ArticleResearch square2026
Non-compacted, PET-insensitive amyloid states increase after systemic inflammation and predict neuritic damage across Aβ pathology models and Alzheimer patients.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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23 authors.
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Abstract
Neuroinflammation is a key modulator of Alzheimer's disease (AD) risk, yet the impact of non-genetic inflammatory risk factors - such as systemic inflammation - remains poorly defined. Building on our previous work, here we show that 9 months after systemic lipopolysaccharide (LPS) challenge in APP23 mice, microglia-plaque interaction is disturbed and shifts Aβ aggregates toward a less compacted state, as revealed by conformation-sensitive amyloid dyes. Importantly, these structural changes are associated with increased plaque-associated neuritic dystrophy, phenocopying the effects of microglial risk genes. Generalising these findings, we show that across aging in APP23 and APPPS1 mice, and in AD patient tissue, non-compacted amyloid and microgliosis - but not compacted amyloid - are consistent predictors of neuritic damage. Notably, both in mouse and human tissue,
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