Article

Non-compacted, PET-insensitive amyloid states increase after systemic inflammation and predict neuritic damage across Aβ pathology models and Alzheimer patients

2026-01-13

Abstract excerpt

<title>Abstract</title> <p>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...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 3c4d7949-54cd-51d1-b7f0-77052b65ce78
DOI: 10.21203/rs.3.rs-8269406/v1

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Non-compacted, PET-insensitive amyloid states increase after systemic inflammation and predict neuritic damage across Aβ pathology models and Alzheimer patientsDOI 10.21203/rs.3.rs-8269406/v1Read

Whole-Brain Single-Neuron Atlas Reveals Microglial Security Hole Accelerating Neuronal VulnerabilitySemantic proximity Read

APOE4 Drives Uniquely Dysfunctional Human Microglial States in Alzheimer’s DiseaseSemantic proximity Read

Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.Semantic proximity Read

Mouse and human microglial phenotypes in Alzheimer’s disease are controlled by amyloid plaque phagocytosis through Hif1αSemantic proximity Read

Microglia-Associated Neuroinflammation in Alzheimer’s DiseaseSemantic proximity Read

Microglia determine ß-amyloid plaque burden but are non-essential for downstream pathologySemantic proximity Read

Phagocytes as Plaque Catalysts: Human Macrophages Actively Generate Pathogenic Aβ42 Fibrils with Seeding and Cross-Seeding PotencySemantic proximity Read

Rethinking Anti-Inflammatory Therapy in Alzheimer’s Disease: From Broad Suppression to Stage–State–Space Neuroimmune ReprogrammingSemantic proximity Read

Galectin-3 drives neuroinflammatory amyloid remodeling by stabilizing intermediate Aβ species and altering lysosomal processingSemantic proximity Read

Hypothesis: Modulation of microglial phenotype in Alzheimer's disease drives neurodegeneration.Semantic proximity Read

Microglia phenotypes are associated with subregional patterns of concomitant tau, amyloid-β and α-synuclein pathologies in the hippocampus of patients with Alzheimer's disease and dementia with Lewy bodies.Semantic proximity Read

The Hidden Role of Non-Canonical Amyloid β Isoforms in Alzheimer’s DiseaseSemantic proximity Read