Intracellular amyloid-β in Alzheimer's disease

By F. LaFerla, K. Green, S. Oddo. Nature Reviews Neuroscience, 2007

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Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “…had suggested that significant amounts of APP were processed to Aβ intracellularly (Greenfield et al. 1999), and evidence provides support for BACE1 in the TGN (Huse et al. 2002) and for intracellular Aβ accumulation in neurons from patients with early AD (Gouras et al 2000; LaFerla et al 2007).”
Pathological roles of MAPK signaling pathways in human diseases. (2010, background): “Amyloidogenic Aβ is produced by β-secretase-mediated cleavage of APP at amino acid 83, whereas non-amyloidogenic Aβ, which is not toxic to neurons, is generated by α-secretase-mediated APP cleavage at amino acid 99 [24,25].”
Autophagy, amyloidogenesis and Alzheimer disease (2007, background): “In its pathologic oligomeric state, A exerts a range of cytotoxic actions considered important to the evolution of neurodegeneration in AD (Selkoe, 2001; Watson et al., 2005; Small et al., 2001; Laferla et al., 2007; Lee et al., 2006).”