Reticulons and β-secretase

Wataru Araki

Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP

　　Cerebral accumulation of amyloid β-protein (Aβ) is the main pathological feature of Alzheimer’s disease (AD).　β-Secretase cleavage of amyloid precursor protein (APP) is catalyzed by the membrane-bound aspartyl protease BACE (β-site APP cleaving enzyme).　Inhibition of BACE is one of the attractive therapeutic approaches for AD.　Recently, we and others identified Nogo-B (reticulon 4-B) and its homologue reticulon 3 as BACE-interacting membrane proteins.　These reticulon family proteins appear to negatively modulate Aβ production through physical association with BACE.　The role of reticulon proteins in the regulation of BACE function is discussed.

Address correspondence to Dr. Wataru Araki, Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP (4-1-1, Ogawahigashi, Kodaira, Tokyo 187-8502, Japan)