3.4.23.45	drug development	therapeutic interventions that potentiate BACE2 may prevent Alzheimer’s disease	
3.4.23.45	medicine	samples from frontal cortex of both Alzheimer's disease-affected individuals and age-matched controls show substantial total amounts of BACE2 protein and enzymatic activity. BACE2 activity does not change significantly in the brain of patients with Alzheimer's disease, and is not related to amyloid beta-peptide concentration	
3.4.23.45	medicine	in patients with preclinical to late-stage Alzheimer's disease, including amnestic mild cognitive impairment, and age-matched controls, cases of frontotemporal dementia, and Down's syndrome, BACE2 protein and enzymatic activity increase as early as preclinical Alzheimer's disease and are found in neurons and astrocytes. Although the levels of total BACE2 mRNA are unchanged, the mRNA for BACE2 splice form C (missing exon 7) increases in parallel with BACE2 protein and activity. BACE1 and BACE2 are strongly correlated with each other at all levels. BACE2 is also elevated in frontotemporal dementia but not in Down's syndrome, even in patients with substantial amyloid beta deposition	
3.4.23.45	medicine	enzyme inhibition is a treatment of type 2 diabetes	
3.4.23.45	pharmacology	the enzyme is a potential target for development of inhibitors in Alzheimer's disease therapy and treatment of Down syndrome