Axonal organelle buildup from loss of AP-4 complex function causes exacerbation of amyloid plaque pathology and gliosis in Alzheimers disease mouse model (Updated November 11, 2024).

The article discusses how the loss of Adaptor protein-4 (AP-4) complex function can lead to an increase in lysosome buildup in axons, exacerbating amyloid plaque pathology and gliosis in an Alzheimer's disease mouse model. The study found that the loss of AP-4 complex function resulted in larger and more abundant amyloid plaques in specific brain regions, such as the hippocampus and corpus callosum, while also increasing microglial association with the plaques. This research highlights the critical role of AP-4-dependent axonal lysosome transport in regulating amyloid precursor protein processing. [Extracted from the article]

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