Role of sorLA in trafficking and processing of APP

Principal Investigator

Project Summary

A hallmark of the brain in Alzheimer's disease is the occurrence of “plaques,” dense deposits of proteinaceous material that are toxic to nerve cells. Plaques are mainly composed of a small peptide called the amyloid-beta (Aβ), which is derived from a larger protein in nerve cells, the amyloid precursor protein (APP). Dr. Anderson has identified a novel protein in nerve cells called sorLA that seems to play an important role in the APP breakdown into Aβ. His studies suggest that sorLA prevents APP from going into specific compartments of the nerve cell where breakdown into Aβ occurs. He believes that raising sorLA levels will prevent Aβ production, and therefore significantly decrease, or even eliminate, plaque accumulation in the brain. If confirmed, Dr. Anderson's studies could be used to develop new ways to combat Alzheimer's disease through drugs designed to increase sorLA levels in the brain.


Andersen, O.M. and Willnow, T.E. (2006) Lipoprotein receptors in Alzheimer's disease. Trends Neurosci. Dec;29(12):687-94.  

Willnow, T.E. and Andersen, O.M. (2006) Pin-pointing APP processing. Mol. Interv. Jun;6(3):137-9.  

Andersen, O.M., Schmidt, V., Spoelgen, R., Gliemann, J., Behlke, J., Galatis, D., McKinstry, W.J., Parker, M.W., Masters, C.L., Hyman, B.T., Cappai, R. and Willnow, T.E. (2006) Molecular dissection of the interaction between amyloid precursor protein and its neuronal trafficking receptor SorLA/LR11. Biochemistry. Feb 28;45(8):2618-28.  

First published on: June 11, 2008

Last modified on: February 25, 2024