of blood–brain barrier permeability, b) assessing the extent to which inflammatory changes in the brain result from the passage of peripheral agents or molecules (e.g., viruses, cytokines) versus brain-restricted alterations, c) identifying which brain cell types are responsible for increased IRF7 expression and activity, d) characterizing the inflammatory changes associated with elevated IRF7 levels and e) determining the extent to which increased IRF7 contributes to cognitive deficits.
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