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FROM EXTRAPARENCHYMAL CLEARANCE TO ASTROCYTIC SEQUESTRATION: AGING AND AMYLOID PATHOLOGY RESHAPE WASTE PATHWAYS
Clara Romera Niñoand 8 co-authors
Section of Physiology, Department of Biochemistry and Physiology, Faculty of Pharmacy and Food Sciences, Universitat de Barcelona
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-076
Presentation
Date TBA
Board: PS05-09AM-076
Event Information
Poster Board
PS05-09AM-076
Poster
View posterAbstract
Recent studies have identified several IgM-reactive histological structures as components of glial and meningeal waste-handling pathways in the mouse brain, including PAS-positive polyglucosan granules, extraparenchymal (EP) IgM⁺ granules, and IgM⁺ astrocytes. However, how these structures are affected by aging and amyloid pathology remains poorly understood.
Here, we examined brain tissue from APP/PS1 mice and C57BL/6 littermate controls at 3, 6, 12, and 22 months of age to assess age- and pathology-dependent changes in these IgM-associated elements.
PAS-positive granules increased markedly with age and showed a region-specific association with amyloid pathology, particularly in the hippocampus and piriform cortex. In contrast, EP IgM⁺ granules were most abundant in young mice and declined progressively with aging, independently of amyloid deposition. IgM⁺ astrocytes increased robustly with age and were consistently more abundant in APP/PS1 mice compared to controls. Triple immunofluorescence revealed co-expression of IgM and the complement component C3 in these astrocytes, indicating a complement-associated reactive phenotype. Correlation analyses demonstrated a strong relationship between β-amyloid plaque burden and IgM⁺ astrocytes, and a moderate, region-dependent association with PAS-positive granules.
Overall, these findings reveal a coordinated remodeling of brain waste-handling structures driven by aging and amyloid pathology, highlighting dynamic glial responses that may contribute to altered proteostasis in Alzheimer’s disease.
Here, we examined brain tissue from APP/PS1 mice and C57BL/6 littermate controls at 3, 6, 12, and 22 months of age to assess age- and pathology-dependent changes in these IgM-associated elements.
PAS-positive granules increased markedly with age and showed a region-specific association with amyloid pathology, particularly in the hippocampus and piriform cortex. In contrast, EP IgM⁺ granules were most abundant in young mice and declined progressively with aging, independently of amyloid deposition. IgM⁺ astrocytes increased robustly with age and were consistently more abundant in APP/PS1 mice compared to controls. Triple immunofluorescence revealed co-expression of IgM and the complement component C3 in these astrocytes, indicating a complement-associated reactive phenotype. Correlation analyses demonstrated a strong relationship between β-amyloid plaque burden and IgM⁺ astrocytes, and a moderate, region-dependent association with PAS-positive granules.
Overall, these findings reveal a coordinated remodeling of brain waste-handling structures driven by aging and amyloid pathology, highlighting dynamic glial responses that may contribute to altered proteostasis in Alzheimer’s disease.
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