al., 2017). Another study ascribes a neurotoxic function for APOE4 that can be ameliorated with a small-molecular structure corrector, predicting a novel and potentially protective AD therapy (Wang et al., 2018). An innovative single-cell analytical platform for detecting secreted Aβ and soluble amyloid precursor protein-alpha (sAPPα) revealed heterogeneity in secretion profiles from cells harboring APP mutations (Liao et al., 2016). These include subpopulations of cells that secret high levels of Aβ, but not sAPPα, cells that secret both Aβ and sAPPα (enriched for GABAergic markers), and cells that secret Aβ levels (enriched for astrocyte markers) (Liao et al., 2016). Finally, 3D organoid models of AD have been able to recapitulate both amyloid deposition, and hyperphosphorylated tau accumulation in somato-dendritic compartments, both from patients with familial mutations (Raja et al., 2016) and from patients with late onset disease (Lee et al., 2016).
