LYZL4 and Alzheimer disease: Finally, Aβ is taken up by endosomes, which ultimately fuse with autophagosomes/lysosomes for degradation.[33] A failure to degrade aggregated Aβ1–42 in late endosomes or secondary lysosomes is a mechanism known to contribute to the intracellular accumulation of Aβ in AD.[34] In order to investigate the potential mechanisms by which Lyzl4 promotes the degradation of Aβ in microglia, we infected primary microglia cultured on coverslips with pLVX‐IRES‐tdTomato lentivirus and treated them with a 2 μm Aβ oligomer solution.