ESR 9 vision / project
Contribution of the BBB in amyloid-b biology in Alzheimer’s disease
We show that BACE-1, the proteinase generating neurotoxic β-amyloid (Aβ), is expressed in BBB ECs and
becomes up-regulated in an AD mouse model. Hence we hypothesize that BACE-1 at the BBB contributes to AD
pathogenesis by Aβ production, leading to BBB dysfunction.
Aim 1: Investigate the factors regulating BACE-1 expression and function at the BBB
Aim 2: Evaluate the role of BACE-1 for APP processing at the BBB in transgenic mouse models
Aim 3: Investigate the impact of BACE-1 at the BBB on drugs targeting BACE-1 in AD
Aim 1: To identify pathways to be involved in BACE-1 regulation at the BBB.
Aim 2: To identify the contribution of endothelial BACE-1 to AD and CAA pathogenesis, and to identify AD-relevant genes regulated in mice deficient in endothelial BACE-1 (BACE-1∆bEC).
Aim 3: To identify the value of endothelial BACE-1 inhibition as a therapeutic target.
Johann Wolfgang Goethe University Frankfurt, Edinger-Institute Neurology, Germany
Main SupervisorStefan Liebner
Early Stage Researcher