Fibrillar Aβ causes profound microglial metabolic perturbations in a novel APP knock-in mouse model

Abstract excerpt

Microglial dysfunction is believed to play a pathogenic role in Alzheimer’s disease (AD). Here, we characterize the amyloid-β related pathology and microglial responses in an engineered APP knock-in mouse model of familial AD. This model recapitulates key pathological features of AD such as a progressive accumulation of parenchymal amyloid plaques and vascular amyloid deposits, altered glial responses and neurodeg...

Topics

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• Alzheimer's disease research and treatments
• Amyloid beta-Peptides
• Amyloid beta-Protein Precursor
• Calcium-Binding Proteins
• Cerebral Cortex
• Laser Capture Microdissection
• Neuroinflammation and Neurodegeneration Mechanisms
• Plaque, Amyloid

Identifiers and source

Literature Corpus work

a4e8ffd8-e5a8-5a74-9385-c6cc586089fa

DOI

10.1101/2021.01.19.426731