APP fragment can regulate production of beta amyloid
Wednesday 11 April 2012
In its healthy state, APP is thought to be involved in synaptic formation and repair. In Alzheimer's disease, APP degenerates and produces beta amyloid (the primary component of amyloid plaque) and also sAPP-α.
Clearly, high levels of beta amyloid are toxic. However, high levels of sAPP-α appear to be beneficial: the researchers showed that reduction of sAPP-α led to an increase of beta amyloid activity.
This is due to the interaction between sAPP-α and the BACE1 enzyme. BACE1 (beta-secretase) initiates the formation of beta amyloid, while sAPP-α reduces or blocks this activity.
The research team, led by Dr. Jun Tan, Professor of Psychiatry, continues to investigate ways of monitoring and adjusting sAPP-α levels, as well as enhancing its association with BACE1.