Since we have previously shown that Aβ34 is a common intermediate in the enzymatic processing of two distinct Aβ degradation pathways6, the present study examines the levels and metabolism of Aβ34 in the brains of BACE1-deficient mice, in brain and CSF of rats treated with a BACE1-specific inhibitor, a cultured human neuronal cell line (SH-SY5Y), and CSF samples from individuals at various clinical stages of AD. Here, BACE1 is linked to Alzheimer disease.