Although brain and CSF levels of BACE1 have been found to be elevated in AD patients and to correlate with brain amyloid load and decrease in hippocampus volume, and though increased generation of amyloid β is clearly the driving pathogenic factor in early-onset AD patients carrying certain variant genes, a classic study comparing brain turnover of amyloid β in patients with sporadic AD and healthy controls concluded that a diminished capacity to catabolize or export amyloid β is the chief reason why amyloid β accumulates in the brain of sporadic AD patients [145,146,147,148,149,150]. Here, BACE1 is linked to Alzheimer disease.